首页> 外文期刊>World Journal of Gastroenterology >Effect of Chinese medicine Qinggan Huoxuefang on inducing HSC apoptosis in alcoholic liver fibrosis rats.
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Effect of Chinese medicine Qinggan Huoxuefang on inducing HSC apoptosis in alcoholic liver fibrosis rats.

机译:中药清肝活血方对酒精性肝纤维化大鼠HSC凋亡的影响。

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AIM: To investigate the effect of Qinggan Huoxuefang (QGHXF) on improvement of liver function and pathology in rats, and to analyze the mechanism. METHODS: Wistar rats were divided into three groups at random: normal control group (12),micro-amount carbon tetrachloride group (CCl(4))(12) and model group A (60). The model group A was ingested with the mixture (500 mL/L alcohol, 8 mL/kg per day; corn oil, 2 mL/kg per day; pyrazole, 24 mg/kg per day) once a day and intraperitoneal injections of 0.25 mL/kg of a 250 mL/L solution of CCl(4) in olive oil twice a week for 12 wk. The CCl(4) group received intraperitoneal injections only. At the end of 8 wk the model group A (60) was divided into 5 subgroups: model group, Xiaochaihu Chongji (XCH) group, QGHXF high dose group, moderate dose group and low dose group, and were given the drugs respectively. At the end of 12 wk, all the rats were killed and blood samples collected, as well as liver tissue. Blood samples were used for evaluation of alanine transaminase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyltransferase (gamma-GT). Liver specimens were obtained for routine HE, apoptosis gene array and flow cytometry analysis. RESULTS: A liver fibrosis animal model was successfully established. Fibrosis was obviously reduced in QGHXF high dose group, and no fibrosis formed in CCl(4) group. Compared with model group the QGHXF group and XCH group could obviously decrease the level of ALT, AST, ALP, and GGT (P<0.05). QGHXF high dose group was better than XCH group in ALT (615+/-190 vs 867+/-115), and AST(1,972+/-366 vs 2,777+/-608). Moreover, QGHXF could reduce liver inflammation, fibrosis-induced hepatic stellate cell (HSC) apoptosis and regulate apoptosis gene expression. The HSC apoptosis rates of QGHXF groups were 22.4+/-3.13, 13.79+/-2.26 and 10.07+/-1.14, higher than model group, 6.58+/-1.04 (P<0.05). Compared to model group, 39 genes were up-regulated, 11 solely expressed and 17 down-regulated in high dose group. CONCLUSION: QGHXF can improve liver fibrosis and induce HSC apoptosis.
机译:目的:探讨清肝活血方(QGHXF)对大鼠肝功能和病理的改善作用,并分析其机制。方法:Wistar大鼠随机分为三组:正常对照组(12),微量四氯化碳组(CCl(4))(12)和模型组A(60)。每天一次向模型组A摄入混合物(500 mL / L酒精,每天8 mL / kg;玉米油,每天2 mL / kg;吡唑,每天24 mg / kg),并经腹腔注射0.25每周两次,每次250 mL / L CCl(4)在橄榄油中的250 mL / L CCl(4)溶液。 CCl(4)组仅接受腹膜内注射。在第8周结束时,模型组A(60)分为5个亚组:模型组,小柴胡冲剂(XCH)组,QGHXF高剂量组,中剂量组和低剂量组,并分别给予药物治疗。在12周结束时,杀死所有大鼠并收集血液样本以及肝组织。血液样本用于评估丙氨酸转氨酶(ALT),天冬氨酸转氨酶(AST),碱性磷酸酶(ALP),γ-谷氨酰转移酶(γ-GT)。获得肝标本用于常规HE,凋亡基因阵列和流式细胞术分析。结果:成功建立了肝纤维化动物模型。 QGHXF高剂量组纤维化明显减少,而CCl(4)组未形成纤维化。与模型组相比,QGHXF组和XCH组可明显降低ALT,AST,ALP和GGT水平(P <0.05)。 QGHXF高剂量组在ALT(615 +/- 190对867 +/- 115)和AST(1,972 +/- 366对2,777 +/- 608)方面优于XCH组。此外,QGHXF可以减轻肝脏炎症,纤维化诱导的肝星状细胞(HSC)凋亡并调节凋亡基因的表达。 QGHXF组的HSC凋亡率分别为22.4 +/- 3.13、13.79 +/- 2.26和10.07 +/- 1.14,高于模型组的6.58 +/- 1.04(P <0.05)。与模型组相比,高剂量组有39个基因上调,有11个单独表达,有17个下调。结论:QGHXF可改善肝纤维化并诱导HSC凋亡。

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