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柴胡疏肝散调控Th17/Treg平衡对乙型病毒性肝炎小鼠肝功能的影响及其机制
作者:李转  王提  王慧莹 
单位:华中科技大学同济医学院附属武汉市金银潭医院 感染科, 湖北 武汉 430014
关键词:乙型病毒性肝炎 柴胡疏肝散 Th17细胞 Treg细胞 免疫 小鼠 
分类号:R373.2
出版年·卷·期(页码):2024·52·第四期(606-611)
摘要:

目的:探究柴胡疏肝散(CHSGS)调控Th17/Treg平衡对乙型病毒性肝炎(简称乙肝)小鼠肝功能的影响和机制。方法: 将小鼠分为对照组、乙型肝炎病毒(HBV)组和HBV+CHSGS组,每组15只。除对照组外,其他两组均采用HBV(1×106 mL, 30 mL·kg-1) 感染以构建乙肝模型。建模成功后,HBV+CHSGS组通过CHSGS灌胃(30 g·mL-1,30 mL·kg-1)干预,对照组和HBV组灌胃等量生理盐水。6周后检测小鼠肝功能、肝脏单个核细胞中Th17和Treg变化以及RORγ和FOXP3蛋白的表达。 结果:与对照组比较,HBV组的谷丙转氨酶(ALT) [(85.24±17.03)U·L-1]、天门冬氨酸氨基转移酶(AST) [(315.39±37.61)U·L-1]、肝脏单个核细胞中Th17(5.22%±0.51%)、Treg(9.96%±0.95%)、Th17/Treg值(0.52±0.07)、RORγ和FOXP3蛋白均升高(P<0.05)。HBV+CHSGS组的ALT[(60.75±8.46)U·L-1]、AST [(201.44±21.87)U·L-1]、肝脏单个核细胞中Th17(3.67%±0.37%)、Th17/Treg值(0.26±0.04)和RORγ蛋白低于HBV组,而Treg(14.30%±1.13%)和FOXP3蛋白高于HBV组(P<0.05)。 结论: CHSGS抑制Th17、促进Treg分化,改善HBV感染引起的Th17/Treg比例异常,从而调控免疫炎症反应保护乙肝小鼠的肝功能。

Objective: To explore the effect and mechanism of Chaihu Shugan powder(CHSGS) regulating Th17/Treg balance on liver function in mice with hepatitis B. Methods: We divided mice into control, hepatitis B virus(HBV) and HBV+CHSGS group.Each group has 15 mice. The hepatitis B model was established by HBV(1×106 mL, 30 mL·kg-1) infection. CHSGS(30 g·mL-1, 30 mL·kg-1) was intervened by intragastric administration. After 6 weeks, liver function, Th17 and Treg changes in liver mononuclear cells, and the expression of RORγ and FOXP3 proteins were detected. Results: Compared with the control group,alanine aminotransferase(ALT) [(85.24±17.03) U·L-1], aspartate aminotransferase(AST) [(315.39±37.61) U·L-1], Th17(5.22%±0.51%), Treg(9.96%±0.95%), Th17/Treg ratio(0.52±0.07), RORγ and FOXP3 proteins were all increased(P<0.05). ALT [(60.75±8.46) U·L-1], AST [(201.44±21.87) U·L-1], Th17(3.67%±0.37%), Th17/Treg ratio(0.26±0.04) and RORγ protein in HBV+CHSGS group were lower than those in the HBV group, while Treg(14.30%±1.13%) and FOXP3 proteins were higher than those in the HBV group(P<0.05). Conclusion: CHSGS can inhibit Th17 and promote the differentiation of Treg, so as to improve the abnormal Th17/Treg ratio caused by HBV, and regulate the immune inflammatory response to protect liver function of mice with HBV.

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