论文部分内容阅读
目的:研究抗氧化剂N-乙酰半胱氨酸(NAC)对小鼠肝脏缺血再灌注损伤模型中肝肺组织的保护作用及机制。方法:制备BALB/c小鼠肝部分缺血再灌注损伤模型,将小鼠随机分为3组:假手术组(SH组),缺血再灌注组(I/R组)和NAC组(I/R-NAC组)。分别于再灌注后1 h、3 h取静脉血测定血清TNF-α浓度和ALT水平;取肺组织标本测湿干质量比及病理。同时取肝、肺组织行RT-PCR以观测Toll样受体2/4(TLR2/4)表达。结果:肺组织病理结果显示I/R组肺组织毛细血管充血,肺泡结构破坏,肺泡间质中性粒细胞浸润,肺泡腔内不同程度渗出及少量红细胞。肺湿干质量比显示肺水肿。缺血再灌注后静脉血清TNF-α浓度和ALT水平较假手术组显著升高。受损肝叶和肺组织内均出现TLR2/4 mR-NA高表达,NAC干预后,肺水肿明显减轻;TLR2/4 mRNA表达受到抑制;血清TNF-α浓度和ALT水平较I/R组明显下降。结论:N-乙酰半胱氨酸抑制再灌注后TLR2/4的活化,降低TNF-α的分泌,从而减轻缺血再灌注肝、肺组织的损伤。
Objective: To study the protective effect and mechanism of antioxidant N-acetyl cysteine (NAC) on liver and lung tissue in a mouse model of hepatic ischemia-reperfusion injury. Methods: The model of partial ischemia-reperfusion injury in BALB / c mice was established. The mice were randomly divided into 3 groups: sham operation group (SH group), ischemia / reperfusion group (I / R group) and NAC group / R-NAC group). Serum levels of TNF-α and ALT were measured by venous blood at 1 and 3 h after reperfusion. The wet-dry weight ratio and pathology of lung tissue were measured. At the same time, liver and lung tissues were taken for RT-PCR to observe the expression of Toll-like receptor 2/4 (TLR2 / 4). Results: Pathological results of lung tissue showed capillary congestion, destruction of alveolar structure, infiltration of alveolar interstitial neutrophils, exudation of alveolar in different degree and a few erythrocytes in I / R group. Lung wet-dry mass ratio shows pulmonary edema. The levels of TNF-α and ALT in venous serum after ischemia-reperfusion were significantly higher than those in sham operation group. The expression of TLR2 / 4 mR-NA was high in the damaged liver and lung tissues. Pulmonary edema was significantly reduced after NAC intervention. The expression of TLR2 / 4 mRNA was inhibited. The serum TNF-α and ALT levels were significantly higher than those in I / R group decline. CONCLUSION: N-acetylcysteine can inhibit the activation of TLR2 / 4 and decrease the secretion of TNF-α after reperfusion, thereby reducing the damage of liver and lung tissue after ischemia-reperfusion.