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作者	单位	E-mail
蔡景治	联勤保障部队第 904医院江苏无锡 214000	zs15209@163.com
郑扬	联勤保障部队第 904医院江苏无锡 214000
仲伟明	联勤保障部队第 904医院江苏无锡 214000
刘波	联勤保障部队第 904医院江苏无锡 214000

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中文摘要:

摘要目的：基于Bcl-2/CytC调控网络探讨槲皮素对肝硬化大鼠微循环及肝脏病变的影响。方法：选取清洁级SD大鼠45 只，随机数字表法分为A组、LC组、QUE low group、QUE high group，ETV组，10 只/组，除10只健康大鼠外其余均建立肝硬化模型，QUE low group采用槲皮素50 mg/kg灌胃，QUE high group采用槲皮素100 mg/kg灌胃，ETV组采用恩替卡韦分散片0.5 mg/次灌胃，A组与LC组均用生理盐水灌胃，均1 次/d，共计14 d。采用ELISA检测大鼠血清中丙氨酸氨基转移酶（ALT）、天门冬氨酸氨基转移酶（AST)、总胆固醇（TC）、甘油三酯（TG）水平及血栓素A2（TXA2）、血管紧张素II（AngⅡ）、前列环素（PGI2）含量，HE染色比较各组肝组织形态，免疫印迹检测大鼠肝组织中Bcl-2、Bax、细胞色素C(CytC)蛋白表达。结果：与A group相比，LC group的ALT、AST、TC、TG、TXA2、AngII表达均较高，PGI2、CytC、Bax较低（P<0.05）；与LC组比较，QUE low group的ALT、AST、TC、TG、TXA2、AngII均降低，PGI2、CytC、Bax升高（P<0.05）；与QUE low group比较，ETV group的ALT、AST、TC、TG、TXA2、AngII均降低，PGI2、CytC、Bax升高（P<0.05）；与ETV group比较，QUE high group的ALT、AST、TC、TG、TXA2、AngII均降低，PGI2、CytC、Bax升高（P<0.05）。A组大鼠肝脏组织完好；LC group大鼠肝组织损伤严重；QUE low group大鼠肝间质仍有纤维组织增生及炎症浸润现象；ETV组仍有肝细胞变性及炎性因子；QUE high group大鼠肝组织变性反应及汇管区炎症降低。与A group比较，LC group有明显肝纤维化、肝细胞变性坏死及炎细胞浸润（P＜0.05）；与LC group比较，QUE low group大鼠肝脏纤维化等有所缓解（P＜0.05）；与QUE low group比较，ETV group大鼠肝脏纤维化、变性坏死及炎细胞浸润缓解（P＜0.05）；与ETV group比较，QUE high group大鼠肝脏纤维化、变性坏死及炎细胞浸润改善（P＜0.05）。结论：槲皮素对肝硬化大鼠的肝组织具有一定保护作用，改善肝功能和肝脏微循环、肝脏病变，其机制可能调节Bcl-2、Bax和CytC等相关蛋白有关。

英文摘要:

ABSTRACT Objective: To investigate the effects of quercetin on microcirculation and liver lesions in cirrhotic rats based on Bcl-2/CytC regulatory network. Methods: Forty-five clean SD rats were selected and divided into group A, LC group, QUE Low group, QUE High group, ETV group, 10 rats per group by random number table method. Liver cirrhosis model was established except for 10 healthy rats. QUE Low group was given quercetin 50 mg/kg intragastric administration. QUE High group was given quercetin 100 mg/kg intragastric administration, ETV group was given Entecavir dispersible tablets 0.5 mg/time intragastric administration, group A and LC were given normal saline intragastric administration, once A day, for A total of 14 days. The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG) and the contents of thrombin A2 (TXA2), angiotensin II (Ang ⅱ) and prostacyclin (PGI2) in serum of rats were detected by ELISA. Liver morphology of each group was compared by HE staining. Western blotting was used to detect the expression of bcl-2, Bax and cytochrome C(CytC) proteins in rat liver tissue. Results: Compared with A group, ALT, AST, TC, TG, TXA2 and AngII expressions were higher in LC group, while PGI2, CytC and Bax were lower(P<0.05). Compared with LC group, ALT, AST, TC, TG, TXA2 and AngII in QUE Low group were decreased, while PGI2, CytC and Bax were increased(P<0.05). Compared with QUE Low group, ALT, AST, TC, TG, TXA2 and AngII of ETV group decreased, while PGI2, CytC and Bax increased(P<0.05). Compared with ETV group, ALT, AST, TC, TG, TXA2 and AngII in QUE High group were decreased, while PGI2, CytC and Bax were increased(P<0.05). The liver tissues of group A were intact. The liver tissue of LC group rats was severely damaged. QUE Low group rats still had fibrous tissue hyperplasia and inflammatory infiltration in liver interstitium. ETV group still had hepatocyte degeneration and inflammatory factors. In QUE High group, the degeneration reaction of liver tissue and inflammation of portal area were decreased. Compared with A group, LC group had obvious liver fibrosis, liver cell degeneration and necrosis and inflammatory cell infiltration(P<0.05). Compared with LC group, liver fibrosis was alleviated in QUE Low group (P<0.05); Compared with QUE Low group, liver fibrosis, degeneration necrosis and inflammatory cell infiltration were alleviated in ETV group(P<0.05). Compared with ETV group, liver fibrosis, degeneration necrosis and inflammatory cell infiltration were improved in QUE High group (P<0.05). Conclusion: Quercetin has a protective effect on liver tissue of cirrhotic rats, improving liver function, liver microcirculation and liver lesions, and its mechanism may regulate bcl-2, Bax, CytC and other related proteins.

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