Vitexin exhibits inhibition of carbohydrate hydrolase with IC50 of 244 μM and shows antioxidant activity in DPPH bleaching assay (IC50 = 24.2 μM). It is an apigenin flavone c-glycosidea isolated and purified from the seeds of Vitex trifolia L. with antinociceptive, antimyeloperoxidase, and anti-inflammatory activities.
Vitexin exhibits inhibition of carbohydrate hydrolase with IC50 of 244 μM and shows antioxidant activity in DPPH bleaching assay (IC50 = 92.5 μM [0.4 μg/mL])[3]. It is an apigenin flavone c-glycosidea isolated and purified from the seeds of Vitex trifolia L. with antinociceptive, antimyeloperoxidase, and anti-inflammatory activities[4]. The MCAO (middle cerebral artery occlusion)-induced brain infarction was obviously decreased by vitexin. Vitexin suppressed the autophagy dysfunction to attenuate MCAO-induced cerebral ischemic stroke via mTOR/Ulk1 pathway[5]. Vitexin inhibited growth and induced apoptosis of ACHN and OS-RC-2 cells in a dose-dependent manner, and promoted excessive autophagy by reducing p62 levels and increasing Beclin1 and LC3II levels[6]. The systemic administration of vitexin (1.25; 2.5 and 5 mg/kg; i.p.) exhibited selective protection against chemically-induced seizures. The higher dose of vitexin protected 100% of animals against the tonic-clonic seizures triggered by GABA antagonists. The results from open-field, elevated plus-maze, and light-dark box tests indicated the anxiolytic properties of vitexin at similar range of doses described for the anticonvulsant action screening[7]. Vitexin protected melanocytes from oxidative stress by activating MAPK-Nrf2/ARE signaling pathway[8]. Vitexin was not cytotoxic (IC50 > 200 µg/ml) in RAW 264.7 and at all doses tested it effectively reduced leukocyte migration in vivo, particularly neutrophils in the peritoneal lavage, independently of the inflammatory stimulus used. It also reduced TNF-α, IL-1β and NO releases in the peritoneal cavity of LPS-challenged mice. Vitexin had low cytotoxicity and was able to reduce the releases of TNF-α, IL-1β, NO, PGE2 and increase in IL-10 release by LPS activated RAW 264.7 cells. Vitexin was also able to regulate transcriptional factors for pro-inflammatory mediators, reducing the expression of p-p38, p-ERK1/2 and p-JNK in LPS-elicited cells[9].
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