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Flavonoids are strong anti-inflammatory compounds. There is evidence that naringin shows anti-inflammatory activity in an air-pouch model of inflammation in which this flavonoid normalized the elevated TNF-α concentration and normalized inflammatory cell infiltration. Liver is known to be affected by the proinflammatory secretion of adipose tissue. Chronic activation of NF-κB by cytokines has been directly linked to the development of insulin resistance. LPS-induced TNF release followed by liver injury was investigated in rats. Naringin supplementation decreased TNF release and improved liver injury. Enhanced expressions of the cell adhesion molecules in human umbilical vein endothelial cells due to high glucose were significantly attenuated by pretreatment with naringin (10–50 μg/mL). In that study, naringin suppressed a high-glucose–induced increment of NF-κB expression. Nuclear factor-erythroid 2–related factor 2 (Nrf2) mediated regulation of cellular antioxidant production, and the anti-inflammatory mechanism plays an important role against various degenerative diseases. Recent evidence suggests that naringin upregulates NAD(P)H:quinone oxidoreductase 1, HO-1, GST P1, and γ-glutamylcysteine ligase mRNA expression followed by activation of Nrf2 and decreased expression of proinflammatory mediators such as TNF-α, cyclooxygenase-2, and inducible NO synthase in 3-nitropropionic acid–induced rats.
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