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Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Mol+Med+Rep 2017 ; 15 (3): 1079-86 Nephropedia Template TP
Mol Med Rep 2017[Mar]; 15 (3): 1079-86 PMID28098903show ga
Diabetes mellitus (DM) is a chronic metabolic disease, where the predominant pathogenesis is pancreatic ?-cells dysfunction or injury. It has been well established that inflammation leads to a gradual exhaustion of pancreatic ?-cell function with decreased ?-cell mass likely resulting from pancreatic ?-cells apoptosis or death. Vitexin, a major bioactive flavonoid compound in plants has numerous pharmacological properties, including antioxidant, anti-inflammatory and antimyeloperoxidase. Whether vitexin can protect pancreatic ?-cells against lipopolysaccharide (LPS)-induced pro-inflammatory cytokine production and apoptosis has received little attention. The present study investigated the potential effects of vitexin on LPS-induced pancreatic ?-cell injury and apoptosis. It was revealed that apoptosis and damage induced by LPS in islet tissue of rats and INS-1 cells was significantly decreased in response to vitexin treatment. In addition, pretreatment with vitexin decreased the levels of the pro-inflammatory cytokines tumor necrosis factor-? and high mobility group box 1 (HMGB1) in LPS-induced rats. Further experiments demonstrated that vitexin pretreatment suppressed the activation of P38 mitogen-activated protein kinase signaling pathways in LPS-induced INS-1 cells. In conclusion, the results indicated that vitexin prevented LPS-induced islet tissue damage in rats, and INS-1 cells injury and apoptosis by inhibiting HMGB1 release. Therefore, the present study provided clear evidence indicating that vitexin may be a viable therapeutic strategy for the treatment of DM.