|摘要: ||本研究在探討普洱茶水萃取物(WEPT)對tert-butyl hydroperoxide (t-BHP)誘發大鼠肝臟損傷與人類肝癌細胞(Hep G2)氧化傷害之保護效果。首先探討於動物模式中餵食WEPT、綠茶水萃取物(WEGT) (0.2、0.5 and 1.0 g/kg b.w.)或沒食子酸(gallic acid; GA) (0.02、0.2g/kg b.w.)與Silymarin (0.2g/kg) 八週後，對t-BHP (0.5mmol/kg b.w. )誘發大鼠肝臟損傷的保護效果。於血液中血清生化值分析的結果顯示，由t-BHP相較於控制組，會造成血清之GOT、GPT值的增加，而WEPT、WEGT或GA與silymarin相較於傷害組(t-BHP)可顯著的降低血清中GOT與GPT。且WEPT可增加血清中多酚類化合物濃度與增加血清總抗氧化能力。在抗氧化酵素方面，預先餵食WEPT則可提升catlase (CAT) 酵素活性，但對superoxide dismutase (SOD)、glutathione peroxidase (GPx)、glutathione reductase (GRd)則無影響。
以細胞模式來探討WEPT之保護作用機制。Hep G2於含WEPT、WEGT、咖啡因、epicatechin (EC)、GA (50-1000μg/mL) 或與t-BHP (2mM) 培養兩小時，結果顯示細胞處理WEPT、WEGT、EC、GA，可以分別降低t-BHP造成的細胞內活性氧(ROS) 與增加GST活性與減緩受t-BHP提升之CAT活性。這些結果顯示WEPT可以減少t-BHP所誘導的細胞毒性，有效的降低t-BHP誘導的氧化壓力。
综合以上結果WEPT於動物與細胞模式中，對t-BHP所誘發之損傷具有保護效用。其保護作用可能來自於自由基的清除與增加Glutathione S-transferase (GST)及CAT酵素活性。
The aim of this study was to investigate the water extract of pu-erh tea (WEPT) against tert-butyl hydroperoxide (t-BHP)-induced hepatic damage in rats and Hep G2 cells, respectively. Before administration of t-BHP (0.5mmol/kg b.w.) to induce hepatic damage, the animals were fed with WEPT and water extract of green tea (WEGT) (0.2, 0.5 and 1.0 g/kg b.w.) or gallic acid (GA)(0.02,0.2g/kg b.w.) and silymarin (0.2g/kg), respectively, for 8 weeks. The results showed that biochemical parameters GOT and GPT levels in serum of t-BHP-induced rats liver damage could increase as compared with control group. Treatment with WEPT, WEGT, GA and silymarin, respectively, could decrease the GOT and GPT levels as compared with negative control (t-BHP). WEPT could significantly increase serum total phenolics content and trolox equivalent antioxidant capacity (TEAC) in rats. In the enzymatic antioxidant, except catalase(CAT), WEPT administration could not increase the enzyme activity of superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GRd) in liver of rats.
Further, Hep G2 cells were incubated with t-BHP (2mM) in the presence/absence of WEPT, WEGT, caffeine, epicatechin (EC) and GA (50-1000μg/mL) for 2h, respectively. The results showed that the levels of intracellular reactive oxygen specie (ROS) and glutathione S-transferase (GST) were decreased and increased, respectively, as compared to t-BHP treatment. After WEPT, WEGT, EC, and GA treatment, only WEPT inhibit the t-BHP increased activites of catalsae in cells. The result showed that WEPT decrease t-BHP-induced toxicity in Hep G2 cells by inhibiting t-BHP-induced oxidative stress.
In conclusion, WEPT exhibited potent protective effects against t-BHP induced liver iniury in rat and cytotoxicity in Hep G2 cells. These protective abilities may be attributed to WEPT scavenging free radicals and increasing the GST and CAT activities.