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目的:探讨胆石六号汤剂治疗豚鼠胆囊炎的作用机制。方法:将40只豚鼠随机分为4组,即空白对照组、模型组、消炎利胆片组(0.40g/kg)、胆石六号汤剂7.70g/kg组。除空白组以为,其余各组连续7 d皮下注射盐酸林可霉素建立豚鼠胆囊炎模型。治疗21天后,HE染色观察肝脏和胆囊病理组织学改变,ELISA测定各组胆汁和血清中肿瘤坏死因子-α(TNF-α)、环氧合酶-2(COX-2)的含量,RT-PCR检测胆囊和肝脏组织中TNF-α、COX-2、核转录因子-κB(NF-κB)基因表达的变化,Western blotting检测胆囊和肝脏组织中NF-κB蛋白表达的变化。结果:与模型组相比,胆石六号汤剂可以减轻胆囊和肝脏的炎性病变,血清和胆汁中的TNF-α浓度为44.53、41.05 ng/L,COX-2浓度为50.72、48.45U/L,均较模型组明显降低(P<0.01);肝脏组织TNF-α、COX-2、NF-κB mRNA的表达量分别为120.82、93.00、89.54,胆囊组织中的表达为140.56,131.31,160.82,均较模型组减少;NF-κB蛋白在肝脏和胆囊的表达降低分别为19.54、18.41。结论:胆石六号汤剂治疗胆囊炎可能是通过抑制NF-κB通路,从而抑制TNF-α、COX-2的产生而实现的。
Objective: To explore the mechanism of gallstone 6 decoction in treating guinea pig cholecystitis. Methods: Forty guinea pigs were randomly divided into four groups: blank control group, model group, Xiaoyanlidan tablet group (0.40g / kg), and Chitosan No.61.70g / kg group. In addition to the blank group that the rest of the group 7 days continuous subcutaneous injection of lincomycin hydrochloride guinea pig cholecystitis model. After 21 days of treatment, the pathological changes of liver and gallbladder were observed by HE staining. The content of tumor necrosis factor-α (TNF-α) and cyclooxygenase-2 (COX-2) PCR was used to detect the gene expression of TNF-α, COX-2 and NF-κB in gallbladder and liver tissues. The expression of NF-κB in gallbladder and liver tissue was detected by Western blotting. Results: Compared with the model group, gallstone Liuhuang decoction could relieve inflammatory lesions of gallbladder and liver. The concentrations of TNF-α in serum and bile were 44.53 and 41.05 ng / L, the COX-2 concentrations were 50.72 and 48.45 U / L were significantly lower than those in model group (P <0.01). The expression of TNF-α, COX-2 and NF-κB mRNA in liver tissue were 120.82, 93.00 and 89.54, respectively, and the expression in gallbladder tissue was 140.56, 131.31 and 160.82 , Were decreased compared with the model group; NF-κB protein in the liver and gallbladder expression decreased 19.54,18.41. Conclusion: The treatment of cholecystitis by Ganshuang No.6 decoction may be achieved by inhibiting the NF-κB pathway and inhibiting the production of TNF-α and COX-2.