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Effect of Naringin on Inflammation

Obesity, metabolic syndrome, and diabetes are strongly correlated with inflammatory response. Inflammation is a complex process. In obesity, inflammatory processes are characterized by infiltration of inflammatory cells (generally macrophages, mast cells) in inflamed organ/tissues, especially in adipose tissue. Adipose tissue itself is considered an endocrine organ and secretes various adipocytokines such as TNF-α, IL-6, and leptin. Various reports also suggest that inflammatory cytokine concentrations are higher in individuals suffering metabolic syndrome and obesity. Among the cytokines released in obesity, TNF-α is the most common inflammatory cytokine found in plasma of obese individuals. TNF-α is responsible for insulin resistance and β-cell damage in islets of the pancreas. TNF-α–mediated impairment of insulin signaling is probably due to activation of Ser/Thr kinases, which act on insulin receptor and insulin receptor substrate (IRS) molecules, making them poor substrates for insulin-mediated tyrosine phosphorylation.

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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