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发酵乳杆菌CQPC07通过调节高脂饮食诱导的肥胖小鼠的抗氧化能力和脂质代谢来减轻肥胖、炎症和血脂异常。

Lactobacillus fermentum CQPC07 attenuates obesity, inflammation and dyslipidemia by modulating the antioxidant capacity and lipid metabolism in high-fat diet induced obese mice.

作者信息

Wu Ya, Li Xueya, Tan Fang, Zhou Xianrong, Mu Jianfei, Zhao Xin

机构信息

Chongqing Collaborative Innovation Center for Functional Food, Chongqing University of Education, Xuefu Main Street 9 Nan'an District, Chongqing, 400067, People's Republic of China.

Chongqing Engineering Research Center of Functional Food, Chongqing University of Education, Xuefu Main Street 9 Nan'an District, Chongqing, 400067, People's Republic of China.

出版信息

J Inflamm (Lond). 2021 Feb 2;18(1):5. doi: 10.1186/s12950-021-00272-w.

DOI:10.1186/s12950-021-00272-w
PMID:33531053
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7852154/
Abstract

BACKGROUND

Obesity is an epidemic disease in the world, the treatment and prevention of obesity methods have gained great attention. Lactobacillus is the main member of probiotics, and the physiological activity of it is specific to different strains. This study systematically explored the anti-obesity effect and possible mechanism of Lactobacillus fermentum CQPC07 (LF-CQPC07), which was isolated from pickled vegetables.

RESULTS

LF-CQPC07 effectively controlled the weight gain of mice caused by a high-fat diet. The results of pathological sections indicated that LF-CQPC07 alleviated hepatocyte damage and fat accumulation in adipocytes. The detection of biochemical indictors revealed that LF-CQPC07 decreased the levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG), and increased the level of high-density lipoprotein cholesterol (HDL-C). Additionally, LF-CQPC07 caused the decrease in the amounts of inflammatory cytokines interleukin (IL)-1β, tumor necrosis factor-α (TNF-α), IL-6, and interferon-γ (IFN-γ), and the increase in the amounts of the anti-inflammatory cytokines IL-10 and IL-4. LF-CQPC07 also decreased the amounts of alanine aminotransferase (ALT), aspartate transaminase (AST), and alkaline phosphatase (ALP). Confirmed by qPCR, LF-CQPC07 enhanced the mRNA expression of catalase (CAT), gamma glutamylcysteine synthetase 1 (GSH1), copper/zinc superoxide dismutase (SOD1), manganese superoxide dismutase (SOD2), and glutathione peroxidase (GSH-Px). It also increased the mRNA expression levels of carnitine palmitoyltransferase 1 (CPT1), peroxisome proliferator-activated receptor alpha (PPAR-α), lipoprotein lipase (LPL), and cholesterol 7 alpha hydroxylase (CYP7A1), and decreased that of PPAR-γ and CCAAT/enhancer binding protein alpha (C/EBP-α) in the liver of mice.

CONCLUSION

This research confirmed that LF-CQPC07 is capable of ameliorating obesity, improving hyperlipemia, and alleviating chronic low-grade inflammation and liver injury accompanied with obesity. Its mechanism may be the regulation of antioxidant capacity and lipid metabolism. Therefore, LF-CQPC07 has enormous potential to serve as a potential probiotic for the prevention or treatment of obesity.

摘要

背景

肥胖是一种全球性的流行性疾病,肥胖的治疗和预防方法备受关注。乳酸杆菌是益生菌的主要成员,其生理活性因菌株而异。本研究系统地探讨了从泡菜中分离出的发酵乳杆菌CQPC07(LF-CQPC07)的抗肥胖作用及其可能的机制。

结果

LF-CQPC07有效控制了高脂饮食引起的小鼠体重增加。病理切片结果表明,LF-CQPC07减轻了肝细胞损伤和脂肪细胞内的脂肪积累。生化指标检测显示,LF-CQPC07降低了总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)和甘油三酯(TG)的水平,并提高了高密度脂蛋白胆固醇(HDL-C)的水平。此外,LF-CQPC07使炎性细胞因子白细胞介素(IL)-1β、肿瘤坏死因子-α(TNF-α)、IL-6和干扰素-γ(IFN-γ)的量减少,抗炎细胞因子IL-10和IL-4的量增加。LF-CQPC07还降低了丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)和碱性磷酸酶(ALP)的量。经qPCR证实,LF-CQPC07增强了过氧化氢酶(CAT)、γ-谷氨酰半胱氨酸合成酶1(GSH1)、铜/锌超氧化物歧化酶(SOD1)、锰超氧化物歧化酶(SOD2)和谷胱甘肽过氧化物酶(GSH-Px)的mRNA表达。它还提高了肉碱棕榈酰转移酶1(CPT1)、过氧化物酶体增殖物激活受体α(PPAR-α)、脂蛋白脂肪酶(LPL)和胆固醇7α羟化酶(CYP7A1)在小鼠肝脏中的mRNA表达水平,并降低了PPAR-γ和CCAAT/增强子结合蛋白α(C/EBP-α)的表达水平。

结论

本研究证实LF-CQPC07能够改善肥胖、改善高脂血症,并减轻肥胖伴随的慢性低度炎症和肝损伤。其机制可能是对抗氧化能力和脂质代谢的调节。因此,LF-CQPC07作为预防或治疗肥胖的潜在益生菌具有巨大潜力。

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