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"[ABSTRAKLatar belakang: Prematuritas merupakan salah satu kelainan yang masih menjadimasalah global. Kejadian prematuritas tidak hanya terjadi di negara berkembangtetapi juga di negara maju. Beberapa kondisi ibu hamil dapat memicu keadaanhipoksia dalam rahim sehingga menyebabkan kelahiran prematur. Keadaanplasenta menggambarkan kesejahteraan janin intra uteri. Kondisi hipoksia selulermemicu ekspresi HIF-1α yang menjadi faktor transkripsi bagi CA9 sebagaipenanda hipoksia. Penelitian ini bertujuan menganalisis pengaruh hipoksiaterhadap plasenta prematur.Metode: Sampel menggunakan plasenta prematur yang hipoksia (H) dan nonhipoksia(N) sebagai kontrol. Parameter yang dinilai adalah struktur histologisplasenta (Hematoksilin-Eosin), regulator hipoksia HIF-1α (imunohistokimia), danpenanda hipoksia CA9 (ELISA).Hasil: Penilaian struktur histologis menunjukkan adanya perbedaan jumlahpembuluh darah fetus antara kedua kelompok secara bermakna, dimana padakelompok hipoksia jumlah pembuluh darah fetus lebih banyak dibandingkankelompok non-hipoksia. Distribusi intensitas ekspresi HIF-1α kedua kelompokjuga berbeda bermakna. Rerata kadar CA9 kedua kelompok tidak berbedabermakna, namun terdapat kecenderungan rerata kadar CA9 kelompok hipoksialebih tinggi 28% dibandingkan yang non-hipoksia.Kesimpulan: Pengaruh hipoksia terhadap plasenta prematur pada tingkatmolekuler berupa stabilitas protein HIF-1α yang menyebabkan peningkatanjumlah pembuluh darah fetus dan terjadi kecenderungan peningkatan sintesisprotein CA9.

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ABSTRACTBackground: Prematurity is a disorder that is still a global problem. Incidence ofprematurity is a problem in developing and also in developed countries. Certaincondition accompanying pregnancies may trigger uterine hypoxia, causingpremature birth. The placental condition is related with the intra-uterine fetalcondition. Cellular hypoxic condition caused by systemic chronic hypoxia, lead tostabilization of HIF-1α protein, a transcription factor of CA9. This study aimed toanalyze the effect of hypoxia on the premature placenta.Methods: Samples from hypoxic premature placenta (H) and non-hypoxicpremature placenta (N) were collected. Parameters assessed were histologicalstructure of the placenta (Hematoxylin-Eosin), expression of HIF-1α(immunohistochemistry) and the level of CA9 (ELISA).Results: Assessment of histological structure showed the number of fetal bloodvessels were differed significantly between the two group, wherein the hypoxiagroup was more than the non-hypoxia. The distributions of HIF-1α expressionbetween the two groups were also differed significantly. The average level of CA9between two groups were not significant, but there is a tendency of higher level ofCA9 in the hypoxia group (28% higher compared to the non-hypoxia group).Conclusion: It is concluded that the effect of the hypoxia on premature placentain this study occured at molecular level and lead to HIF-1α protein stability thatcauses an increase of the number of fetal blood vessel and synthesis of CA9protein.;Background: Prematurity is a disorder that is still a global problem. Incidence ofprematurity is a problem in developing and also in developed countries. Certaincondition accompanying pregnancies may trigger uterine hypoxia, causingpremature birth. The placental condition is related with the intra-uterine fetalcondition. Cellular hypoxic condition caused by systemic chronic hypoxia, lead tostabilization of HIF-1α protein, a transcription factor of CA9. This study aimed toanalyze the effect of hypoxia on the premature placenta.Methods: Samples from hypoxic premature placenta (H) and non-hypoxicpremature placenta (N) were collected. Parameters assessed were histologicalstructure of the placenta (Hematoxylin-Eosin), expression of HIF-1α(immunohistochemistry) and the level of CA9 (ELISA).Results: Assessment of histological structure showed the number of fetal bloodvessels were differed significantly between the two group, wherein the hypoxiagroup was more than the non-hypoxia. The distributions of HIF-1α expressionbetween the two groups were also differed significantly. The average level of CA9between two groups were not significant, but there is a tendency of higher level ofCA9 in the hypoxia group (28% higher compared to the non-hypoxia group).Conclusion: It is concluded that the effect of the hypoxia on premature placentain this study occured at molecular level and lead to HIF-1α protein stability thatcauses an increase of the number of fetal blood vessel and synthesis of CA9protein., Background: Prematurity is a disorder that is still a global problem. Incidence ofprematurity is a problem in developing and also in developed countries. Certaincondition accompanying pregnancies may trigger uterine hypoxia, causingpremature birth. The placental condition is related with the intra-uterine fetalcondition. Cellular hypoxic condition caused by systemic chronic hypoxia, lead tostabilization of HIF-1α protein, a transcription factor of CA9. This study aimed toanalyze the effect of hypoxia on the premature placenta.Methods: Samples from hypoxic premature placenta (H) and non-hypoxicpremature placenta (N) were collected. Parameters assessed were histologicalstructure of the placenta (Hematoxylin-Eosin), expression of HIF-1α(immunohistochemistry) and the level of CA9 (ELISA).Results: Assessment of histological structure showed the number of fetal bloodvessels were differed significantly between the two group, wherein the hypoxiagroup was more than the non-hypoxia. The distributions of HIF-1α expressionbetween the two groups were also differed significantly. The average level of CA9between two groups were not significant, but there is a tendency of higher level ofCA9 in the hypoxia group (28% higher compared to the non-hypoxia group).Conclusion: It is concluded that the effect of the hypoxia on premature placentain this study occured at molecular level and lead to HIF-1α protein stability thatcauses an increase of the number of fetal blood vessel and synthesis of CA9protein.]"

"ABSTRAKLatar Belakang: Keadaan hipoksia akan menimbulkan respons adaptasi untuk mempertahankan homeostasis tubuh. Perubahan fisiologis (peningkatan denyut jantung, nadi, dan frekuensi pernafasan) terjadi untuk menjamin penyediaan oksigen terutama untuk otak. Faktor transkripsi HIF-1 yang penting untuk mengatasi hipoksia, terdiri atas dua subunit yaitu HIF-1α dan HIF-1β yang dalam keadaan hipoksia membentuk heterodimer dan mengatur ekspresi sejumlah gen target untuk mengatasi hipoksia. Hipoksia akan menyebabkan produksi H+ oleh sel meningkat. Paru akan mengurangi keadaan melalui eksresi CO2 dan H2O. Proses ini membutuhkan enzim anhidrase karbonat (CA). Peran EKA yang disintesis di paru diperlukan untuk menaikan tekanan darah.Tujuan: Penelitian ini bertujuan untuk mengetahui respons HIF-1α, CA dan EKA pada paru tikus yang mengalami hipoksia sistemik kronik.Metode: 25 ekor tikus jantan Sprague-Dawley dibagi secara acak dalam 5 kelompok dan 4 kelompok diinduksi hipoksia normobarik sistemik selama 1, 3. 5, dan 7 hari. Dilakukan pengukuran protein HIF-1α (ELISA), ekspresi relatif mRNA HIF-1α, CA9 dan Ace1 (real time RT-PCR satu langkah). Aktivitas enzim CA total dan aktivitas EKA total (metode spektrofotometri).Hasil: Ekspresi mRNA HIF-1α meningkat pada hari ke 5 induksi hipoksia (ANOVA, p=0,006), protein HIF-1α mengalami peningkatan hingga hari ke 7 hipoksia (ANOVA, p=0,038), dan keduanya berkorelasi sedang dan bermakna (Pearson, R=0,426). Ekspresi mRNA CA9 dan aktivitas CA total meningkat pada hipoksia (p>0,05), dan berkorelasi sedang. Ekspresi mRNA Ace1 meningkat seiring dengan lamanya induksi (p>0,05), sedangkan aktivitas EKA total meningkat pada hari ke 3 hipoksia, dan berkorelasi sangat lemah. Hasil uji korelasi juga menunjukkan hubungan yang kuat antara protein HIF-1α dengan ekspresi mRNA Ace1, namun sangat lemah dengan ekspresi mRNA CA9.Kesimpulan: Terjadi peningkatan HIF-1α, CA dan EKA selama induksi hipoksia pada paru tikus. Protein HIF-1α meregulasi ekspresi CA9 dan Ace1.

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ABSTRACT

Background: Hypoxia will cause adaptation response to maintain the body homeostasis. Physiological changes (increased heart rate, pulse, and respiratory rates) occur to supply oxygen especially brain. The transcription factor HIF-1 is important to overcome hypoxia condition, which composed of two subunits: HIF-1α and HIF-1β to form a heterodimer, and then regulate the expression of a target gene. Hypoxia causes increase H+ production in the cells. Lungs will decrease this condition through CO2 and H2O excretion. This process requires the enzyme carbonic anhydrase (CA). The blood pressure increases during hypoxia and ACE which is synthesized in the lung required increasing the blood pressure through renin angiotensin system (RAS).

Aims: To analyze response of HIF-1α, carbonic anhydrase, and angiotensin converting enzyme in the chronically hypoxia.

Methods: The lung tissues of 25 young male Sprague-Dawley rats were exposed to chronic systemic hypoxia (O2 10%: N290%) for 1, 3, 5, and 7 days. mRNA expression of HIF-1α, CA9, and Ace1 (one step real time RT-PCR). HIF-1α protein was determined with ELISA. The activities of CA and ACE were measured spectrophotometrically.

Results: mRNA expression of HIF-1α increased in 5 days after induction (ANOVA, p=0,006), and protein HIF-1α was found to be the highest at 7 days after induction (ANOVA, p=0,038), and both of them was correlated significant. The highest expression of CA9 and specific activities of total CA were measured in 5 days after induction (p<0,05). Expression of Ace1 increased during induction, but not the specific activities of ACE total. A Strong correlation was found between HIF-1α protein with Ace1 mRNA expression, but not with CA9 mRNA expression.

Conclusions: During chronic hypoxia, an increase HIF-1α, CA and ACE. HIF-1α protein can regulate CA9, and Ace1 expression."