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目的 在过去临床实践的基础上 ,欲探讨复方抗纤二号抗肝纤维化的治疗机制。 方法 雄性Wistar大鼠分成五组 ,除正常对照外 ,余四组大鼠肝纤维化造模均采用腹腔注射猪血清 (0 .5ml /次 ,2次 /周 )。抗纤二号早期治疗组在第三周给予中药灌胃 ,1g/10 0 g每天一次。抗纤二号晚期治疗组在造模第九周给予中药灌胃 ,1g/10 0g每天一次。γ -干扰素治疗组在造模第九周每天皮下注射 10万单位的干扰素。模型组和正常对照组给等量的生理盐水灌胃。在 12周杀大鼠 ,HE和Masson染色观察肝纤维化的形成 ,RT -PCR检测肝组织中I ,III型胶原mRNA的表达 ,免疫组化观察I ,III型胶原蛋白的表达。 结果 病理学观察 ,抗纤二号早期治疗组显著逆转了猪血清诱导的肝纤维化 ,与模型组比较 ,经HE和Masson染色抗纤二号治疗组能明显降解纤维化大鼠肝中的胶原 (P <0 .0 5 )。PT -PCR分析I ,III型胶原mRNA的表达在抗纤二号治疗组均明显减少。同时分析表明I ,III型胶原蛋白的表达在抗纤二号治疗组均明显减少。 结论 抗纤二号能逆转免疫引起的肝纤维化 ,这是由于能促进肝脏胶原的降解作用 ,最终导致肝纤维化的逆转。肝纤维化的早期治疗用药优于后期的治疗。
Objective To explore the therapeutic mechanism of compound anti-fibrosis-2 anti-fibrosis on the basis of past clinical practice. Methods Male Wistar rats were divided into five groups. In addition to the normal controls, liver fibrosis models in the other four rats were injected intraperitoneally with pig serum (0.5 ml/time, 2 times/week). The anti-fibric early-treatment group received gavage of traditional Chinese medicine in the third week, once daily at 1g/10 0 g. The anti-fibrosis 2 advanced treatment group was given intragastric administration at the ninth week of modeling, 1g/10 0g once daily. In the IFN-gamma treatment group, 100,000 units of interferon were injected subcutaneously every day during the ninth week of model establishment. The model group and the normal control group were given an equal volume of normal saline. The rats were sacrificed at 12 weeks. HE and Masson staining were used to observe the formation of hepatic fibrosis. RT-PCR was used to detect the mRNA expression of type I and type III collagen in the liver. Immunohistochemistry was used to observe the expression of collagen type I and type III. RESULTS: Pathological observations showed that the anti-fibrin II early treatment group significantly reversed liver fibrosis induced by porcine serum. Compared with the model group, the anti-fibrosis II group treated with HE and Masson significantly degraded fibrotic collagen in rat liver. (P <0. 0 5). The expression of type I and type III collagen mRNA in PT-PCR analysis was significantly decreased in the anti-fibrosis treatment group. At the same time analysis showed that the expression of type I and type III collagen was significantly reduced in the anti-fibrosis treatment group. Conclusion Anti-fibrosis can reverse liver fibrosis induced by immunity, which is due to the promotion of liver collagen degradation, and ultimately lead to the reversal of liver fibrosis. The early treatment of liver fibrosis is better than the later treatment.