Naringin Dihydrochalcone, an artificial sweetener derived from naringin—a prominent flavanone glycoside found in tomatoes and various citrus fruits—displays a range of biological activities including antioxidant, anti-inflammatory, and antiapoptotic effects. It notably impedes the NF-κB signaling pathway[1].
体内研究
Naringin treatment significantly attenuates renal injury in diabetic rats and notably increases their body weight. It effectively reduces collagen deposition and renal interstitial fibrosis in these rats. Moreover, Naringin administration correlates with decreased levels of reactive oxygen species (ROS) and malondialdehyde (MDA), along with increased activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px)[1].
Oral intake of naringin substantially ameliorates learning and memory capabilities and significantly augments the insulin signaling pathway[3].
体外研究
Naringin inhibits the NF-κB signaling pathway activation and restricts high glucose-induced proliferation, inflammatory response, and oxidative stress injury in HBZY-1 cells[1].
Naringin diminishes AGS cancer cell proliferation in a dose- and time-dependent manner. It significantly reduces the phosphorylation of PI3K and its downstream targets p-Akt and p-mTOR at a concentration of 2 mM in Naringin-treated AGS cells. Additionally, Naringin induces autophagic cell death and activates autophagy-related proteins in AGS cells[2].
Naringin confers protection to PC12 cells against 3-NP neurotoxicity. It reduces lactate dehydrogenase release in 3-NP-challenged PC12 cells and bolsters the antioxidant defense by enhancing the activities of enzymatic antioxidants and elevating levels of reduced glutathione[3].
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