副干酪乳杆菌FM-M9-1对D-半乳糖诱导氧化损伤小鼠的修复机制

Mechanism by Which Lactobacillus paracasei FM-M9-1 Repairs D-Galactose-Induced Oxidative Damage in Mice

目的:分析副干酪乳杆菌FM-M9-1修复氧化损伤的作用机制。方法:利用D-半乳糖诱导氧化损伤模型小鼠,以高、低剂量((5.01±0.05)×10^(10)、(5.01±0.05)×10~8 CFU/m L)FM-M9-1活菌体灌胃小鼠,以VC作为阳性药物对照,60 d后测定小鼠的肾和肝组织中超氧化物歧化酶(superoxide dismutase,SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)活力及丙二醛、蛋白质羰基含量,同时利用荧光实时定量聚合酶链式反应法分析小鼠肝脏和肾脏组织Sod、Gsh-Px、Nrf2和Trx基因的表达水平。结果:FM-M9-1能不同程度地提高小鼠肝和肾组织中的GSH-Px和SOD活力,降低蛋白质羰基和丙二醛含量,提高与抗氧化功能相关的Sod、Gsh-Px、Nrf2和Trx基因的表达水平。结论:FM-M9-1上调小鼠体内抗氧化相关基因Sod、Gsh-Px、Nrf2和Trx的表达,提高抗氧化酶SOD、GSH-Px活力,抑制体内的蛋白质和脂肪的氧化损伤,最终达到修复小鼠体内氧化损伤的目的。

Objective:To analyze the mechanism by which Lactobacillus paracasei FM-M9-1 repairs oxidative damage in mice.Methods:A mouse model of oxidative damage was induced by D-galactose.The model mice were gavaged with strain FM-M9-1 at low and high doses of(5.01±0.05)×1010 and(5.01±0.05)×108 CFU/mL for 60 successive days,separately.Vitamin C was used as a positive control drug.Afterwards,the activity of superoxide dismutase(SOD)and glutathione peroxidase(GSH-Px)and the contents of malondialdehyde(MDA)and protein carbonyl groups in renal and hepatic tissues were measured.We also examined the expression levels of Sod,Gsh-Px,Nrf2 and Trx by real-time fluorescent quantitative polymerase chain reaction(qPCR).Results:The administration of FM-M9-1 significantly enhanced SOD and GSH-Px activities and reduced MDA and protein carbonyl contents.At the transcriptional level,qPCR analysis suggested that the gene expression of Sod,Gsh-Px,Nrf2 and Trx in mice administered with FM-M9-1 increased.Conclusion:Strain FM-M9-1 can alleviate oxidative stress by increasing the activities of antioxidant enzymes,inhibiting lipid and protein oxidation,and up-regulating the expression of antioxidant function-related genes.Overall,strain FM-M9-1 is a promising probiotic candidate for application in functional foods and antioxidant supplements.