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PP04 通过调节 C57BL/6N 小鼠的脂代谢改善高脂饮食诱导的高血脂症。

PP04 Ameliorates High-Fat Diet-Induced Hyperlipidemia by Regulating Lipid Metabolism in C57BL/6N Mice.

机构信息

College of Food Science and Engineering, Jilin Agricultural University, Changchun 130118, China.

Jilin Province Innovation Center for Food Biological Manufacture, Jilin Agricultural University, Changchun 130118, China.

出版信息

J Agric Food Chem. 2020 Dec 23;68(51):15154-15163. doi: 10.1021/acs.jafc.0c05060. Epub 2020 Dec 10.

Abstract

In this study, 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 PP04 to evaluate the antihyperlipidemia effect. After 8 weeks, the indicators of hyperlipidemia, liver injury, and inflammation were measured. The treatment of 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 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, 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).

摘要

本研究从东北酸菜中分离得到的 PP04 具有良好的胃肠道耐受性,并能在肠道内稳定定植。用高脂饲料喂养 C57BL/6N 小鼠构建动物模型,并用 PP04 进行治疗,以评估其抗高血脂作用。8 周后,测量高血脂、肝损伤和炎症的指标。PP04 的治疗显著降低了总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、游离脂肪酸(FFAs)、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)的水平。Western blot 结果表明,PP04 通过 AMPK 信号通路改善了高脂饮食诱导的高血脂,该通路通过上调 PPARα 刺激脂肪分解,并通过下调 SREBP-1c、脂肪酸合成酶(FAS)和硬脂酰辅酶 A 去饱和酶-1(SCD1)抑制脂肪生成。此外,PP04 通过触发 Nrf2/CYP2E1 信号通路有效改善了高脂饮食诱导的氧化应激,该通路增强了抗氧化活性,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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