The clinical significance of the analysis of gene amplification and protein expression of α-smooth muscle actin in the liver of patients with CHB
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摘要: 目的研究慢性乙型肝炎(CHB)肝活检组织α-肌动蛋白(α-SMA)的表达,探讨α-SMA在慢性乙型肝炎病毒感染中的作用及意义。方法通过RT-PCR对CHB活检组织的α-SMA进行半定量,结合肝脏组织学和免疫组化,对CHB患者的肝组织α-SMA的表达进行分析。结果在基因水平上,轻度CHB患者α-SMA/β-actin为0.126±0.032,与中度(0.323±0.099,P=0.001)和重度(0.410±0.103,P=0.000)比较差异有统计学意义;但在CHB患者中,中度和重度比较差异无统计学意义(P=0.097)。免疫组化显示:在CHB肝组织,α-SMA主要与坏死性炎症反应有关,贮脂细胞和肝窦内皮细胞表达α-SMA较强。CHB轻度组(G1/G2),α-SMA表达于坏死性炎症反应部位;CHB较重组(G3/G4),则表达于坏死区及其相邻的肝实质表达明显增加,且Kuppfer细胞明显增多。结论 HBV慢性感染状态下,α-SMA的表达上调,可能参与了与肝脏患者的CHB病理过程。Abstract: Objective To investigate the roles and significance of α-smooth muscle actin (α-SMA) expression in liver biopsies of patients with CHB.237 liver biopsy tissues were used to observe the correlation between severity of CHB and the level of expression of α-smooth muscle actin.Methods The expression of α-SMA in the liver biopsies from patients with CHB were semi-quantified by RT-PCR and analysis was performed recombinant with histological and immunochemical methods.Results The expression of α-SMA varied in different liver biopsies.In the mRNA level, the expression quantity of α-SMA in G1/G2 group was 0.126±0.032, in G2/G3 groups was 0.323±0.099 (P=0.001) and in the G3/G4 groups was 0.410±0.103 (P=0.000) .There was significant difference among them.Moreover, in the protein levels, expression of α-SMA in G1/G2 groups was located in the necrosis and inflammation sites.In the G3/G4 groups they were very seriously in the liver Disses space tissues and stellate cells and there were more Kuffer's cells involved in the regions.Conclusion Expression of α-SMA were up-regulated in CHB liver biopsies whether in the mRNA levels or in the protein levels.And their expression and distribution may be involved in CHB pathologic course, which may be a new concept involved in chronic HBV infection progress.
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Key words:
- hepatitis B /
- chronic /
- actin /
- gene amplification
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[1]Chu CM, Shyu WC, Liaw YF.Comparative studies on expression of alpha-smooth muscle actin in hepatic stellate cells in chronic hepatitis B and C[J].Dig Dis Sci, 2008, 53 (5) :1364-1369. [2]Mekonnen GA, IJzer J, Nederbragt H.Tenascin-C in canine hepatitis:Immunohistochemical localization and correlation with necro-inflammatory activity, fibrotic stage, and expression of alpha-smooth muscle actin, cytokeratin 7 and CD3+cells[J].Vet Pathol, 2007, 44 (6) :803-813. [3]Muhanna N, Doron S, Wald O, et al.Activation of hepatic stellate cells after phagocytosis of lymphocytes:A novel pathway of fibrogenesis[J].Hepatology, 2008, 48 (3) :963-977. [4]孙永红, 陈青锋, 肖萍, 等.乙型肝炎病毒基因型与临床病理分级分期的关系[J].临床荟萃, 2008, 23 (8) :566-568. [5]Yoshida T.MCAT elements and the TEF-1 family of transcription factors in muscle development and disease[J].Arterioscler Thromb Vasc Biol, 2008, 28 (1) :8-17. [6]王昭, 周总光.肌动蛋白在炎症反应中的作用[J].中国微循环, 2002, 6 (2) :117-119. [7]王珍祥, 吴军, 易萱, 等.反义及正义平滑肌肌动蛋白逆转录病毒载体的构建与表达[J].中国美容杂志, 2003, 12 (3) :229-232. [8]任桂芳, 叶立红, 黄燕, 等.乙型肝炎患者肝组织粘着斑激酶、肌动蛋白的表达及意义[J].中国临床肝脏病杂志, 2006, 22 (6) :410-412. [9]Guo GH, Tan DM, Zhu PA, et al.Hepatitis B virus X protein promotes proliferation and upregulates TGF-beta1 and CTGF in human hepatic stellate cell line, LX-2[J].Hepatobiliary Pancreat Dis Int, 2009, 8 (1) :59-64. [10]付德才, 杨世忠, 孙钰玮, 等.甲珠对肝纤维化大鼠仪α-SMA和TGF-β1表达的影响[J].世界华人消化杂志, 2008, 16 (3) :253-258. [11]Wu MS, Liao CW, Du WY, et al.Enhanced expression of transforming growth factor-beta 1 in inflammatory cells, alpha-smooth muscle actin in stellate cells, and collagen accumulation in experimental granulomatous hepatitis caused by Toxocara canis in mice[J].Acta Trop, 2008, 105 (3) :260-268. [12]胡昆鹏, 林楠, 林继宗, 等.人骨髓间质干细胞对肝星状细胞的体外调控[J].中国组织工程研究与临床康复, 2009, 13 (27) :5257-5260. [13]曹力波, 李兵, 李佐军, 等.水飞蓟素对肝纤维化小鼠的保护作用及机制探讨[J].中国药理学通报, 2009, 25 (6) :794-796. [14]Gulbove M.Immunohistochemical localization of collagenⅢand typeⅣ, laminin, tenascin and alpha smooth muscle actin in the human liver in peliosis[J].Pathol Res Pract, 2002, 198 (12) :803-812. [15]Akpolat N, Yahsi S, Godekmerdan A, et al.The value of alpha-SMA in the evaluation of hepatic fibrosis severity in hepatitis B infection and cirrhosis development:a histopathological and immunohistochemical study[J].Histopathology, 2005, 47 (3) :276-280. [16]Iwaisako K, Hatano E, Taura K, et al.Loss of Sept4 exacerbates liver fibrosis through the dysregulation of hepatic stellate cells[J].J Hepatol, 2008, 49 (5) :768-778.
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