| 摘要: | 在洛神花粗萃物之活性分析中發現其具有抑制黃螵呤氧化？之抗氧化活性,經成分分析在乙酸乙酯層得一具強抗氧化之成分,經Mass, IR,NMR等儀器分析得知結構為二羥苯甲酸即原兒茶酸,以下乃針對原兒茶酸於初代肝細胞進行一連串抗氧化活性之探討。 原兒茶酸廣布於植物界如根、葉、花、果實,有報告指出其具有抑制致癌物所引發之癌症,如Diethylnitrosamine誘導之肝癌, Azoxymethane引發之大腸癌等,然其機制仍不甚清楚。本研究利用t-butylhydroperoxide (t-BHP)誘導肝細胞氧化性損傷之模式,探討原兒茶酸之抗氧化活性。初代肝細胞在t-BHP (1.5mM)處理半小時即造成肝細胞大量釋放乳酸去氫？(LDH),丙氨酸轉氨？(ALT)及大量形成脂肪過氧化產物---丙二醛酸(MDA),而加入原兒茶酸0.05mg/ml及0.10mg/ml可有意義的抑制以上之作用。另外原兒茶酸亦抑制t-BHP (0.1mM;1h)所導致之粒線體膜去極化(Uptake of rhodamine 123)及不正常之DNA修補作用(UDS),而在DPPH試驗中原兒茶酸可消去自由基。 由以上結果顯示原兒茶酸具有抑制氧化性傷害所造成之肝毒性及基因毒性而此作用可能與其消去自由基之能力有關。
Hibiscus protocatechuic acid (PCA), a simple phenolic compound isolated from Hibiscus sabdariffa L., was studied for its protective effects against oxidative damage induced by tert-butylhydroperoxide (t-BHP) in a primary culture of rat hepatocytes. It had been reported that exposure of isolated hepatocytes to t-BHP results in leakage of lactate dehydrogenase (LDH) and alanine transaminase (ALT), peroxidation of cellular lipids, and depolarization of mitochondria. The present investigations showed that PCA at concentrations of 0.05mg/ml and 0.10mg/ml significantly decreased the leakage of LDH (p<0.05 and p<0.01) and ALT (p<0.05) and the formation of malondialdehyde (MDA; p<0.01 and p<0.001) induced by 30 min treatment with t-BHP (1.5mM) in primary cultured rat hepatocytes. PCA also attenuated t-BHP (0.10mM) induced mitochondrial depolarization as determined by a retention test of rhodamine 123 and DNA repair synthesis as evidenced by unscheduled DNA synthesis (UDS). In addition, PCA exhibited an effective ability to quench 1,1-diphenyl-2-picrylhydrazyl radicals (DPPH). In conclusion, PCA demonstrated protective effects against hepatotoxicity and genotoxicity induced by t-BHP. One of mechanisms of PCA's protective effect may be associated with its property of scavenging free radicals. |
