富氢水对乙醇诱导的胃损伤和肝损伤的保护作用与机制

发布时间：2018-06-09 00:14

本文选题：乙醇 + 胃损伤　；参考：《兰州大学》2017年硕士论文

【摘要】：目的本研究旨在探讨富氢水对乙醇诱导的急性胃损伤和慢性肝损伤的保护作用与机制,并研究富氢水是否会对机体产生毒副作用。方法建立小鼠急性乙醇性胃损伤和慢性乙醇性肝损伤的动物模型,分为4组:正常对照组,单独富氢水组,乙醇造模组和富氢水治疗组。观察慢性乙醇性肝损伤模型的小鼠生存情况。测量急性乙醇性胃损伤模型小鼠的胃黏膜损伤指数。HE染色观察胃、肝组织的病理学改变。检测慢性乙醇性肝损伤模型血清中ALT、AST、TB和DB的水平。WST-1法检测小鼠血清及胃、肝组织中氧化指标SOD活力。TAB法检测小鼠血清及胃、肝组织中氧化指标MDA水平。ELISA法检测小鼠血清中炎症因子IL-6和TNF-α的水平。免疫组织化学和RT-PCR法检测胃和肝组织凋亡因子Caspase-3、Bax、Caspase-9、Fas和Caspase-8的表达水平。P0.05表示有显著性差异。结果1.对于急性乙醇性胃损伤模型,与正常对照组相比,乙醇造模组小鼠胃黏膜损伤指数显著升高(P0.001),胃组织病理损伤程度重,氧化指标血清SOD/MDA显著降低(P0.001),氧化指标血清SOD,血清和胃组织MDA,炎症因子IL-6及凋亡因子Caspase-3,Bax,Fas的蛋白和Caspase-3,Bax,Fas,Caspase-9的mRNA表达水平显著升高(P0.001,P0.001,P0.001,P0.001,P0.001,P0.001,P0.001,P0.001,P=0.047,P=0.002,P=0.001)。与乙醇造模组相比,富氢水治疗组胃黏膜损伤指数显著降低(P0.001),胃组织病理损伤减轻,血清SOD活力显著升高(P0.001),血清及胃组织SOD/MDA显著升高(P=0.002,P0.001),血清及胃组织MDA水平显著降低(P0.001,P0.001),血清中IL-6水平显著降低(P0.001),胃组织中的Caspase-3,Bax的蛋白和Caspase-3,Bax,Fas的mRNA表达水平显著降低(P0.001,P=0.001,P0.001、P=0.005,P0.001)。与正常对照组相比,单独富氢水组胃黏膜损伤指数,氧化指标,炎症因子及凋亡因子的表达均无统计学意义(P0.05)。2.对于慢性乙醇性肝损伤模型,与正常对照组相比,乙醇造模组生存率显著降低(P0.001),肝组织病理损伤程度重,血清ALT和AST显著升高(P0.001,P0.001),氧化指标血清及肝组织SOD/MDA显著降低(P=0.002、P0.001),血清及肝组织MDA,炎症因子TNF-α及凋亡因子Bax,Caspase-8的蛋白和Fas的mRNA的表达水平显著升高(P0.001,P0.001,P=0.001,P0.001,P0.001,P0.001)。与乙醇造模组相比,富氢水治疗组小鼠生存率显著升高(P=0.019),肝组织病理损伤减轻,血清ALT和AST显著降低(P0.001、P=0.002),肝组织SOD/MDA显著升高(P0.001),血清及肝组织MDA水平显著降低(P=0.001,P0.001),血清中TNF-α的水平显著降低(P0.001),肝组织中凋亡因子的表达水平均无统计学意义(P0.05)。与正常对照组相比,单独富氢水组小鼠生存率,血清ALT,AST,TB,DB,氧化指标,炎症因子及凋亡因子的表达均无统计学意义(P0.05)。结论富氢水可以减轻乙醇诱导的急性胃损伤和慢性肝损伤程度,对急性乙醇性胃损伤可能的主要作用机制为抗氧化、抗炎和抗凋亡,而对慢性乙醇性肝损伤可能的主要作用机制为抗氧化和抗炎。富氢水是安全可靠的,未发现对机体存在明显毒副作用。
[Abstract]:Objective to explore the protective effect and mechanism of hydrogen rich water on ethanol induced acute gastric injury and chronic liver injury, and to study the toxic and side effects of hydrogen rich water on the body. Methods the animal models of acute ethanol induced gastric injury and chronic alcoholic liver injury in mice were set up into 4 groups: normal control group and separate hydrogen rich water group, The survival of chronic alcoholic liver injury models in mice was observed by ethanol model and hydrogen rich water treatment group. The gastric mucosal injury index.HE staining of acute ethanol induced gastric injury model mice was measured to observe the pathological changes of the stomach and liver tissues. The serum levels of ALT, AST, TB and DB in the serum of chronic alcoholic liver injury were detected by.WST-1 method in the detection of mice. Serum and gastric, liver tissue oxidation index SOD activity.TAB method to detect the serum and stomach of mice and the level of MDA level of oxidation index in liver tissue to detect the level of inflammatory factors IL-6 and TNF- alpha in the serum of mice. Immunohistochemistry and RT-PCR method were used to detect the apoptosis factor Caspase-3 of gastric and liver tissues, Bax, Caspase-9, Fas and Caspase-8. Results 1. for acute ethanol induced gastric injury. Compared with the normal control group, the gastric mucosal damage index of the ethanol model mice was significantly increased (P0.001), the pathological damage of the gastric tissue was heavy, the serum SOD/MDA was significantly reduced (P0.001), the oxidation index serum SOD, the serum and gastric tissue MDA, and the inflammatory factor IL-6 were significantly higher than those of the normal control group. Caspase-3, Bax, Fas protein and Caspase-3, Bax, Fas, Caspase-9 significantly increased the level of mRNA expression (P0.001, P0.001, P0.001, P0.001), compared with the ethanol model group, the gastric mucosal injury index of the hydrogen rich treatment group decreased significantly, the pathological damage of the gastric tissue was reduced, blood was reduced. The serum and gastric tissue SOD/MDA increased significantly (P=0.002, P0.001), and the serum and gastric tissue MDA levels decreased significantly (P0.001, P0.001) in serum and gastric tissue (P0.001, P0.001). The level of IL-6 in serum and gastric tissue decreased significantly (P0.001), Caspase-3 in the gastric tissue, and the expression level of Bax protein and SOD decreased significantly. 5, P0.001). Compared with the normal control group, the expression of gastric mucosal damage index, oxidation index, inflammatory factor and apoptosis factor in the individual rich hydrogen group had no statistical significance (P0.05).2. for chronic alcoholic liver injury model, compared with the normal control group, the survival rate of ethanol model was significantly lower (P0.001), the degree of pathological damage of liver tissue was heavy, serum level was heavy. ALT and AST significantly increased (P0.001, P0.001), the oxidation index serum and liver tissue SOD/MDA decreased significantly (P=0.002, P0.001), serum and liver MDA, inflammatory factor TNF- alpha and apoptotic factor Bax, Caspase-8 protein and Fas. The survival rate of the mice in the treatment group was significantly increased (P=0.019), the pathological damage of the liver tissue was reduced, the serum ALT and AST were significantly decreased (P0.001, P=0.002), the liver tissue SOD/MDA was significantly increased (P0.001), the serum and liver MDA levels were significantly decreased (P=0.001, P0.001), the level of TNF- alpha in the serum was significantly reduced (P0.001), the expression level of apoptosis factors in liver tissues were all There was no statistical significance (P0.05). Compared with the normal control group, the survival rate of mice in the hydrogen rich water group alone, the expression of serum ALT, AST, TB, DB, oxidation index, inflammatory factor and apoptosis factor were not statistically significant (P0.05). Conclusion the hydrogen rich water can reduce the severity of acute gastric injury and chronic liver injury induced by ethanol, and the acute ethanol induced gastric injury may be reduced. The main mechanism of action is antioxidation, anti-inflammatory and anti apoptosis, and the main mechanism of action on chronic alcoholic liver injury is antioxidant and anti-inflammatory. The hydrogen rich water is safe and reliable, and there is no obvious toxic side effect on the body.
【学位授予单位】：兰州大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R57

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