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背景:肝脏是对缺血再灌注损伤最敏感的器官之一。黄酮类化合物落新妇甙可作为递氢体清除氧自由基,从而可能在减轻肝脏缺血再灌注损伤等方面发挥作用。目的:观察落新妇甙对肝脏热缺血再灌注损伤的保护作用,对其机制进行初步探讨。方法:C57BL/6小鼠随机分为4组:假手术组、模型组、小剂量干预组和大剂量干预组。干预组小鼠于缺血前24h和1h分别给予10或40mg/kg的落新妇甙腹腔注射,然后建立70%部分肝缺血再灌注模型。采集血液和肝脏组织样本。检测血清丙氨酸氨基转移酶活性,ELISA测血清肿瘤坏死因子α水平,化学比色法测定肝组织中超氧化物歧化酶、丙二醛含量。肝脏组织病理学检测。Westernblot检测肝组织中肿瘤坏死因子α蛋白含量,RT-PCR检测肿瘤坏死因子αmRNA。结果与结论:落新妇甙干预能有效降低血清丙氨酸氨基转移酶水平,干预组肝组织丙二醛含量较模型对照组明显下降(P<0.01);而超氧化物歧化酶含量明显上升(P<0.01);干预组血清肿瘤坏死因子α含量较模型组对照组明显下降(P<0.01);小、大剂量干预组肝组织中肿瘤坏死因子α蛋白表达与模型组模型对照组比较渐次降低,与半定量RT-PCR结果相符(小剂量干预组P<0.05,大剂量干预组P<0.01)。落新妇甙保护肝脏热缺血再灌注损伤显示出剂量-效应关系趋势。结果提示,落新妇甙干预能减轻小鼠肝脏热缺血再灌注损伤后的炎症反应和脂质过氧化损伤,有效改善肝功能和肝脏病理损害;机制可能在于其能抑制缺血再灌注损伤肝组织中肿瘤坏死因子α的高表达。
BACKGROUND: The liver is one of the most sensitive organs for ischemia-reperfusion injury. The flavonoids assemblages of women and children can act as hydrogenerators to scavenge oxygen free radicals, which may play a role in reducing hepatic ischemia-reperfusion injury. OBJECTIVE: To observe the protective effect of Astilbin on female liver warm ischemia reperfusion injury, and to discuss its mechanism. Methods: C57BL/6 mice were randomly divided into 4 groups: sham operation group, model group, low-dose intervention group and large-dose intervention group. The mice in the intervention group were given an intraperitoneal injection of 10 or 40 mg/kg of astilbin before and 24 hours before ischemia, and then a 70% partial hepatic ischemia-reperfusion model was established. Blood and liver tissue samples were collected. Serum alanine aminotransferase activity was measured. Serum tumor necrosis factor alpha levels were measured by ELISA. Superoxide dismutase and malondialdehyde levels in liver tissues were determined by chemical colorimetry. Histopathological examination of the liver. The content of tumor necrosis factor-α protein was detected by Western blot, and the tumor necrosis factor-α mRNA was detected by RT-PCR. RESULTS AND CONCLUSION: The intervention of the new women and children can effectively reduce serum alanine aminotransferase levels. The content of malondialdehyde in the liver tissue of the intervention group was significantly lower than that of the model control group (P<0.01), and the content of superoxide dismutase was significantly increased ( P<0.01); Serum tumor necrosis factor-α content in the intervention group was significantly lower than that in the model group (P<0.01); Tumor necrosis factor-α protein expression in the liver tissue of the small and high-dose intervention group was gradually decreased compared with the model group of the control group. , Consistent with semi-quantitative RT-PCR results (P<0.05 for low-dose interventions, P<0.01 for large-dose interventions). Emergence of new women’s cockroaches protects the liver from warm ischemia-reperfusion injury and shows a dose-response relationship. The results suggest that intervention of astilbin and momordica can reduce the inflammatory reaction and lipid peroxidation injury after hepatic warm ischemia-reperfusion injury in mice, and effectively improve liver function and liver pathological damage; the mechanism may be that it can inhibit the liver from ischemia-reperfusion injury. High expression of tumor necrosis factor alpha in tissues.