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- 2017
胸腺素α1对急性肝衰竭大鼠血浆TNF-α与IL-10的影响
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Abstract:
摘要： 目的 探讨胸腺素α1(Tα1)对急性肝衰竭大鼠血浆TNF-α与IL-10的影响。方法 构建急性肝衰竭大鼠模型后分组，干预组大鼠注射Tα1，检测不同时间点大鼠血浆ALT、AST、TBIL含量及血浆TNF-α、IL-10水平，获取的肝组织标本进行HE染色。结果 ①模型组及干预组ALT、AST、TBIL随时间均呈上升趋势，同一时间点，干预组ALT、AST、TBIL明显低于模型组(P<0.05)。②模型组及干预组肝组织均出现明显肝组织结构紊乱，肝细胞明显坏死，炎性细胞浸润等急性肝衰竭表现，且两组均随着时间不断加重。同一时间点，干预组肝细胞坏死程度较模型组轻，浸润的炎性细胞也较模型组少。③模型组及干预组TNF-α、IL-10均明显高于对照组(P<0.05)。模型组及干预组TNF-α、IL-10随时间均呈上升趋势。同一时间点，干预组TNF-α明显低于模型组；干预组IL-10明显高于模型组。结论 Tα1对急性肝衰竭大鼠具有保护作用，可明显改善肝细胞炎症及坏死，其机制可能与下调炎性细胞因子TNF-α水平，上调抗炎性细胞因子IL-10水平有关。
ABSTRACT: Objective To investigate the effects of thymosin α1 (Tα1) on plasma TNF-α and IL-10 of rats with acute liver failure. Methods The model of acute liver failure in rats was established. The rats in intervention group were injected with Tα1; their plasma ALT, AST and TBIL contents as well as plasma TNF-α and IL-10 levels were assayed at different time points for HE staining of liver sections. Results ① ALT, AST and TBIL in model group and intervention group increased over time. Plasma ALT, AST and TBIL were significantly lower in intervention group than in model group at the same time point (P<0.05). ② Manifestations of acute liver failure such as structural disorder of liver tissue, obvious necrosis of liver cells and infiltration of inflammatory cells were observed in model group and intervention group, and worsened over time. At the same time point, liver cell necrosis and infiltration of inflammatory cells were less severe than those in model group. ③ TNF-α and IL-10 were significantly higher in model and intervention groups than in control group (P<0.05). Plasma TNF-α and IL-10 showed a rising trend over time in the former groups (P<0.05). At the same time point, TNF-α was significantly lower but IL-10 was significantly higher in intervention group than in model group. Conclusion Thymosin α1 has a protective effect on acute hepatic failure in rats, and it can significantly alleviate liver inflammation and necrosis. The mechanism is related to inhibition of pro-inflammatory cytokine TNF-α and upregulation of anti-inflammatory cytokine IL-10
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