机构地区:[1]厦门大学附属东南医院/解放军联勤保障部队第909医院感染病科,福建省厦门市363000
出 处:《实用肝脏病杂志》2021年第3期323-326,共4页Journal of Practical Hepatology
基 金:福建省科技厅科研基金资助项目(编号:20180349)。
摘 要:目的研究原儿茶酸对豆蛋白A(ConA)所致的免疫性肝损伤小鼠肝组织丙二醛(MDA)、一氧化氮(NO)、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-PX)水平的影响。方法随机将60只小鼠分为对照组、模型组、小、中、大剂量(2.5 mg.kg^(-1).d^(-1)、5 mg.kg^(-1).d^(-1)、10 mg.kg^(-1).d^(-1))原儿茶酸和(0.2 g.kg^(-1).d^(-1))联苯双酯处理组。在对照组和模型组给予等量生理盐水灌胃,在药物处理组分别给予不同剂量的药物灌胃,连续10 d。在末次给药1 h,一次性经尾静脉注射ConA,诱导免疫性肝损伤模型。分别检测血清白介素-4(IL-4)、IL-6、肿瘤坏死因子-α(TNF-α)和肝组织匀浆MDA、NO、SOD和GSH-PX活性。结果不同剂量原儿茶酸和联苯双酯处理组动物肝、脾指数显著降低,血清ALT和AST水平显著降低,血清IL-4、IL-6和TNF-α水平显著降低(P<0.05);模型组肝匀浆MDA和NO水平分别为(5.2±0.5)nmol/mg和(8.0±0.9)μmol/L,经小、中、大剂量原儿茶酸处理后,分别降至【(4.7±0.4)nmol/mg、(4.3±0.3)nmol/mg和(3.9±0.3)nmol/mg及(6.8±0.8)μmol/L、(6.2±0.7)μmol/L和(5.8±0.7)μmol/L,P<0.05】;模型组肝匀浆SOD和GSH-PX水平分别为(59.4±3.6)U/mg和(85.2±9.6)U/mg,经小、中、大剂量原儿茶酸处理后,分别升高至【(74.2±4.4)U/mg、(85.2±5.3)U/mg和(99.2±5.9)U/mg及(107.3±13.4)U/mg、(115.2±12.8)U/mg和(139.3±12.9)U/mg,P<0.05】。结论原儿茶酸可以减轻ConA引起的小鼠免疫性肝损伤,可能是通过提高了肝组织内源性抗氧化酶活力,增强了对氧自由基的清除能力有关。Objective The aim of this study was to investigate the effects of protocatechuic acid(PA)on hepatic malondialdehyde(MDA),nitric oxide(NO),superoxide dismutase(SOD)and glutathione peroxidase(GSH-PX)activities in mice with concanavalin A(ConA)-induced immune liver injury.Methods 60 Kunming mice were randomly divided into control,model,low-dose,middle-dose and high-dose(2.5 mg.kg^(-1).d^(-1)、5 mg.kg^(-1).d^(-1)、10 mg.kg^(-1).d^(-1))of PA-intervened and 0.2 g.kg^(-1).d^(-1) of bifendate-intervened group,with 10 in each.The mice in control group and in model group were intragastricly given normal saline for 10 days,and in other groups were intragastricly given PA or bifendate for 10 days.One hour after the last administration,the ConA were injected through tail vein once to induce immune liver injury models.Serum interleukin-4(IL-4),IL-6,tumor necrosis factor-α(TNF-α)and the MDA,NO,SOD and GSH-PX activities in hepatic homogenate were assayed.Results The liver indexes,spleen indexed,serum ALT and AST,serum IL-4,IL-6 and TNF-αin any dose of PA-intervened groups decreased significantly compared to those in the model(P<0.05);the hepatic MDA and NO activities in model group were(5.2±0.5)nmol/mg and(8.0±0.9)μmol/L,while they both decreased to[(4.7±0.4)nmol/mg,(4.3±0.3)nmol/mg and(3.9±0.3)nmol/mg or(6.8±0.8)μmol/L,(6.2±0.7)μmol/L and(5.8±0.7)μmol/L,respectively,P<0.05]in low-dose,middle-dose and large-dose of PA-intervened groups;the hepatic SOD and GSH-PX activities in model were(59.4±3.6)U/mg and(85.2±9.6)U/mg,while they both increased to[(74.2±4.4)U/mg,(85.2±5.3)U/mg and(99.2±5.9)U/mg or(107.3±13.4)U/mg,(115.2±12.8)U/mg and(139.3±12.9)U/mg,respectively,P<0.05]in low-dose,middle-dose and large-dose of PA-intervened groups.Conclusion PA could alleviate ConA-induced liver injury in mice,which might be related to the increased activity of endogenous antioxidant enzymes in liver tissues.
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