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目的观察小鼠冠状病毒性肝炎肝细胞中caspase-3介导的凋亡机制变化,探讨藏茵陈对其干预作用及相关机制。方法将24只小鼠随机分成对照组、模型组、阳性对照组和藏茵陈组,造模成功后用赖氏法测定小鼠血清肝功能2项,苏木素-伊红染色光镜观察小鼠肝脏病理变化,用酶标仪检测肝匀浆caspase-3活性,用荧光定量PCR检测肝组织中Fas和caspase-3 mRNA含量。结果与对照组比较,模型组小鼠ALT、AST活力分别为(225.349±9.904)、(180.823±17.34)U/L,明显升高;病理切片显示肝脏损伤明显,caspase-3活性(0.371±0.051)、Fas和caspase-3 mRNA含量(1.93±0.08、0.867±0.102)均明显升高;藏茵陈干预后ALT、AST分别为(181.906±20.164)和(139.824±12.153)U/L,Fas和caspase-3 mRNA含量为(1.673±0.047)和(0.518±0.103),明显低于模型组(P<0.05),病理切片显示,藏茵陈组小鼠肝脏损伤与模型组比较有所改善。结论 Fas诱导的caspase-3细胞凋亡可能是小鼠冠状病毒性肝炎的致病机制之一,藏茵陈可通过抑制细胞凋亡并改善肝脏损伤程度。
Objective To observe the changes of caspase-3-mediated apoptosis in hepatocarcinogenesis of coronavirus in mice and to explore its mechanism of intervention and its mechanism. Methods Twenty-four mice were randomly divided into control group, model group, positive control group and Tibetan Yinchen group. After successful modeling, the liver function of mice was determined by Lai’s method. Liver pathology was observed by hematoxylin-eosin staining The activity of caspase-3 in liver homogenate was detected by microplate reader. The contents of Fas and caspase-3 mRNA in liver tissue were detected by real-time PCR. Results Compared with the control group, the ALT and AST activities in the model group were (225.349 ± 9.904) and (180.823 ± 17.34) U / L, respectively, which were significantly higher than those in the control group. The pathological sections showed that the liver injury was obvious and the activity of caspase- (1.93 ± 0.08,0.867 ± 0.102), respectively. The levels of ALT and AST were (181.906 ± 20.164) and (139.824 ± 12.153) U / L, respectively. The levels of Fas and caspase- 3 mRNA levels were (1.673 ± 0.047) and (0.518 ± 0.103) in the model group, respectively, which were significantly lower than those in the model group (P <0.05). The pathological sections showed that the liver injury in the Tibetan Yinchen group was improved compared with the model group. Conclusion Fas-induced apoptosis of caspase-3 cells may be one of the pathogenic mechanisms in mouse coronavirus. Tibetan Yin-Chen can inhibit apoptosis and improve liver injury.