Rosmarinic Acid Attenuates Sodium Taurocholate-Induced Acute Pancreatitis in Rats by Inhibiting Nuclear Factor-κB Activation.
| Autor: | Fan, Yu-Ting, Yin, Guo-Jian, Xiao, Wen-Qin, Qiu, Lei, Yu, Ge, Hu, Yan-Ling, Xing, Miao, Wu, De-Qing, Cang, Xiao-Feng, Wan, Rong, Wang, Xing-Peng, Hu, Guo-Yong |
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| Předmět: |
ANIMAL experimentation
BIOPHYSICS CARBOXYLIC acids ENZYME-linked immunosorbent assay HISTOLOGICAL techniques IMMUNOENZYME technique IMMUNOHISTOCHEMISTRY RESEARCH methodology MEDICINAL plants PANCREATITIS POLYMERASE chain reaction RATS RESEARCH funding STATISTICS WESTERN immunoblotting PLANT extracts DATA analysis DESCRIPTIVE statistics IN vitro studies MANN Whitney U Test KRUSKAL-Wallis Test ONE-way analysis of variance |
| Zdroj: | American Journal of Chinese Medicine; 2015, Vol. 43 Issue 6, p1117-1135, 19p, 3 Charts, 4 Graphs |
| Abstrakt: | Rosmarinic Acid (RA), a caffeic acid ester, has been shown to exert anti-inflammation, anti-oxidant and antiallergic effects. Our study aimed to investigate the effect of RA in sodium taurocholate ()-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 β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) levels, and inhibited NF-κB translocation in pancreas. In vitro, pretreating the fresh rat pancreatic acinar cells with 80 μ mol/L RA 2 h before 3750 nmol/L sodium taurocholate or 10 ng/L TNF-α administration significantly attenuated the reduction of isolated pancreatic acinar cell viability and inhibited the nuclear activation and translocation of NF-κB. 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-κB. These findings might provide a basis for investigating the therapeutic role of RA in managing acute pancreatits. [ABSTRACT FROM AUTHOR] |
| Databáze: | Complementary Index |
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