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目的研究肿瘤坏死因子-α(TNF-α)在小鼠酒精性肝损伤过程中的表达与意义。方法将50只健康雄性小鼠按照体重随机分为2组:对照组(n=10),模型组(n=40)。用56°红星二锅头经酒精灌胃(15 m L·kg-1)诱导小鼠肝损伤1,2,3,4周,建立小鼠酒精性肝损伤模型,分别于0(对照组小鼠)与1,2,3,4周,各取10只小鼠于眼球取血,用赖式法检测血清谷草转氨酶(AST)的活性;以颈椎脱臼法处死小鼠,取小鼠肝,用蛋白印迹法测定肝组织TNF-α的表达量。结果小鼠肝AST酶的活性在0,1,2,3,4周分别为(112±22),(126±24),(967±30),(1010±35),(206±23)U·L~(-1),与对照组相比,差异均有统计学意义(均P<0.05)。模型组的小鼠肝AST酶的活性在第1周缓慢上升,第2周迅速上升,于第3周达到高峰,第4周开始下降,但仍高于对照组。TNF-α相对积分光密度在0,1,2,3,4周分别为1.15±0.12,1.10±0.08,2.13±0.16,2.16±0.15,1.16±0.11,与对照组相比,第1周略有下降,第2周迅速上升,第3周达到高峰,第4周出现下降,仍高于对照组,差异均有统计学意义(均P<0.01)。结论在酒精灌胃诱导的小鼠肝损伤的进程早期,TNF-α促使肝细胞的损伤和坏死,并参与了后期肝的修复再生。
Objective To study the expression and significance of tumor necrosis factor-α (TNF-α) in mice with alcoholic liver injury. Methods Fifty healthy male mice were randomly divided into two groups according to body weight: control group (n = 10) and model group (n = 40). The model of alcoholic liver injury in mice was established by intraperitoneal injection of 56 ° Red Star Erguotu with alcohol (15 m L · kg-1) for 1, 2, 3 and 4 weeks. The mice were sacrificed at 0 (control group) At 1, 2, 3, and 4 weeks, 10 mice in each group were sacrificed on the eyeball, and serum aspartate aminotransferase (AST) activity was measured by Lai method. The mice were sacrificed by cervical dislocation, The expression of TNF-α in liver tissue was measured by Western blot. Results The activities of AST in mice liver were (112 ± 22), (126 ± 24), (967 ± 30), (1010 ± 35) and (206 ± 23) at 0, U · L ~ (-1), compared with the control group, the difference was statistically significant (P <0.05). The activity of AST in mouse liver increased slowly in the first week, rose rapidly in the second week, reached the peak in the third week and then decreased in the fourth week, but still higher than that in the control group. The relative integral optical density of TNF-α was 1.15 ± 0.12, 1.10 ± 0.08, 2.13 ± 0.16, 2.16 ± 0.15 and 1.16 ± 0.11 at 0, 1, 2, 3 and 4 weeks respectively. Compared with the control group, (P <0.01). The difference was statistically significant (P <0.01). The difference was statistically significant (P <0.01). Conclusion In the early stage of liver injury induced by ethanol, TNF-α can promote the injury and necrosis of hepatocytes and participate in the repair and regeneration of liver in the late stage.