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通过腹腔注射四氯化碳诱导小鼠急性肝损伤,检测小鼠血清中GOT和GPT的活力,肝脏匀浆液中SOD的活力和MDA的含量,筛选黑莓籽保护小鼠急性肝损伤的有效部位及其作用机制。结果显示,石油醚部位高低剂量组和正丁醇部位中低剂量组均能显著性地降低小鼠血清中GPT和GOT的活力,降低小鼠肝脏匀浆液中MDA含量和升高SOD活力(P<0.05);乙酸乙酯部位中低剂量组均能显著性地降低小鼠血清中GPT和GOT的活力(P<0.05),但降低小鼠肝脏匀浆液中MDA含量和升高SOD活力不具有显著性(P>0.05);黑莓籽油高中低剂量组能显著性地降低小鼠血清中GOT的活力和小鼠肝脏匀浆液中MDA含量,及升高SOD活力(P<0.05),降低GPT活力不具有显著性但低于模型组(P>0.05)。黑莓籽石油醚部位、乙酸乙酯部位、正丁醇部位和黑莓籽油是黑莓籽保护肝损伤的有效部位,抗氧化机制是石油醚部位、正丁醇部位和黑莓籽油保肝作用机制之一。
Acute liver injury was induced by intraperitoneal injection of carbon tetrachloride in mice. The activity of GOT and GPT in serum, the activity of SOD and the content of MDA in liver homogenates were detected. The effective parts of acute liver injury protected by blackberry seed were screened. Its mechanism of action. The results showed that low and middle dose of petroleum ether and low and middle dose of n-butanol could significantly reduce the activity of GPT and GOT, decrease the content of MDA in liver homogenate and increase the activity of SOD (P < 0.05). Both middle and low dose ethyl acetate group could significantly reduce the activity of GPT and GOT in serum of mice (P <0.05), but the content of MDA in liver homogenate and the activity of SOD were not significant (P> 0.05). Blackberry seed oil high and medium low dose group could significantly reduce the activity of GOT in mice serum and the content of MDA in liver homogenate, and increase the activity of SOD (P <0.05), and lower the activity of GPT Not significant but lower than model group (P> 0.05). Blackberry seeds petroleum ether, ethyl acetate, n-butanol and blackberry seed oil is blackberry seed protection of liver injury is an effective part of the antioxidant mechanism is the petroleum ether part of n-butanol and blackberry seed oil liver mechanism of action one.