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目的探讨黄连素对四氯化碳(CCl4)诱导的小鼠急性肝损伤的保护作用及其机制。方法 30只C57小鼠,♂,随机分为对照组、CCl4组和黄连素组,每组10只。黄连素组在CCl4注射前1 h腹腔注射黄连素(10 mg·kg?1),CCl4组和黄连素组腹腔注射CCl4橄榄油溶液(0.5%,5 m L·kg?1),对照组腹腔注射橄榄油溶液(0.5%,5 m L·kg?1)。24 h后麻醉下处死小鼠,收集血清和肝脏标本,采用生化检测ALT和AST,HE染色后观察肝脏病理学形态,Western blot检测JAK2和STAT3,p-JAK2和p-STAT3。RT-PCR和ELISA检测炎症因子白介素-6(IL-6)和白介素8(IL-8)和肿瘤坏死因子-α(TNF-α)的表达和分泌。结果与对照组相比,CCl4组病理改变明显增加,p-JAK2、p-STAT3蛋白表达量明显增加,JAK2和STAT3表达无明显变化,IL-6、IL-8和TNF-?表达和分泌明显增加。与CCl4组相比,黄连素组病理改变明显减轻,p-JAK2、p-STAT3表达明显减少,IL-6、IL-8和TNF-?表达和分泌也明显减少,但JAK2和STAT3表达仍无明显变化。结论黄连素预处理可通过抑制JAK2/STAT3信号通路激活而减少炎症反应,从而减轻CCl4诱导的急性肝损伤。
Objective To investigate the protective effect of berberine on carbon tetrachloride (CCl4) -induced acute liver injury in mice and its mechanism. Methods Thirty C57 mice were randomly divided into control group, CCl4 group and berberine group, with 10 in each group. In the berberine group, berberine (10 mg · kg -1) was injected intraperitoneally 1 hour before CCl 4 injection. CCl 4 group and berberine group were intraperitoneally injected with CCl 4 olive oil solution (0.5%, 5 m L · kg -1) Inject olive oil solution (0.5%, 5 m L · kg -1). Mice were sacrificed 24 h after anesthesia. Serum and liver samples were collected. ALT and AST were detected by biochemical methods. Pathological changes of liver were observed by HE staining. JAK2, STAT3, p-JAK2 and p-STAT3 were detected by Western blot. The expression and secretion of interleukin-6 (IL-6), interleukin 8 (IL-8) and tumor necrosis factor-α (TNF-α) were detected by RT-PCR and ELISA. Results Compared with the control group, the expression of p-JAK2 and p-STAT3 in CCl4 group was significantly increased, the expression of JAK2 and STAT3 was not significantly changed, and the expression and secretion of IL-6, IL-8 and TNF- increase. Compared with CCl4 group, the pathological changes in the berberine group were significantly reduced, the expressions of p-JAK2 and p-STAT3 were significantly decreased, and the expressions and secretion of IL-6, IL-8 and TNF-α were also significantly decreased, but the expression of JAK2 and STAT3 was still absent obvious change. Conclusion Berberine preconditioning can reduce the inflammatory reaction by inhibiting the activation of JAK2 / STAT3 signaling pathway and thus reduce CCl4-induced acute liver injury.