Hasil Pencarian  ::  Simpan CSV :: Kembali

Abstrak :
Sindrom metabolik disebabkan oleh pola makan yang tidak sehat seperti diet tinggi lemak, karbohidrat dan fruktosa serta gaya hidup yang menetap. Hal tersebut menyebabkan akumulasi lemak pada berbagai jaringan. Obesitas menyebabkan akumulasi lemak baik di jaringan adiposa dan nonadiposa, salah satunya pada ginjal. Akumulasi lemak yang berlebih pada ginjal menyebabkan disfungsi seluler. Salah satu mekanisme yang menyebabkannya adalah peningkatan stres oksidatif. Tujuan penelitian ini yaitu untuk mengevaluasi efek 6-gingerol terhadap perbaikan fungsi ginjal akibat sindrom metabolik dengan pemberian diet tinggi lemak, fruktosa 55% dan streptozotocin pada tikus. Tikus yang diinduksi menjadi sindrom metabolik (SM) akan diberikan 6-Gingerol dosis 50 mg/kgBB, 100 mg/kgBB dan 200 mg/kgBB selama 8 minggu. Hewan coba dilakukan terminasi setelah 8 minggu pemberian 6-gingerol, lalu dilakukan pengambilan organ, urin dan darah untuk dianalisis parameter ekspresi gen NADPH Oksidase-4 (NOX-4), NADPH Oksidase (NOX-2), P47phox , aktivitas Glutathione peroksidase (GPx), kadar Malondialdehyde (MDA), klirens kreatinin, urea serum, aktivitas N-acetyl-β-Dglukosaminidase (NAG), kadar protein urin dan histopatologi ginjal dengan pewarnaan Hemaktosilin & Eosin dan Masson trichrome. Hasil dari penelitian ini menunjukkan bahwa pemberian 6-gingerol dosis 100 mg/kgBB dan 200 mg/kgBB dapat menurunkan ekspresi gen NOX-4, P47phox, dan meningkatkan aktivitas GPx walaupun kadar MDA tidak menurun. Pemberian 6-gingerol dosis 200 mg/kgBB dapat meningkatkan klirens kreatinin, menurunkan aktivitas NAG urin dan menurunkan kadar protein urin. 6-Gingerol dosis 100 mg/kgBB dan 200 mg/kgBB dapat menurunkan total akumulasi lemak, menurunkan tubulointetstisial inflamasi dan memperbaiki penebalan membran glomerulus secara histopatologi. Namun tidak dapat menurunkan fibrosis pada tubulointerstisial. Berdasarkan dari hasil penelitian, maka 6-gingerol memiliki potensi dalam memperbaiki kondisi stres oksidatif dan fungsi ginjal pada tikus sindrom metabolik. ......Metabolic syndrome is caused by unhealthy eating patterns such as high fat, carbohydrates, and fructose diets as well as a sedentary lifestyle. This causes fat accumulation in various tissues. Obesity causes fat accumulation in both adipose and non-adipose tissue, which is the kidneys. Excessive fat accumulation in the kidneys causes cellular dysfunction. One mechanism that causes is increased oxidative stress. This study aimed to evaluate the effect of 6-gingerol on the improvement of kidney function due to metabolic syndrome by administering a high-fat diet, 55% fructose, and streptozotocin to rats. Rats that are induced to develop the metabolic syndrome will be given 6-gingerol at doses of 50 mg/kgBW, 100 mg/kgBW, and 200 mg/kgBW for 8 weeks. The experimental animals were terminated after 8 weeks of 6-gingerol administration, then organs, urine, and blood were taken to determine the gene expression parameters of NADPH Oxidase-4 (NOX-4), NADPH Oxidase (NOX-2), P47phox, Glutathione peroxidase (GPx) activity, Malondialdehyde (MDA) levels, creatinine clearance, serum urea, Nacetyl-β-D-glucosaminidase (NAG) activity, urine protein levels, and kidney histopathology with Hematoxylin & Eosin and Masson trichrome staining. The results of this study show that administration of 6-gingerol at doses of 100 mg/kgBW and 200 mg/kgBW can reduce the expression of the NOX-4, P47phox genes, and increase GPx activity even though MDA levels do not decrease. Administration of 6-gingerol at a dose of 200 mg/kgBW can increase creatinine clearance, reduce urinary NAG activity, and reduce urinary protein levels. 6- Gingerol at 100 mg/kgBW and 200 mg/kgBW can decrease total fat vacuoles, decrease tubulointerstitial inflammation, and improve histopathological glomerular membrane thickening even though tubulointerstitial fibrosis do not decrease. Based on the research results, 6-gingerol has the potential to improve oxidative stress conditions and kidney function in metabolic syndrome rat.

Abstrak :
[ABSTRAK
Latar Belakang: Penyakit ginjal kronik (PGK) merupakan penyakit progresif dan ireversibel yang mempunyai berbagai komplikasi serius serta belum ada terapi yang dapat memperbaiki kerusakan ginjal yang telah terjadi. Beberapa studi menunjukkan stres oksidatif berperan dalam patogenesis penyakit ini. Stres oksidatif terjadi akibat ketidakseimbangan produksi ROS dan pertahanan antioksidan. Nrf2 merupakan faktor transkripsi yang terlibat dalam mekanisme pertahanan sel dalam mengatasi stres oksidatif. Penelitian ini bertujuan untuk mengetahui aktivitas kuersetin sebagai aktivator Nrf2 dalam menghambat progresivitas penyakit ginjal yang diinduksi nefrektomi 5/6. Metode: Tikus Sprague-Dawley jantan dikelompokkan secara acak dalam kelompok kontrol normal (C), kontrol nefrektomi 5/6 (Nx), nefrektomi 5/6 yang diberi kuersetin dengan dosis 100 mg/kgbb/hari/p.o. (NxQ), nefrektomi 5/6 dan diberi kaptopril dengan dosis 10 mg/kgbb/hari/p.o. (NxK). Hewan coba diterminasi diakhir perlakuan untuk diambil darah, urin, dan organ ginjalnya. Pemeriksaan yang dilakukan adalah pemeriksaan proteinuria, kreatinin urin dan plasma, ureum plasma, kadar MDA plasma dan jaringan, aktivitas glutation peroksidase (GPx), kerusakan jaringan (histopatologi) dan ekspresi Nrf2 (imunohistokimia). Hasil: Hasil penelitian menunjukkan bahwa nefrektomi 5/6 dapat menimbulkan peningkatan proteinuria, ureum plasma, dan derajat fibrosis ginjal secara signifikan. Nefrektomi 5/6 cenderung meningkatkan kreatinin plasma, kadar MDA ginjal, aktivitas GPx, dan menurunkan MDA plasma serta ekspresi Nrf2. Kuersetin tidak mempengaruhi proteinuria, ureum dan kreatinin plasma, dan derajat fibrosis ginjal. Kuersetin cenderung menurunkan kadar MDA dan meningkatkan aktivitas enzim GPx serta ekspresi Nrf2. Kesimpulan: Kuersetin tidak mempengaruhi proteinuria, ureum dan kreatinin plasma serta kerusakan struktur jaringan atau fibrosis ginjal. Kuersetin cenderung menurunkan kadar MDA dan meningkatkan aktivitas enzim GPx serta cenderung meningkatkan ekspresi Nrf2.

---

ABSTRACT
Background: Chronic Kidney Disease (CKD) is a progressive and irreversible condition that has several serious complications and currently there has no single therapy that can repair kidney damage was occurred. Some studies suggest a role of oxidative stress in the pathogenesis of this disease. Oxidative stress is caused by an imbalance of ROS production and antioxidant defenses. Nrf2 is a transcription factor involved in cell defense mechanisms againts oxidative stress. This study was aimed to determine the quercetin activity as Nrf2 activator in inhibit the progression of 5/6 nephrectomy induced CKD in male rats. Method: Sprague-Dawley rats were randomly divided into normal control group (C), untreated 5/6 nephrectomy (Nx), quercetin-treated 5/6 nephrectomy, NxQ (100 mg / kg / day orally), captopril-treated 5/6 nephrectomy, NxK (10 mg / kg / day orally). Animal models was sacrificed at the end of intervention to take blood to measure creatinine, urea, and MDA, urine to measure protein and creatinine, and kidney organ to measure levels of MDA, glutathione peroxidase (GPx) activity, and renal damage (histopathology) and Nrf2 expression (immunohistochemistry). Results: The results showed that 5/6 nephrectomy may cause an increased of proteinuria, plasma urea, and grade of renal fibrosis significantly. 5/6 nephrectomy has trend to increased plasma creatinine, renal MDA levels, GPx activity, and decreased plasma MDA and Nrf2 expression. Quercetin did not decrease proteinuria, plasma urea and creatinine, and renal fibrosis grading. Quercetin tend to reduced levels of MDA, increased GPx enzyme activity, and expression of Nrf2. Conclusion: Quercetin does not affect proteinuria, plasma urea,plasma creatinine, and tissue damage or kidney fibrosis. Quercetin tend to reduced levels of MDA and increased the activity of GPx and Nrf2 expression.;Background: Chronic Kidney Disease (CKD) is a progressive and irreversible condition that has several serious complications and currently there has no single therapy that can repair kidney damage was occurred. Some studies suggest a role of oxidative stress in the pathogenesis of this disease. Oxidative stress is caused by an imbalance of ROS production and antioxidant defenses. Nrf2 is a transcription factor involved in cell defense mechanisms againts oxidative stress. This study was aimed to determine the quercetin activity as Nrf2 activator in inhibit the progression of 5/6 nephrectomy induced CKD in male rats. Method: Sprague-Dawley rats were randomly divided into normal control group (C), untreated 5/6 nephrectomy (Nx), quercetin-treated 5/6 nephrectomy, NxQ (100 mg / kg / day orally), captopril-treated 5/6 nephrectomy, NxK (10 mg / kg / day orally). Animal models was sacrificed at the end of intervention to take blood to measure creatinine, urea, and MDA, urine to measure protein and creatinine, and kidney organ to measure levels of MDA, glutathione peroxidase (GPx) activity, and renal damage (histopathology) and Nrf2 expression (immunohistochemistry). Results: The results showed that 5/6 nephrectomy may cause an increased of proteinuria, plasma urea, and grade of renal fibrosis significantly. 5/6 nephrectomy has trend to increased plasma creatinine, renal MDA levels, GPx activity, and decreased plasma MDA and Nrf2 expression. Quercetin did not decrease proteinuria, plasma urea and creatinine, and renal fibrosis grading. Quercetin tend to reduced levels of MDA, increased GPx enzyme activity, and expression of Nrf2. Conclusion: Quercetin does not affect proteinuria, plasma urea,plasma creatinine, and tissue damage or kidney fibrosis. Quercetin tend to reduced levels of MDA and increased the activity of GPx and Nrf2 expression., Background: Chronic Kidney Disease (CKD) is a progressive and irreversible condition that has several serious complications and currently there has no single therapy that can repair kidney damage was occurred. Some studies suggest a role of oxidative stress in the pathogenesis of this disease. Oxidative stress is caused by an imbalance of ROS production and antioxidant defenses. Nrf2 is a transcription factor involved in cell defense mechanisms againts oxidative stress. This study was aimed to determine the quercetin activity as Nrf2 activator in inhibit the progression of 5/6 nephrectomy induced CKD in male rats. Method: Sprague-Dawley rats were randomly divided into normal control group (C), untreated 5/6 nephrectomy (Nx), quercetin-treated 5/6 nephrectomy, NxQ (100 mg / kg / day orally), captopril-treated 5/6 nephrectomy, NxK (10 mg / kg / day orally). Animal models was sacrificed at the end of intervention to take blood to measure creatinine, urea, and MDA, urine to measure protein and creatinine, and kidney organ to measure levels of MDA, glutathione peroxidase (GPx) activity, and renal damage (histopathology) and Nrf2 expression (immunohistochemistry). Results: The results showed that 5/6 nephrectomy may cause an increased of proteinuria, plasma urea, and grade of renal fibrosis significantly. 5/6 nephrectomy has trend to increased plasma creatinine, renal MDA levels, GPx activity, and decreased plasma MDA and Nrf2 expression. Quercetin did not decrease proteinuria, plasma urea and creatinine, and renal fibrosis grading. Quercetin tend to reduced levels of MDA, increased GPx enzyme activity, and expression of Nrf2. Conclusion: Quercetin does not affect proteinuria, plasma urea,plasma creatinine, and tissue damage or kidney fibrosis. Quercetin tend to reduced levels of MDA and increased the activity of GPx and Nrf2 expression.]

Abstrak :
Pemanfaatan teknologi nuklir terutama radiasi gamma telah menjadi bagian penting di bidang kedokteran. Radiasi gamma dapat menghasilkan spesies oksigen reaktif (ROS) yang menyebabkan kerusakan biologis pada sel normal. Antioksidan adalah senyawa kimia yang dapat mencegah reaksi berantai radikal bebas. Pada penelitian ini dilakukan eksplorasi kemampuan dari bawang putih, petai, jengkol, tomat dan NAC dalam melindungi sel tehadap radiasi gamma. Kelompok perlakuan terdiri atas: A (kontrol), B (radiasi), C (bawang putih+radiasi), D (petai+radiasi), E (jengkol+radiasi), F (tomat+radiasi) dan G (NAC+radiasi). Tiap kelompok terdiri atas 4 ekor tikus jantan. Paparan radiasi gamma dilakukan setelah pemberian bahan alam selama 8 hari berturut-turut. Uji biokimia berupa pengukuran konsentrasi Malondialdehid (MDA), Glutation (GSH), 8-hidroksi-2-deoksiguanosin (8-OHdG), aktivitas spesifik Glutation Peroksidase (GPx), Katalase (CAT) serta uji immunofluoresensi foci γH2AX pada limfosit dan plasma. Hasil penelitian menunjukkan bahwa paparan radiasi gamma dapat menyebabkan peningkatan signifikan pada konsentrasi MDA, GSH, 8-OHdG dan jumlah foci γH2AX serta penurunan signifikan pada aktivitas spesifik GPx dan CAT (p<0.05). Sementara itu, pemberian ekstrak bawang putih, jengkol, tomat dan NAC mampu secara signifikan mengurangi radikal bebas akibat radiasi gamma. Kesimpulan dari penelitian ini adalah bawang putih, jengkol, tomat dan NAC mampu melindungi tikus terhadap stres oksidatif akibat radiasi gamma. ......Application of nuclear technology, especially gamma radiation, has become an important part of the medical field. Gamma radiation exposure can produce reactive oxygen species (ROS) which cause biological damage to normal cells. Antioxidants are chemical compounds that can prevent free radical chain reaction. This study has been focused to explore the capability some materials of garlic, petai, jengkol, tomatoes and N-acetylcystein (NAC) in counteracting free radicals caused by gamma radiation. This research was divided into 7 treatment groups, namely A (control), B (radiation), C(garlic+radiation), D(petai+radiation), E(jengkol+radiation), F(tomato+radiation) and G(NAC+radiation). Each group consists of 4 male rats. The irradiation were given after 8 days the suplement had been given. Detection of  malondialdehyde (MDA), glutathione (GSH), glutathione peroxidase (GPx), catalase (CAT), 8-hydroxy-2-deoxyguanosine (8-OHdG) by biochemical, and γ-H2AX foci by immunoflouresence assay were made from lymphocytes and plasma. The results showed that gamma radiation cause a significant increase in MDA, GSH, 8-OHdG concentration and the number of foci γH2AX and a significant decrease in GPx and CAT specific activity (p <0.05). Giving garlic extract, jengkol bean, tomato and NAC can significantly reduce free radicals due to gamma radiation. The conclusion is garlic, jengkol bean, tomato and NAC can protect mice against oxidative stress due to gamma radiation.

Abstrak :
ABSTRAK
Endometriosis merupakan penyakit ginekologi ditandai dengan implantasi jaringan endometrium di luar rongga uterus, berhubungan erat dengan proses inflamasi kronis. Stres oksidatif menjadi aktivator terjadinya proses inflamasi kronis di endometriosis. Oktil galat terbukti lebih efektif menekan proses inflamasi dibandingkan asam galat dan heptil galat pada sel kultur primer endometriosis. Penelitian ini bertujuan menganalisis pengaruh oktil galat pada proses inflamasi dan stres oksidatif pada tikus Wistar model endometriosis. Tiga puluh ekor tikus Wistar dibagi menjadi tiga kelompok, yaitu kelompok uji, kontrol endometriosis dan kelompok normal. Kelompok uji dilakukan autotransplantasi lalu diberikan suspensi oktil galat dan CMC selama satu bulan. Kelompok endometriosis dilakukan autotransplantasi lalu diberikan larutan CMC selama satu bulan, sedangkan kelompok normal hanya dilakukan laparotomi. Seluruh tikus kemudian dieuthanasia, dari kelompok uji dan kontrol endometriosis diambil jaringan endometriosisnya sedangkan dari kelompok sehat diambil jaringan endometriumnya untuk dianalisis. Analisis MDA (Malondialdhyde) dan SOD (Superoxide Dismutase) dilakukan secara spektofotometri, kadar NF-ĸB dengan ELISA dan IL-1β (Interleukin-1 Beta) dengan LUMINEX. Pemberian oktil galat pada kelompok uji tidak menurunkan kadar MDA namun berpotensi menekan kondisi stres oksidatif dengan meningkatkan kadar SOD. Oktil galat terbukti menekan aktivasi NF-ĸB secara signifikan, namun tidak menekan kadar IL-1β. Oktil galat berperan sebagai antiinflamasi pada tikus Wistar model endometriosis dengan cara induksi peningkatan SOD dan hambatan langsung pada translokasi nuklear NF-ĸB.

---

ABSTRACT
Endometriosis is a gynecological disease characterized by the implantation of endometrial tissue outside the uterine cavity, related to the chronic inflammatory process. Oxidative stress activates the occurrence of chronic inflammatory in endometriosis. Octyl gallate is more effective in suppressing the inflammatory process than gallic acid and heptil gallate in primary endometriosis culture cells. This study aimed to analyze the effect of octyl gallate on the inflammatory process and oxidative stress in endometriosis Wistar rat models. 30 Wistar rats were divided into three groups, the test group, endometriosis control and normal groups. The test group was autotransplantated and then given a suspension of octyl galate and CMC for one month. The endometriosis group was autotransplanted and then given a CMC solution for one month, while the normal group only underwent laparotomy. All rats were then euthanized, from the test and endometriosis group the endometriosis tissue was taken while from the normal group endometrial tissue was taken for analysis. MDA and SOD were measured using spectrophotometry, NF-ĸB with ELISA and IL-1β with LUMINEX. Induction of octyl gallate in the test group did not reduce MDA levels but could potentially suppress oxidative stress conditions by increasing SOD levels. Octyl gallate significantly inhibit the NF-ĸB activation, but not suppressing IL-1β levels significantly. Octyl gallate act as anti-inflammatory agent in endometriosis Wistar rat model through the enhancement of SOD and direct inhibition to nuclear translocation of NF-ĸB.

Abstrak :
Latar Belakang: Salah satu penyebab kematian pada pasien penyakit ginjal kronis adalah gangguan kardiovaskular. Adanya hipertrofi pada ventrikel kiri dijadikan surrogate marker kondisi kardiomiopatik dan progresivitas penyakit ginjal kronis. Penelitian terbaru menunjukkan adanya peran FGF23 dalam menstimulasi terjadinya hipertrofi jantung dan meningkatkan aktivitas sistem renin-angiotensin-aldosteron serta berfungsi sebagai faktor parakrin dengan peran dalam remodelling jantung. Metode: Penelitian ini dilakukan dengan menggunakan tikus model nefrektomi 5/6 yang diberikan terapi irbesartan, simvastatin dan kombinasi keduanya selama satu bulan. Tekanan darah diukur pada saat sebelum dan sesudah pemberian obat. Tikus kemudian ditempatkan pada kandang metabolik selama 24 jam untuk pengambilan urin. Nekropsi dilakukan untuk mengambil darah dan jantung. Pemeriksaan yang dilakukan antara lain pemeriksaan indeks massa ventrikel kiri jantung, volume dan kadar protein dalam urin, kadar urea dan kreatinin dalam serum, serta kadar FGF23 dan hormon PTH dalam serum. Hasil: Hasil dari pemeriksaan tersebut menunjukkan bahwa penggunaan irbesartan dapat menurunkan tekanan darah dan indeks massa ventrikel kiri secara signifikan. Penggunaan irbesartan, simvastatin dan kombinasi keduanya tidak menunjukkan penurunan yang signifikan terhadap hasil pemeriksaan fungsi ginjal, kadar hemoglobin, indeks massa ventrikel kiri, FGF23 dan hormon paratiroid. Kesimpulan: Dari hasil penelitian ini, dapat disimpulkan bahwa baik penggunaan irbesartan, simvastatin, maupun keduanya memiliki kecenderungan untuk mengurangi kejadian kardiomiopatik uremik pada tikus model nefrektomi 5/6 ......Introduction: Cardiovascular events is one of the causes of chronic renal disease’s mortality. Left ventricular hypertrophy was a surrogate marker for cardiomyopathy and progressivity of chronic renal disease. Latest study mentioned about the role of FGF23 on stimulating cardiac hypertrophy and renin-angiotensin-aldosterone activity and also a paracrine factor of cardiac remodeling. Methods: This study was done using 5/6 nephrectomy rats getting irbesartan, simvastatin and combination of both treatments for 30 days. Blood pressure was measured before and after the treatment. Urine sample was collected for 24 hours for protein assay. Sacrificing the animals was done at the end of study to harvest the heart and blood sample. Heart sample was weighed and measured for left ventricle mass index. Blood sample was used for hemoglobin assay. Serum sample was used for urea, creatinine, FGF23 and PTH assay. Result: Irbesartan significantly lowered the blood pressure and cardiac mass index, but not significantly improved renal function, hemoglobin level, left ventricular mass index, FGF23 and PTH hormone. Simvastatin and combination of both treatments did not significantly improve renal function, hemoglobin level, left ventricular mass index, FGF23 and PTH hormone. Conclusion: The use of irbesartan, simvastatin and both combinations tend to improve uremic cardiomyopathy condition on 5/6 nephrectomy rats’ heart.

Abstrak :
Efek lunasin sebagai anti-inflamasi, antioksidan, anti kanker dan anti metastasis telah lama diketahui. Lunasin melalui motif RGD pada strukturnya dapat berikatan dengan integrin dan menghambat jalur persinyalan FAK/Src/ERK/NFkB sehingga aktivasi NF-kB menurun. Hal ini akan menyebabkan penurunan aktifitas proliferasi dan peningkatan apoptosis. Penelitian ini bertujuan untuk mempelajari efek lunasin dalam menghambat karsinogenesis kolorektal dan mempelajari protein-protein yang terlibat dalam mekanisme tersebut. Penelitian ini menggunakan bahan biologi tersimpan (BBT) blok parafin jaringan kolon mencit BALB/c yang diinduksi AOM dan DSS yang terdiri dari 6 kelompok yaitu kelompok normal yang tidak diinduksi dan diberi perlakuan, kelompok kontrol negatif yang hanya diinduksi AOM dan DSS, kelompok kontrol positif yang diinduksi dan diberi aspirin, kelompok lunasin dosis rendah, sedang dan tinggi masing-masing yang diinduksi dan diberi lunasin 75, 150 dan 200 mg/BB. Jaringan kolon hewan diambil dan dilakuan pulasan hematoksilin eosin dan imunohistokimia untuk mengukur ekspresi Ki67, C-myc dan Bcl-2. Kuantifikasi ekspresi Ki67, C-myc dan Bcl-2 dari hasil pulasan imunohistokimia dilakukan dengan menggunakan metode H-score. Data H-score diolah dan dianalisa menggunakan uji statistik Kruskall Wallis. Ekspresi Ki67, C-myc dan Bcl-2 berbeda signifikan pada setiap kelompok (p=0,000). Lunasin dapat menurunkan ekspresi Ki67, C-myc dan Bcl-2 pada kolon model hewan karsinogenesis kolorektal yang diinduksi AOM dan DSS. ...... The effects of Lunasin as anti-inflammatory, antioxidant, anti-cancer and antimetastatic effects have long been known. Lunasin through the RGD motive on its structure can bind to integrins and inhibit the FAK/Src/ERK/NF-kB signaling pathway and supress NF-kB activation. It causes decreasing of proliferative activity and increasing of apoptosis. This study aims to study the effect of lunasin in inhibiting colorectal cancer carcinogenesis and investigate the proteins involved in this mechanism. This study used stored biological material (BBT), paraffin blocks, colon tissue of BALB/c mice induced by AOM and DSS which consisted of 6 groups, the normal group that was not induced and treated, the negative control group that was only induced by AOM and DSS, the positive control group. who were induced and given aspirin, the low, medium and high dose lunasin groups were induced and given lunacin 75, 150 and 200 mg/kgBW, respectively. Colon tissue was taken and stained with hematoxylin eosin and immunohistochemistry to measure the expression of Ki67, C-myc and Bcl-2. The quantification of Ki67, C-myc and Bcl-2 expressions from the results of immunohistochemical stains was done using the H-score method. The H-score data were processed and analyzed using the Kruskall Wallis statistical test. Expressions of Ki67, C-myc and Bcl-2 were significantly different in each group (p = 0.000). Lunasin can decrease the expression of Ki67, C-myc and Bcl-2 in colon animal models of AOM and DSS-induced colorectal cancer.

Abstrak :
Ibu hamil yang bekerja di tempat yang bising dapat secara langsung merasakan efek dari kebisingan tersebut. Kebisingan tersebut bukan hanya mempengaruhi ibu hamil tetapi juga janin yang dikandungnya. Terdapat banyak studi yang membuktikan efek negatif bising terhadap janin. Studi tersebut menjelaskan bahwa pajanan suara dari gelombang monoton (bising) yang terus menerus berpengaruh negatif terhadap neurogenesis. Sedangkan suara dari gelombang ritmis (musik) dapat meningkatkan neurogenesis dan sinaptogenesis yang nantinya akan berpengaruh langsung terhadap fungsi memori. Maka akan dilihat apakah efek positif dari gelombang ritmis dapat meredam atau menjadi terapi bagi bagian otak yang sudah mendapat efek negatif dari gelombang monoton tersebut. Studi ini mennggunakan telur ayam yang sudah difertilisasi dibagi kedalam empat kelompok, yaitu kelompok yang dipajan suara ritmis, monoton, gabungan suara monoton dan ritmis, dan kelompok yang tidak mendapat pajanan (kontrol). Pajanan suara ritmis memiliki intensitas 65 dB dan suara monoton 110 dB. Hasil yang didapat yaitu terdapat perbedaan bermakna densitas optik protein postsynapticddensity 95 dan Waktu Uji T-Maze antara kelompok suara ritmis, monoton dan gabungan. Serta tidak terdapat perbedaan bermaknaprotein postsynapticddensity 95 dan Waktu Uji T-Maze antara kelompok suara gabungan dan kelompok kontrol. ......Pregnant women who work in noisy places can directly feel the effects of the noise. The noise not only affects pregnant women but also the fetus they contain. There are many studies that prove the negative effects of noise on the fetus. The study explained that continuous exposure to sound from monotonous (noisy) waves negatively influences neurogenesis. While the sound of rhythmic waves (music) can increase neurogenesis and synaptogenesis which will directly affect the memory function of. Then it will be seen whether the positive effects of rhythmic waves can reduce or be a therapy for the part of the brain that has gotten the negative effects of these monotonous waves. Methode tha used in this study is Fertilized chicken eggs were divided into four groups, namely groups that were exposed to rhythmic, monotonous sounds, combined monotonous and rhythmic sounds, and groups that did not receive exposure (control). Rhythmic sound exposure has an intensity of 65 dB and a monotone sound of 110 dB. The results is there were significant differences optical density postsynapticdensity-95 and T-Maze time between rhythmic, monotonous and combined sound groups. And there is no significant differenceoptical density postsynapticdensity-95 and T-Maze time between the combined sound group and the control group.

Abstrak :
Latar Belakang: Kondisi hipoksia akan meningkatkan pembentukan dan pelepasan spesies oksigen reaktif (ROS). Sel mampu melindungi diri terhadap kerusakan akibat pembentukan ROS yang terjadi secara alami, tetapi pembentukan radikal bebas yang berlebihan, akan terjadi stres oksidatif yang menyebabkan kerusakan terutama pada jantung sehingga diperlukan antioksidan. Acalypha indica dan Centella asiatica terbukti memiliki efek antioksidan dan melindungi banyak organ dari kondisi hipoksia, sehingga penelitian dilakukan dengan tujuan untuk melihat efek antioksidan kombinasi ekstrak etanol Acalypha indica dan Centella asiatica pada organ jantung tikus Spraque-Dawley pascahipoksia. Metode: Tiga puluh lima ekor tikus Sprague-Dawley jantan diinduksi hipoksia selama 7 hari dalam ruang khusus, kemudian diberi perlakuan. Ekstrak etanol Acalypha indica dan Centella asiatica diberikan secara kombinasi dan tunggal kepada kelompok tikus yang telah dibagi menjadi grup A (hipoksia dan diberi air), B (hipoksia dan diberi kombinasi Acalypha indica 200 mg/kgBB dan Centella asiatica 150 mg/kgBB), C (hipoksia dan diberi kombinasi Acalypha indica 250 mg/kgBB dan Centella asiatica 100 mg/kgBB), D (hipoksia dan diberi Acalypha indica 250 mg/kgBB), E (hipoksia dan diberi Centella asiatica 150 mg/kgBB), F (hipoksia dan diberi vitamin C 100mg/kgBB) dan kelompok normal selama 7 hari. Parameter yang diamati adalah ekspresi mRNA HIF-1a, kadar MDA, aktivitas enzim SOD dan ekspresi mRNA cTnI. Hasil: Hasil uji dianalisis dengan uji one way anova. Tidak terdapat perbedaan bermakna pada ekspresi HIF-1a antara grup A dengan kelompok tikus normal (p>0,05). Kadar MDA meningkat signifikan pada grup A (p<0,05) dibanding tikus normal. Grup D mengalami penurunan kadar MDA secara signifikan (p<0,05) dibanding grup A. Aktivitas SOD menurun signifikan pada grup A (p<0,05) dibanding tikus normal. Grup B dan E (p<0,05) mengalami peningkatan aktivitas SOD secara signifikan dibanding grup A. Grup B meningkat signifikan (p<0,05) dibanding grup E. Tidak terdapat perbedaan bermakna antar kelompok perlakuan pada Ekspresi cTnI. Tidak terdapat korelasi antara kadar MDA dan aktivitas SOD serta ekspresi mRNA HIF-1a dan mRNA cTnI. Kesimpulan: Pemberian kombinasi ekstrak Acalypha indica 200 mg/kgBB dan Centella asiatica 150 mg/kgBB tidak dapat membantu memproteksi kerusakan jantung pascahipoksia.

---

Background: The condition of hypoxia will increase the formation and release of reactive oxygen species (ROS). Cells have mechanisms to protect themselves against damage caused by ROS generation occurring naturally. If the excessive formation of free radicals, oxidative stress will occur that cause damage, especially to the heart so that the necessary antioxidants. Acalypha indica and Centella asiatica has been shown to have antioxidant effects and protecting many organs from hypoxic conditions, so that the research was conducted to see the effect of the antioxidant combination Acalypha indica and ethanol extracts of Centella asiatica on cardiac organ Spraque Dawley rats pascahipoksia. Methods: Thirty-five male Sprague-Dawley rats induced hypoxia for 7 days in a specific chamber, later treated. Acalypha indica extract, Centella asiatica extract and the combination of both extract were given to the rats that divided into 7 group, ie groups A (water), B (combination of Acalypha indica 200 mg/kgBB and Centella asiatica 150 mg/kgBB), C (combination of Acalypha indica 250 mg/kgBB and Centella asiatica 100 mg/kgBB), D (Acalypha indica 250 mg/kgBB), E (Centella asiatica 150 mg/kgBB), F (vitamin C 100 mg/kgBB) and normal group. Those treatment were given orally for 7 days after hypoxia. The parameters were mRNA expression of HIF-1a, level of MDA, SOD enzyme activity and mRNA expression of cTnI. Results: There were no significant differences in the expression of HIF-1a between group A with group of normal rats (p>0,05). MDA levels increased significantly in group A (p<0,05) compared to normal rats. Group D decreased MDA levels were significantly (p<0,05) compared to group A. SOD activity decreased significantly in group A (p<0,05) compared to normal rats. Group B and E (p<0,05) increased the activity of SOD significantly compared to group A. Group B increased significantly (p<0,05) compared to group E. There was no significant difference between treatment groups on the mRNA expression of cTnI. There was no correlation between level of MDA and SOD activity so do between expression mRNA HIF-1a and mRNA cTnI. Conclusion: Administration of a combination of Acalypha indica extract 200 mg/kgBB and 150 mg/kgBB of Centella asiatica cannot help protect the heart against cardiac injury after hypoxia.

Abstrak :
ABSTRAK Latar Belakang: Endoksifen merupakan terapi baru pada pengobatan sel kanker payudara yang responsif terhadap endokrin. Studi terdahulu menunjukkan bahwa paparan endoksifen jangka panjang dapat menyebabkan resistensi melalui mekanisme Epithelial-Mesenchymal Transition (EMT). EMT adalah sebuah proses dimana suatu sel epithelial berubah menjadi sel mesenkimal. Proses EMT ditandai dengan adanya modulasi marker-marker epitelial seperti E-cadherin, vimentin dan TGF-β1. Berbagai penelitian telah menunjukan bahwa paparan singkat kurkumin dapat memperbaiki marker-marker EMT. Namun, kurkumin memiliki keterbatasan karena bioavailabilitasnya yang rendah. Oleh karena itu, pada penelitian ini kami menggunakan nanokurkumin untuk mencegah jalur EMT. Metode: ini merupakan penelitian in vitro menggunakan sel MCF-7. Kami membagi sel menjadi beberapa kelompok yaitu: Endoksifen 1000 nM+β-estradiol 1 nM, Endoksifen 1000 nM+β-estradiol 1 nM + nanokurkumin (8.5 μM dan 17 μM), Endoksifen 1000 nM+β-estradiol 1 nM+kurkumin 17 μM dan DMSO selama 8 minggu. Sel kemudian dipanen dan dihitung setiap minggu. Setelah minggu ke-4 dan ke-8 paparan, ekspresi E-cadherin, TGFβ1 dan vimentin diukur menggunakan two-step qRT PCR. Pada minggu ke-8, kadar protein TGF-β1 diukur dengan ELISA, sementara morfologi sel MCF-7 diamati menggunakan mikroskop konfokal. Hasil: Terdapat peningkatan viabilitas sel pada kelompok Endoksifen 1000 nM+β-estradiol 1 nM. Viabilitas sel menurun secara signifikan pada kelompok nanokurkumin dan kurkumin 17 μM, tetapi tidak pada kelompok nanokurkumin 8.5 μM. Analisis marker EMT pada minggu ke-8 menunjukkan terdapat peningkatan ekspresi mRNA vimentin dan TGF-β1 sementara ekspresi mRNA E-cadherin dan kadar protein TGF-β1 tampak menurun. Hasil menunjukkan bahwa pemberian nanokurkumin pada semua dosis tidak mampu memperbaiki ekspresi vimentin, TGF-β1, dan E-cadherin. Tidak tampak perbedaan yang signifikan antara nanokurkumin dan kurkumin terhadap modulasi marker-marker EMT pada sel kanker payudara yang dipaparkan endoksifen berulang. Pengamatan morfologi menggunakan mikroskop konfokal menunjukkan adanya sel mesenkimal baik pada kelompok endoksifen+β-estradiol maupun kelompok yang mendapat nanokurkumin/kurkumin. Kesimpulan: nanokurkumin tidak mampu mencegah aktivasi EMT walaupun dapat menurunkan viabilitas sel pada penggunaan jangka panjang. Meskipun nanokurkumin lebih terakumulasi di dalam sel. tidak tampak perbedaan potensi dibandingkan dengan kurkumin dalam menurunkan marker EMT.

---

ABSTRACT Background: Endoxifen is a novel therapy in the treatment of endocrine responsive type of breast cancer. Previous study showed that long-term exposure of endoxifen may lead to resistance through the mechanism of Epithelial-Mesenchymal Transition (EMT). EMT is a process where epithelial cells turn into mesenchymal cells. EMT is characterized by the modulation of epithelial markers such as E-cadherin, vimentin and TGF-β. Various studies have shown that short term treatment with curcumin may improve EMT markers. However, the efficacy of curcumin is limited by its low bioavailability. In this study, we use nanocurcumin to prevent the activation of EMT. Methods: This is an in vitro study in MCF-7. We exposed the cells to several groups, which are: endoxifen 1000nM + β-estradiol 1 nM, endoxifen 1000nM + β-estradiol 1 nM + nanocurcumin (8.5 μM and 17 μM), endoxifen 1000nM + β-estradiol 1 nM + curcumin 17 μM and DMSO, for 8 consecutive weeks. Cells were then harvested and counted weekly. After 4 and 8 weeks of treatments, E-cadherin, TGF-β and vimentin expressions were measured using a two-step qRT PCR. At week 8, protein level of TGF-β1 was measured by ELISA, while MCF-7 cell morphology was observed using confocal microscope. Results: MCF-7 cell viability was increased in endoxifen + β-estradiol group. Cell viability was significantly decreased in nanocurcumin and curcumin 17 μM, but not in nanocurcumin 8.5 μM group. Analysis of EMT markers at week 8 indicates that there were increase in vimentin and TGF-β mRNA expressions, while E-cadherin mRNA expressions and TGF-β1 protein concentrations were shown to decrease. The results showed that administration of nanocurcumin in all the dose administered were incapable improving the expressions of vimentin, TGF-β1 and E-cadherin. There were no significant differences between nanocurcumin and curcumin on the modulation of EMT?s markers in breast cancer cells exposed to repeated endoxifen and estradiol. Morphological observation using confocal microscope showed the presence of mesenchymal cells both in the endoxifen+β-estradiol group and the group given nanocurcumin/curcumin. Conclusion: nanocurcumin is incapable to prevent the activation of EMT, although it may reduce cell viability on a long-term use. Although nanocurcumin are more accumulated in the cells, they show no difference in efficacy compared with curcumin in reducing EMT markers.

Abstrak :
ABSTRAK Brown dan James, secara skematik, melalui teori pelipatan dan segmental juxtaposisi ventrodorsal embrionik menegaskan bahwa foregut primitif memiliki komponen dorsal dan ventral yang berbeda dikarenakan pelipatan sefalokaudal pada bidang-bidang primordial lempeng embrionik trilaminar. Namun masih belum jelas apakah semua segmen endodermal usus terbentuk dari komponen ventral dan dorsal akibat pelipatan sefalokaudal atau ada bagian segmen endodermal usus yang hanya terbentuk akibat pelipatan lateral embrionik. Nkx2.1 ditemukan di anterior ventral foregut sebagai salah satu penentu pola dorsoventral pada awal pembentukan foregut dan juga merupakan faktor transkripsi spesifik untuk perkembangan primordium paru. Endodermal foregut ventral bagian kaudal, yang terbentuk dari segmen embrionik rostal, merupakan endodermal primordium paru sehingga Nkx2.1 dapat menjadi kandidat penentu batas akhir pelipatan sefalokaudal sebelah sefalik. Untuk itu, perlu dipahami pola ekspresi Nkx2.1 pada proses pelipatan sefalokaudal. Desain penelitian adalah deskriptif observasional, menggunakan embrio tikus Sprague Dawley usia ED 9.5, ED10, ED10.5 dan ED1, kemudian diperiksa ekspresi protein Nkx2.1 dengan menggunakan teknik imunohistokimia. Ekspresi Nkx2.1 di foregut ventral pertama kali terlihat pada embrio ED 11 dan tidak terekspresi di seluruh usus depan bagian ventral, tetapi mempunyai pola khusus, yaitu terekspresi pada primordium tiroid, setinggi kaudal lengkung faring pertama dan pada usus depan bagian ventral setinggi jantung, mulai setinggi kanalis atrioventrikularis hingga distal sinus venosus. Batas lateral ekspresi Nkx2.1 di endodermal foregut tidak tegas. Pada batas akhir pelipatan, Nkx2.1 tidak terekspresi sehingga Nkx2.1 tidak dapat dijadikan penanda batas akhir pelipatan sefalokaudal sebelah sefalik.

---

ABSTRACT Brown and James, schematically, through theory of embryonic folding and segmental ventrodorsal juxtapositioning, assert that primitive foregut has different dorsal and ventral parts because cephalocaudal folding in the fields of primordial embryonic trilaminar plate. But it is unclear whether all segments of endoderm gut is formed from the ventral and dorsal components cause cephalocaudal folding or any part endoderm segment of intestine only from embryonic lateral folding. Nkx2.1 was found in the anterior ventral foregut as one determinant of dorsoventral pattern in the early foregut formation and also a specific transcription factor for the development of lung primordium. Ventral part of caudal foregut endoderm, formed from embryonic segment rostal, is endoderm lung primordium so Nkx2.1 may be a candidate determinant cephalic part boundary marker of cephalocaudal folding. For that, we need to understand the pattern of expression of Nkx2.1 during cephalocaudal folding process. The study design was observational descriptive, using embryo rat strain Sprague-Dawley aged E9.5, E10, E 10.5 and E11, then examined the expression of Nkx2.1 protein using immunohistochemical techniques. Nkx2.1 expression in the ventral foregut first seen in embryos E11 and not expressed in the whole ventral foregut, but has a special pattern, which is expressed in the thyroid primordium, as level as caudal first pharyngeal arch and the ventral foregut at heart level, ranging as level as atrioventricularis canal to the distal venous sinuses. The lateral limits of Nkx2.1 expression in endoderm foregut indecisive. At the end of cephalocaudal folding, Nkx2.1 is not expressed so Nkx2.1 can?t be used as a cephalic part boundary marker of cephalocaudal folding.