Juglanin improves lipid metabolism disorder, liver injury, and intestinal integrity in nonalcoholic fatty liver mice

Lipid metabolism disorder and inflammation are essential promoters in pathogenesis of liver injury in type 2 diabetes. Puerarin (PUR) has been reported to exert beneficial effects on many diabetic cardiovascular diseases and chemical-induced liver injuries, but its effects on diabetic liver injury and its mechanism are still unclear. The current study was designed to explore the therapeutic effect and mechanism of PUR on liver injury in a type 2 diabetic rat model induced by a high-fat diet combined with low-dose streptozotocin. The diabetic rats were treated with or without PUR (100 mg/kg/day) by gavaging for 8 weeks, and biochemical and histological changes in liver were examined. Results showed that treatment with PUR significantly attenuated hepatic steatosis by regulating blood glucose and ameliorating lipid metabolism disorder. Liver fibrosis was relieved by PUR treatment. PUR inhibited oxidative stress and inflammation which was associated with inactivation of NF-κB signaling, thereby blocking the upregulation of proinflammatory cytokines (IL-1β, TNF-α) and chemokine (MCP-1). This protection of PUR on diabetic liver injury is possibly related with inhibition on TGF-β/Smad signaling. In conclusion, the present study provides evidence that PUR attenuated type 2 diabetic liver injury by inhibiting NF-κB-driven liver inflammation and the TGF-β/Smad signaling pathway.

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Anthraquinones in the aqueous extract of Cassiae semen cause liver injury in rats through lipid metabolism disorder

Phytomedicine ◽

10.1016/j.phymed.2019.153059 ◽

2019 ◽

Vol 64 ◽

pp. 153059 ◽

Cited By ~ 8

Author(s):

Jinlan Yang ◽

An Zhu ◽

Shuo Xiao ◽

Tao Zhang ◽

Liming Wang ◽

...

Keyword(s):

Lipid Metabolism ◽

Liver Injury ◽

Aqueous Extract ◽

Lipid Metabolism Disorder ◽

Metabolism Disorder

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Dietary Genistein Alleviates Lipid Metabolism Disorder and Inflammatory Response in Laying Hens With Fatty Liver Syndrome

Frontiers in Physiology ◽

10.3389/fphys.2018.01493 ◽

2018 ◽

Vol 9 ◽

Cited By ~ 10

Author(s):

Zengpeng Lv ◽

Kun Xing ◽

Guang Li ◽

Dan Liu ◽

Yuming Guo

Keyword(s):

Lipid Metabolism ◽

Inflammatory Response ◽

Fatty Liver ◽

Laying Hens ◽

Lipid Metabolism Disorder ◽

Metabolism Disorder

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AMPK/PGC-1α/GLUT4-Mediated Effect of Icariin on Hyperlipidemia-Induced Non-Alcoholic Fatty Liver Disease and Lipid Metabolism Disorder in Mice

Biochemistry (Moscow) ◽

10.1134/s0006297921110055 ◽

2021 ◽

Vol 86 (11) ◽

pp. 1407-1417

Author(s):

Wei Lin ◽

Yin Jin ◽

Xiang Hu ◽

Erjiong Huang ◽

Qihan Zhu

Keyword(s):

Lipid Metabolism ◽

Liver Disease ◽

Fatty Liver ◽

Fatty Liver Disease ◽

Lipid Metabolism Disorder ◽

Alcoholic Fatty Liver ◽

Metabolism Disorder ◽

Alcoholic Fatty Liver Disease

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A nanodrug system overexpressed circRNA_0001805 alleviates nonalcoholic fatty liver disease via miR-106a-5p/miR-320a and ABCA1/CPT1 axis

Journal of Nanobiotechnology ◽

10.1186/s12951-021-01108-8 ◽

2021 ◽

Vol 19 (1) ◽

Author(s):

Jian Li ◽

Jing Qi ◽

Yishu Tang ◽

Huaizheng Liu ◽

Kefu Zhou ◽

...

Keyword(s):

Lipid Metabolism ◽

Glycyrrhizic Acid ◽

Cultured Cells ◽

Underlying Mechanism ◽

Luciferase Reporter ◽

Lipid Metabolism Disorder ◽

Nonalcoholic Fatty Liver ◽

Metabolism Disorder ◽

Rbc Membrane ◽

Metalorganic Framework

AbstractOur study aimed to explore the function of circRNA_0001805 in the pathogenesis of NAFLD and the underlying mechanism. A nanodrug system (GA-RM/GZ/PL) was constructed to overexpress circRNA_0001805 specifically in hepatocytes for the treatment of NAFLD. Fat droplet accumulation in cultured cells and mouse hepatic tissues was detected using Oil Red O or H&E staining. The relative expression of circRNAs, genes associated with lipogenesis was quantified by qRT-PCR. Interactions between circRNA_0001805 and miR-106a-5p/miR-320a, between miR-106a-5p/miR-320a and ABCA1/CPT1 were confirmed by dual-luciferase reporter assay. A novel metalorganic framework nanocarrier (GZ) was prepared from glycyrrhizic acid and zinc ions (Zn2+), and this nanocarrier was loaded with the circRNA_0001805 plasmid to construct a nanocore (GZ/PL). Then, this GZ/PL was coated with a galactose-modified RBC membrane (GA-RM) to generate GA-RM/GZ/PL. CircRNA_0001805 expression was downregulated in FFA-challenged primary hepatocytes, HFD-fed mice and NAFLD patients. Overexpressed circRNA_0001805 attenuated NAFLD development by suppressing lipid metabolism disorder and inflammation. CircRNA_0001805 targeted miR-106a-5p/miR-320a, which served as an upstream inhibitor of ABCA1/CPT1 and collaboratively regulated NAFLD progression. GA-RM/GZ/PL targeted hepatocytes, overexpressed circRNA_0001805, released glycyrrhizic acid to reduce the accumulation of lipids in the liver and played a synergistic role against NAFLD-induced lipid metabolism disorder. Graphical Abstract

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SGL 121 Attenuates Nonalcoholic Fatty Liver Disease through Adjusting Lipid Metabolism Through AMPK Signaling Pathway

International Journal of Molecular Sciences ◽

10.3390/ijms21124534 ◽

2020 ◽

Vol 21 (12) ◽

pp. 4534

Author(s):

Da Eun Kim ◽

Bo Yoon Chang ◽

Byeong Min Jeon ◽

Jong In Baek ◽

Sun Chang Kim ◽

...

Keyword(s):

Lipid Metabolism ◽

Liver Disease ◽

Fatty Liver ◽

Nonalcoholic Fatty Liver Disease ◽

Signaling Pathway ◽

Hepg2 Cells ◽

Fatty Liver Disease ◽

Fatty Acid Synthase ◽

Density Lipoprotein ◽

Nonalcoholic Fatty Liver

A ginsenoside F2-enhanced mixture (SGL 121) increases the content of ginsenoside F2 by biotransformation. In the present study, we investigated the effect of SGL 121 on nonalcoholic fatty liver disease (NAFLD) in vitro and in vivo. High-fat, high-carbohydrate-diet (HFHC)-fed mice were administered SGL 121 for 12 weeks to assess its effect on improving NAFLD. In HepG2 cells, SGL 121 acted as an antioxidant, a hepatoprotectant, and had an anti-lipogenic effect. In NAFLD mice, SGL 121 significantly improved body fat mass; levels of hepatic triglyceride (TG), hepatic malondialdehyde (MDA), serum total cholesterol (TC), high-density lipoprotein (HDL), and low-density lipoprotein (LDL); and activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). In HepG2 cells, induced by oxidative stress, SGL 121 increased cytoprotection, inhibited reactive oxygen species (ROS) production, and increased antioxidant enzyme activity. SGL 121 activated the Nrf2/HO-1 signaling pathway and improved lipid accumulation induced by free fatty acids (FFA). Sterol regulatory element-binding protein-1 (SREBP-1) and fatty acid synthase (FAS) expression was significantly reduced in NAFLD-induced liver and HepG2 cells treated with SGL 121. Moreover, SGL 121 activated adenosine monophosphate-activated protein kinase (AMPK), which plays an important role in the regulation of lipid metabolism. The effect of SGL 121 on the improvement of NAFLD seems to be related to its antioxidant effects and activation of AMPK. In conclusion, SGL 121 can be potentially used for the treatment of NAFLD.

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