α-SMA与TGF-β1在大鼠肝纤维化中的表达及相互关系
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摘要
为明确α-SMA和TGF-β1在肝脏纤维化过程中的作用和相互关系,研究首先利用CCl4腹腔注射的方法建立肝脏纤维化大鼠模型,通过组织学、免疫组织化学及蛋白组学方法检测肝脏纤维化过程中病理组织结构变化、α-SMA和TGF-β1的表达情况。结果显示肝脏纤维化模型造模成功,肝脏组织呈现明显纤维化病变特征,α-SMA和TGF-β1的表达呈阳性,且与肝脏纤维化程度呈正相关。α-SMA和TGF-β1是肝脏纤维化过程中的重要细胞因子,能够促进肝脏纤维化的形成,并可能协同参与。
To make clear the effect and relationship between α-SMA and TGF-β1 in liver fibrosis,intraperitoneal injection of CCl4 was usedto make liver fibrosis model in rats,and then histopathological changes were detectedand α-SMA and TGF-β1 were expressedby histopathological method,immunohistochemistry and proteomics method in the process of liver fibrosis.The results showed that the model was successfully built and pathological characteristics were obviously observed.The expression of α-SMA and TGF-β1 was positive and showedpositively correlated with liver fibrosis process.α-SMA and TGF-β1 were important cytokines which could promote the liver fibrosis process,and mightcooperate in formation of liver fibrosis.
To make clear the effect and relationship between α-SMA and TGF-β1 in liver fibrosis,intraperitoneal injection of CCl4 was usedto make liver fibrosis model in rats,and then histopathological changes were detectedand α-SMA and TGF-β1 were expressedby histopathological method,immunohistochemistry and proteomics method in the process of liver fibrosis.The results showed that the model was successfully built and pathological characteristics were obviously observed.The expression of α-SMA and TGF-β1 was positive and showedpositively correlated with liver fibrosis process.α-SMA and TGF-β1 were important cytokines which could promote the liver fibrosis process,and mightcooperate in formation of liver fibrosis.
引文
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[12]武淑琴,吴丹丹,王新,等.不同剂量对乙酰氨基酚诱导大鼠急性肝损伤的研究[J].黑龙江八一农垦大学学报,2015,27(3):40-43.
[13]Tu X,Zhang H,Zhang J,et al.Micro RA-101 suppresses liver fibrosis by targeting the TGF-βsignalling pathway[J].J Pathol,2014,234(1):46-59.
[2]Hernandez-Gea V,Friedman SL.Pathogenesis of liver fibrosis[J].Ann Rev Pathol Mech Dis,2011(6):425-456.
[3]Mederacke I,Hsu CC,Troger JS,et al.Fate tracing reveals hepatic stellate cells as dominant contributors to liver fibrosis independent of its aetiology[J].Nat Commun,2013(6):2823.
[4]Forbes SJ,Parola M.Liver fibrogenie cells[J].Best Pract Res Clin Gastroenterol,2011,25(2):207-217.
[5]武希润,吕敏和,王琦,等.α平滑肌肌动蛋白表达及血浆转化生长因子β1变化在肝纤维化发生发展中的作用[J].中华肝脏病杂志,2004,12(7):400-402.
[6]张云巍,胡亚卓,徐丽娟,等.四氯化碳法制备肝硬化大鼠模型中重要脏器的病理改变[J].世界华人消化杂志,2014,22(1):74-79.
[7]李钰,刘佳,韦丹丹,等.动物病理组织切片制作方法改良的探讨[J].黑龙江畜牧兽医,2014(15):154-157.
[8]肖颖,杨涛涛,周卫民,等.TGF-β/Smad与Wnt/β-catenin在博莱霉素致大鼠肺纤维中的表达及相互作用[J].中国比较医学杂志,2014,24(2):63-69.
[9]曾志萍,郭津生.肝纤维化发生机制及治疗进展[J].世界华人消化杂志,2017,25(7):569-575.
[10]黄艳,黄成,李俊.肝纤维化过程中Kupffer细胞分泌细胞因子对肝星状细胞活化增殖、凋亡的调控[J].中国药理学通报,2010,26(1):9-13.
[11]Duval F,Moreno-Cuevas JE,Gonzalez-Garza MT,et al.Liver fibrosis and protection mechanisms action of medicinal plants targeting apoptosis of hepatocytes and hepatic stellate cells[J].Adv Pharmacol Sci,2014(7):373295.
[12]武淑琴,吴丹丹,王新,等.不同剂量对乙酰氨基酚诱导大鼠急性肝损伤的研究[J].黑龙江八一农垦大学学报,2015,27(3):40-43.
[13]Tu X,Zhang H,Zhang J,et al.Micro RA-101 suppresses liver fibrosis by targeting the TGF-βsignalling pathway[J].J Pathol,2014,234(1):46-59.