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. 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. 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.

中文翻译：

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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

肥胖是世界上的一种流行病，肥胖的治疗和预防方法受到了广泛的关注。乳酸杆菌是益生菌的主要成分，其生理活性对不同菌株具有特异性。本研究系统地探讨了从腌制蔬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理。LF-CQPC07有效地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减轻了肝细胞的损害和脂肪细胞中脂肪的积累。对生化指标的检测表明，LF-CQPC07降低了总胆固醇（TC），低密度脂蛋白胆固醇（LDL-C）和甘油三酸酯（TG）的水平，并增加了高密度脂蛋白胆固醇（HDL-C）的水平。此外，LF-CQPC07导致炎症细胞因子白介素（IL）-1β，肿瘤坏死因子-α（TNF-α），IL-6和干扰素-γ（IFN-γ）的量减少，并且抗炎细胞因子IL-10和IL-4的量。LF-CQPC07还减少了丙氨酸转氨酶（ALT），天冬氨酸转氨酶（AST）和碱性磷酸酶（ALP）的含量。通过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。它还增加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）的mRNA表达水平，脂蛋白脂酶（LPL）和胆固醇7α羟化酶（CYP7A1），并降低了小鼠肝脏中PPAR-γ和CCAAT /增强子结合蛋白α（C /EBP-α）的胆固醇。这项研究证实了LF-CQPC07能够改善肥胖，改善高脂血症，减轻慢性低度炎症和肥胖引起的肝损伤。其机制可能是抗氧化能力和脂质代谢的调节。因此，LF-CQPC07具有巨大的潜力，可以作为预防或治疗肥胖症的潜在益生菌。减轻慢性低度发炎和肝脏损伤并伴有肥胖。其机制可能是抗氧化能力和脂质代谢的调节。因此，LF-CQPC07具有巨大的潜力，可以作为预防或治疗肥胖症的潜在益生菌。减轻慢性低度发炎和肝脏损伤并伴有肥胖。其机制可能是抗氧化能力和脂质代谢的调节。因此，LF-CQPC07具有巨大的潜力，可以用作预防或治疗肥胖症的潜在益生菌。