截断逆挽方对慢加急性肝衰竭模型大鼠血清TNF-α、肝组织p-JNK及c-Jun的影响

发布时间：2018-05-16 07:13

本文选题：慢加急性肝衰竭 + 截断逆挽方　；参考：《首都医科大学学报》2017年02期

【摘要】：目的观察截断逆挽方对慢加急性肝衰竭(acute-on-chronic liver failure,ACLF)大鼠血清肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)含量、肝组织磷酸化c-Jun氨基末端激酶(phosphorylated c-Jun N-terminal kinase,p-JNK)及转录因子cJun表达的影响,探讨该方干预ACLF大鼠的部分作用机制。方法选择SPF级Wistar雄性大鼠70只,采用数字表法随机分为正常对照组、模型组、截断逆挽方组和JNK抑制剂SP600125(anthrapyrazolone)组,予猪血清免疫诱导大鼠形成肝纤维化模型,再联合D-氨基半乳糖/脂多糖(D-galactosamine/lipopolysaccharide,D-Gal N/LPS)急性攻击,建立ACLF大鼠模型。截断逆挽方组在急性攻击前给予截断逆挽方连续灌胃3 d,SP600125组在急性攻击前0.5 h腹腔注射SP600125。各组大鼠分别在急性攻击后4、8、12 h取材。采用酶联免疫吸附法(enzyme-linked immune sorbent assay,ELISA)检测血清TNF-α含量,蛋白印迹法(Western blotting,WB)检测c-Jun蛋白表达量,免疫组织化学法检测肝组织中p-JNK蛋白表达量,HE染色观察肝脏结构病理变化。结果与正常组相比,模型组各时间点血清TNF-α浓度均升高,差异具有统计学意义(P0.01);与对应时间点模型组相比,截断逆挽方组及SP600125组4、8 h血清TNF-α含量明显降低(P0.01),12 h有所升高;与正常组相比,模型组各时间点c-Jun、p-JNK表达量升高(P0.01);与模型组相比,截断逆挽方组、SP600125组在4 h及8 h c-Jun、p-JNK表达减少(P0.05),12 h表达增多。截断逆挽方组及SP600125组两两比较差异无统计学意义(P0.05)。结论截断逆挽方在一定程度上可以减轻ACLF大鼠肝细胞的损伤,其作用机制可能是通过影响JNK信号通路介导的细胞凋亡,从而保护肝细胞,抑制肝衰竭。
[Abstract]:Objective To observe the effect of the truncated reverse arm on the content of serum tumor necrosis factor - alpha (tumor necrosis factor- alpha, TNF- a) in the serum of acute-on-chronic liver failure (ACLF) rats and the expression of the phosphorylated c-Jun amino terminal kinase (phosphorylated c-Jun N-terminal) and the transcription factor of the liver tissue. The partial action mechanism of pre ACLF rats was selected. Methods 70 male rats with SPF grade Wistar were selected and randomly divided into normal control group, model group, truncated reverse arm group and JNK inhibitor SP600125 (anthrapyrazolone) group. The liver fibroization model was formed in pig serum immunized rats, and then D- amino galactose / lipopolysaccharide (D-galactosa) was combined with D-. Mine/lipopolysaccharide, D-Gal N/LPS) acute attack, establish a rat model of ACLF. Truncated the reverse arm group before the acute attack of 3 D, and group SP600125 in group SP600125 before the acute attack, the rats in each group were injected with the 4,8,12 h after the acute attack. The enzyme linked immunosorbent assay (enzyme-linked immune) was used. Sorbent assay, ELISA) was used to detect the content of TNF- alpha in serum. The expression of c-Jun protein was detected by Western blot (Western blotting, WB). The expression of p-JNK protein in liver tissues was detected by immunohistochemistry. The pathological changes of liver were observed by HE staining. Compared with the normal group, the concentration of TNF- alpha in all time points of the model group increased. Study significance (P0.01); compared with the corresponding time point model group, the content of serum TNF- alpha in the truncated reverse arm group and the SP600125 group 4,8 h decreased significantly (P0.01), and the 12 h increased. Compared with the normal group, the p-JNK expression of the model group increased (P0.01) at each time point c-Jun, and the reverse arm group was truncated, and the SP600125 group was expressed in the 4 h and 8 expressions. Decreased (P0.05), 12 h expression increased. There was no significant difference between the truncated reverse arm group and the SP600125 group 22 (P0.05). Conclusion a truncated reverse arm can reduce the damage of liver cells in ACLF rats to a certain extent. The mechanism may be to protect the hepatocytes and inhibit the liver failure through the apoptosis induced by the JNK signaling pathway.

【作者单位】：首都医科大学中医药学院中医络病研究北京市重点实验室;首都医科大学附属北京佑安医院人工肝中心;
【基金】：首都中医药研究专项(14ZY01)~~
【分类号】：R285.5;R-332

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