Rosmarinic Acid Attenuates Sodium Taurocholate-Induced Acute Pancreatitis in Rats by Inhibiting Nuclear Factor-κB Activation
Rosmarinic Acid Attenuates Sodium Taurocholate-Induced Acute Pancreatitis in Rats by Inhibiting Nuclear Factor-κB Activation
复制标题
迷迭香酸通过抑制核因子 kappa B 激活减轻牛磺胆酸钠诱导的大鼠急性胰腺炎
DOI：
10.1142/s0192415x15500640
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发表时间：
2015-01-01
影响因子：
5.7
通讯作者：
Hu, Guo-Yong
中科院分区：
文献类型：
--
作者：
Fan, Yu-Ting;Yin, Guo-Jian;Hu, Guo-Yong
Rosmarinic Acid (RA), a caffeic acid ester, has been shown to exert antiinflammation, anti-oxidant and antiallergic effects. Our study aimed to investigate the effect of RA in sodium taurocholate (NaTC)-induced acute pancreatitis, both in vivo and in vitro. In vivo, RA (50 mg/kg) was administered intraperitoneally 2 h before sodium taurocholate injection. Rats were sacrificed 12 h, 24 h or 48 h after sodium taurocholate injection. Pretreatment with RA significantly ameliorated pancreas histopathological changes, decreased amylase and lipase activities in serum, lowered myeloperoxidase activity in the pancreas, reduced systematic and pancreatic interleukin-1 beta (IL-1 beta), IL-6, and tumor necrosis factor-alpha (TNF-alpha) levels, and inhibited NF-kappa B translocation in pancreas. In vitro, pretreating the fresh rat pancreatic acinar cells with 80 mu mol/L RA 2 h before 3750 nmol/L sodium taurocholate or 10 ng/L TNF-alpha administration significantly attenuated the reduction of isolated pancreatic acinar cell viability and inhibited the nuclear activation and translocation of NF-kappa B. Based on our findings, RA appears to attenuate damage in sodium taurocholate-induced acute pancreatitis and reduce the release of inflammatory cytokines by inhibiting the activation of NF-kappa B. These findings might provide a basis for investigating the therapeutic role of RA in managing acute pancreatits.
