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目的:观察三七总皂苷(PNS)对肝纤维化大鼠细胞因子产生的影响,探讨其抗肝纤维化的作用机制。方法:SD大鼠随机分成正常对照组、模型组、PNS(50、100、200 mg/kg)组和秋水仙碱(Col)组。除正常对照组外其余各组大鼠采用CCl4皮下注射的方法诱导肝纤维化模型,2次/w,连续18 w。于造模第9周起,给药组分别灌胃给予相应的受试药物,正常对照组和模型组给予等体积生理盐水,1次/d,疗程10 w。实验结束后,放射免疫法测定血清IL-1、IL-6、IL-10、TNF-α的含量;同时取固定部位肝脏组织,HE染色观察肝组织病理学改变,免疫组化技术测定肝组织中NF-κB、转化生长因子(TGF)-β蛋白的表达,RT-PCR技术测定肝组织中TGF-β、TNF-αmRNA表达。结果:与模型组比较,PNS(100、200 mg/kg)不仅能减轻大鼠肝纤维化程度,还能显著抑制IL-1、IL-6、NF-κB、TNF-α、TGF-β的表达,升高IL-10的水平。结论:PNS对肝纤维化大鼠具有一定的保护作用,其机制可能与下调促炎因子,上调抑炎因子的产生,调控细胞因子网络平衡有关。
Objective: To observe the effect of Panax Notoginseng Saponins (PNS) on cytokine production in rats with hepatic fibrosis and to explore its mechanism of action against hepatic fibrosis. Methods: SD rats were randomly divided into normal control group, model group, PNS group (50, 100, 200 mg / kg) and colchicine group. Except the normal control group, rats in other groups were induced by CCl4 subcutaneously to induce hepatic fibrosis model twice a week for 18 weeks. From the 9th week of model making, the rats in the treatment group were given the corresponding drugs by intragastric administration. The normal control group and the model group were given equal volume of normal saline once a day for 10 weeks. At the end of the experiment, the contents of IL-1, IL-6, IL-10 and TNF-α in the serum were measured by radioimmunoassay. At the same time, the liver tissue of the fixed part was taken out and the pathological changes of the liver were observed by HE staining. The expression of NF-κB and transforming growth factor-β (TGF-β) in liver tissues was detected by RT-PCR. Results: Compared with model group, PNS (100,200 mg / kg) not only attenuated the degree of hepatic fibrosis in rats, but also significantly inhibited the expressions of IL-1, IL-6, NF-κB, TNF-α and TGF-β Express, increase the level of IL-10. CONCLUSION: PNS has a protective effect on rats with hepatic fibrosis. The mechanism may be related to the downregulation of proinflammatory cytokines, the upregulation of anti-inflammatory cytokines and the regulation of cytokine network balance.