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Pediococcus pentosaceus PP04 Ameliorates High-Fat Diet-Induced Hyperlipidemia by Regulating Lipid Metabolism in C57BL/6N Mice
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2020-12-10 , DOI: 10.1021/acs.jafc.0c05060 Yu Wang 1, 2 , Ying You 1, 2 , Yuan Tian 1, 2 , Haiyue Sun 1, 2 , Xia Li 1, 2 , Xiujuan Wang 1, 2 , Yuhua Wang 1, 2, 3, 4 , Jingsheng Liu 1, 4
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2020-12-10 , DOI: 10.1021/acs.jafc.0c05060 Yu Wang 1, 2 , Ying You 1, 2 , Yuan Tian 1, 2 , Haiyue Sun 1, 2 , Xia Li 1, 2 , Xiujuan Wang 1, 2 , Yuhua Wang 1, 2, 3, 4 , Jingsheng Liu 1, 4
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In this study, Pediococcus pentococcus PP04 isolated from the Northeast pickled cabbage had good gastrointestinal tolerance and can colonize in the intestine stably. C57BL/6N mice were fed a high-fat diet to build animal models and treated with Pediococcus pentosaceus PP04 to evaluate the antihyperlipidemia effect. After 8 weeks, the indicators of hyperlipidemia, liver injury, and inflammation were measured. The treatment of P. pentosaceus PP04 reduced the gain of total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), free fatty acids (FFAs), leptin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), lipopolysaccharides (LPS), and tumor necrosis factor-α (TNF-α) significantly. The western blotting results suggested P. pentosaceus PP04 ameliorated high-fat diet-induced hyperlipidemia by the AMPK signaling pathway, which stimulated lipolysis via upregulation of PPARα and inhibited lipogenesis by downregulation of SREBP-1c, fatty acid synthase (FAS), and stearoyl-CoA desaturase-1 (SCD1) mainly. Furthermore, P. pentosaceus PP04 improved high-fat diet-induced oxidative stress effectively by triggering the Nrf2/CYP2E1 signaling pathway that enhanced the antioxidant activity including superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px).
中文翻译：
戊糖小球菌PP04通过调节C57BL / 6N小鼠的脂质代谢改善高脂饮食诱导的高脂血症
本研究从东北泡菜中分离出戊球菌PP04，具有良好的胃肠道耐受性，可以稳定地在肠道内定植。给C57BL / 6N小鼠喂食高脂饮食以建立动物模型，并用戊糖小球菌PP04处理以评估其抗高脂血症的作用。8周后，测量高脂血症，肝损伤和炎症的指标。戊糖假单胞菌的治疗PP04降低了总胆固醇（TC），甘油三酸酯（TG），低密度脂蛋白胆固醇（LDL-C），游离脂肪酸（FFA），瘦素，丙氨酸氨基转移酶（ALT），天冬氨酸氨基转移酶（AST），脂多糖（ LPS）和肿瘤坏死因子-α（TNF-α）显着。Western blotting结果表明，戊糖假单胞菌PP04通过AMPK信号通路改善了高脂饮食诱导的高脂血症，后者通过上调PPARα刺激脂解作用，并通过下调SREBP-1c，脂肪酸合成酶（FAS）和硬脂酰-糖脂来抑制脂肪生成。主要是CoA去饱和酶1（SCD1）。此外，P。pentosaceus PP04通过触发Nrf2 / CYP2E1信号传导途径来改善高脂饮食诱导的氧化应激，该信号传导途径增强了抗氧化活性，包括超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）。
更新日期：2020-12-23
中文翻译：
戊糖小球菌PP04通过调节C57BL / 6N小鼠的脂质代谢改善高脂饮食诱导的高脂血症
本研究从东北泡菜中分离出戊球菌PP04，具有良好的胃肠道耐受性，可以稳定地在肠道内定植。给C57BL / 6N小鼠喂食高脂饮食以建立动物模型，并用戊糖小球菌PP04处理以评估其抗高脂血症的作用。8周后，测量高脂血症，肝损伤和炎症的指标。戊糖假单胞菌的治疗PP04降低了总胆固醇（TC），甘油三酸酯（TG），低密度脂蛋白胆固醇（LDL-C），游离脂肪酸（FFA），瘦素，丙氨酸氨基转移酶（ALT），天冬氨酸氨基转移酶（AST），脂多糖（ LPS）和肿瘤坏死因子-α（TNF-α）显着。Western blotting结果表明，戊糖假单胞菌PP04通过AMPK信号通路改善了高脂饮食诱导的高脂血症，后者通过上调PPARα刺激脂解作用，并通过下调SREBP-1c，脂肪酸合成酶（FAS）和硬脂酰-糖脂来抑制脂肪生成。主要是CoA去饱和酶1（SCD1）。此外，P。pentosaceus PP04通过触发Nrf2 / CYP2E1信号传导途径来改善高脂饮食诱导的氧化应激，该信号传导途径增强了抗氧化活性，包括超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）。
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