Nobiletin Ameliorates Hepatic Lipid Deposition, Oxidative Stress, and Inflammation by Mechanisms That Involve the Nrf2/NF-κB Axis in Nonalcoholic Fatty Liver Disease

Involvement of Bile Acid Metabolism and Gut Microbiota in the Amelioration of Experimental Metabolism-Associated Fatty Liver Disease by Nobiletin

“…The collection and processing methods for mouse serum and liver tissue were adapted from previous studies [ 24 ]. The serum levels of TC, TG, NEFA, HDL, LDL, ALT, AST, LPS, and INS, as well as the hepatic levels of TC, IL-1Β, and TNF-α were detected using biochemistry kits, following the manufacturers’ specifications.…”

“…NOB provides hepatoprotective effects by regulating the composition of gut microbes [ 22 ] and simultaneously mitigating insulin resistance [ 23 ]. Studies have demonstrated that NOB can ameliorate hepatic lipid deposition, oxidative stress, and inflammation through mechanisms involving the Nrf2/NF-κB axis in NAFLD [ 24 ]. Additionally, NOB has been shown to have beneficial effects in mice deficient dyslipidemia in hepatic AMPK deficient ( Ampkβ 1 −/− ) mice fed a high-fat diet (HFD) [ 25 ].…”

Nobiletin from citrus peel: a promising therapeutic agent for liver disease-pharmacological characteristics, mechanisms, and potential applications

“…In addition, NOB reduces the expression of 4-hydroxy-2-nonenal in the liver and decreases the intracellular redox potential ( Dusabimana et al, 2019 ). NOB also increases hepatic GSH levels and protects hepatocytes by inhibiting endogenous oxidative stress, NF-κB ( Fan et al, 2023 ), JNK ( Li et al, 2020 ; Zhang et al, 2016 ) and PPAR-α pathways ( Ke et al, 2023 ). NOB administration can lead to a decrease in superoxide dismutase activity due to its suppressive effect on drug-induced hepatic lipid peroxidation and ROS generation, which results in redox homeostasis in the liver rather than an improvement in antioxidant capacity ( Fan et al, 2023 ).…”

“…NOB also increases hepatic GSH levels and protects hepatocytes by inhibiting endogenous oxidative stress, NF-κB ( Fan et al, 2023 ), JNK ( Li et al, 2020 ; Zhang et al, 2016 ) and PPAR-α pathways ( Ke et al, 2023 ). NOB administration can lead to a decrease in superoxide dismutase activity due to its suppressive effect on drug-induced hepatic lipid peroxidation and ROS generation, which results in redox homeostasis in the liver rather than an improvement in antioxidant capacity ( Fan et al, 2023 ). Li et al ( Hao et al, 2023 ) established a liver fibrosis model by intraperitoneal injection of carbon tetrachloride (CCl 4 ) to induce oxidative stress, and the experimental group received different doses of NOB for 3 weeks, and found that NOB significantly inhibited ROS production, and the expression of Microtubule-associated protein 1 light chain 3 II and degradation of p62 were significantly increased after NOB treatment.…”