摘要
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 On the basis of clinical practice of treatment for hepatic fibrosis, the mechanism of chinese herbal compound“ kang-xian-er-hao (KXEH)”in treating hepatic fibrosis were further explored and studied. Methods Male wistar rats were divided into five groups. The rat fibrosis model was induced by pig serum,excepted for normal control group(group N),the other four groups were all given intraperitoneal injection of pig serum respectively(0.5ml/once,2 times/week,total 12 weeks). In KXEH early treatment group(group B), the rats were fed with KXEH by gavage, 1g/100 g, once a day at the third week. In KXEH late treatment group(group C) , the rats were fed with KXEH by gavage, 1 g/100g, once a day at the ninth week. In γ-interferon treated group(group D),the rats were subcutaneous injected γ-interferon 10 5 every day at the ninth week .The model group(group A) and group N were fed with the same amount of saline by gavage. Rats were killed at the end of the twelfth week, the pathology of liver fibrosis was observed with HE stain and Masson stain.collagen I mRNA and collagen III mRNA were detected in liver samples with RT-PCR, immunohistochemical observe the expression of collagen I ,III protein. Results Upon pathological examination, the KXEH treatment had significantly reversed pig serum -induced liver fibrosis.In early treatment group B,the KXEH could enhance the degradation of collagen in the rat’s fibrotic liver according to HE and Masson staining compared with the fibrotic model group A(P<0.05). Moreover, in KXEH treatment group(B and C), the expression of collagen I ,III and its protein in liver was markedly reduced respectively according to RT-PCR analysis and immunohistochemistry as compared with group A. Conclusion The result showed that pig serum-induced rat hepatic fibrosis can be obviously reversed by the KXEH treatment.The mechanism of treating hepatic fibrosis with KXEH appears to be due to the enhancement of degradation of collagen in liver, then resulted in hepatic fibrosis be reversed eventually. Therefore the treatment of hepatic fibrosis should be as early as possible.
出处
《实用预防医学》
CAS
2005年第1期37-40,共4页
Practical Preventive Medicine