Latar Belakang: Otak sangat sensitif terbadap kondisi kekurangan oksigen. Terhentinya suplai datah ke otak secara tiba-tiba, seperti yang tetjadi pada hipoksia serebri yang diasosiasikan sehagai stroke, dapat berakibat fatal dan menyehabkan kematian sel-sel neuron otak dalam waktu beberapa menit Hipoksia memicu serangkaian patologis yang disebabkan oleh eksitotoksisitas glutmnat dan produksi berlebih radikal belles yang selanjutnya memicu kaskade kematian sel. BDNF (Brain derived neurotrophic factor), salah satu faktor yang berperan dalam mempertahankan kelangsungan hidup neuron, dilaporkan kadarya menunm pada kendaan hipoksia. Seiling dangan meningkatnya kasus stroke serta prognosisnya yang buruk, merupakan suato kebutnben untuk mencari bahan obat yang dibarepkan dapat memblokir kaskade hipoksia sehingga kematian neuron dapat dicegah. Tanarnan akar kaning atau Acalypha indica Linn adalah tanaman perdu liar yang banyak dijum)lai di selurah daerah di Indonesia dan secara tidak sengaja rehusan akarnya dapat memulihkan kelumpuben akibat stroke. Senyawa flavmoid yang terkendung dalam tanarnan akar kucing memiliki kemampuan antioksidan yang terbukti dapat mencegah kaskade kematian neuron. Tujuan: Mengetahui pengarah pemberian akstrak akar Acalypha indica Linn dalam mcmproteksi neuron tikas pada kendaan hipcksia. Metode: Studi eksperimental in vitro pada kultur sel neuron jaringan hipckumpus tikus Sprague Dow/ey dewasa yang dipajan dengan ekstrak air akar Acalypha indica Linn pada dosis 10 mglml, 15 mglml, dan 20 mglml selama 72 jam. Kemudian seluruh sel diberi perlakuan hipoksia dengan gas 5% W5% C02/N1 balans selama 24 jam. Viabilitas sel diukur dcngan MTT assay, tingkat proliferasinya diukur dengan BrdU dan kadar BDNF medium kultur diperiksa dengan metoda ELISA. Hasil: Viabilitas relatif, tingkat proliferasi neuron dan kadar BDNF endogen pada kultur jaringan llipokarnpus tikus dengan pemberian ekstrak akar kucing pada dosis 10 mg/ml, 15 mg/ml, dan 20 mg/ml meningkat dibandingkan dengan kontrol. Kesimpulan: Ekstrak akar Acalypha indica Linn mampu meningkat viabilitas neuron serta kadar BDNF endogen pada keadaan hipoksia.

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Background: The brain is very sensitive to oxygen deprivation condition. Interruption of the blood supply to the brain suddenly, as happens on cerebral hypoxia is associated as a stroke, can be metal and cause death of brain cells neurons within a few minutes. Hypoxia triggers a ;Series of pathological cascade caused by the glutamate excitotoxicity and free radicals which in turn triggered a cascade of cell death. BDNF{Brain derived neurotrophic factor). is one of the factors maintaining the survival of neurons. is decreased during hypoxic conditions. The increase and a poor prognosis of stroke, represents a need to look for ingredients that are expected to block tile cascade of hypoxia that neuron death can be prevented. Acalypha indica Linn (akar kucing) is a common wild plants that can be found in all regions in Indonesia and accidentally the decoction of the root can cure paralysis caused by stroke. Flavonoid compounds contained in the roots have the proven ability of antioxidants can prevent neuron death caScade.

Objective: To detennine the effect of root extracts of Acalypha indica Linn as a protection of rat neuronal on the state of hypoxia.

Metbods: Experimental in vitro study of cell culture of rat hippocampal neuronal of adult Sprague Dow/ey rat treated with Acalypha indica Linn root water extract at a dose of I 0 mg!ml, 15 mg/ml, and 20 mg/ml for 72 hrs, Then the cells were exposed to hypoxia wil 5% 0,/5% CO,IN 2 balance gas for 24 hours, Cell viability was measured by MTI assay and BrdU for cell proliferation. Levels BDNF medium culture was measured by ELISA methods.

Results: Relative viability, proliferation rate of neuron and endogenous BDNF level of rat hippocampal tissue culture with Acalypha indica Linn roots extract with dosage of 10 mglml, 15 mg/ml, and 20 mg/ m! is increased compared with control.

Conclusion: Acalypha indica Linn root extract can increase neuron viability and the level of endogenous BDNF in hypoxic conditions.