Rosmarinic Acid Attenuates Sodium Taurocholate-Induced Acute Pancreatitis in Rats by Inhibiting Nuclear Factor-κB Activation
| Autor: | Miao Xing, Yanling Hu, Guoyong Hu, Lei Qiu, Xingpeng Wang, Xiaofeng Cang, Yuting Fan, De-Qing Wu, Guojian Yin, Ge Yu, Wenqin Xiao, Rong Wan |
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| Rok vydání: | 2015 |
| Předmět: |
Male
Taurocholic Acid medicine.medical_specialty Sodium Interleukin-1beta chemistry.chemical_element Depsides Proinflammatory cytokine Rats Sprague-Dawley chemistry.chemical_compound In vivo Internal medicine medicine Acinar cell Animals Humans Pancreas Interleukin-6 Plant Extracts Tumor Necrosis Factor-alpha Rosmarinic acid NF-kappa B General Medicine Taurocholic acid medicine.disease Rats Endocrinology Pancreatitis Complementary and alternative medicine chemistry Cinnamates Acute pancreatitis |
| Zdroj: | The American Journal of Chinese Medicine. 43:1117-1135 |
| ISSN: | 1793-6853 0192-415X |
| Popis: | 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 ( 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 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. |
| Databáze: | OpenAIRE |
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