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International Journal of Molecular Medicine 2013-Apr

Anti-inflammatory effects of total alkaloids from Rubus alceifolius Poir [corrected]. on non-alcoholic fatty liver disease through regulation of the NF-κB pathway.

Aðeins skráðir notendur geta þýtt greinar
Skráðu þig / skráðu þig
Krækjan er vistuð á klemmuspjaldið
Jinyan Zhao
Haiyin Zheng
Yan Liu
Jiumao Lin
Xiaoyong Zhong
Wei Xu
Zhenfeng Hong
Jun Peng

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Útdráttur

We aimed to explore the anti-inflammatory effects of total alkaloids inRubus alceifolius Poir [corrected]. (TARAP) on non-alcoholic fatty liver disease, and to investigate the possible molecular mechanisms. A rodent non-alcoholic fatty liver disease (NAFLD) model was established by administration of a modified high-fat diet ad libitum for 8 weeks. Rats were treated with polyene phosphatidylcholine (PP), TARAP low‑dose (0.72 g/kg body weight/day) and TARAP high-dose (1.44 g/kg body weight/day). The model group and the control group received distilled water. After treatment for 4 weeks, the blood samples were obtained from the abdominal aorta, and the levels of serum ALT, AST, GGT, ALP, TG, TC, HDL-C and LDL-C were measured. Changes in liver tissue morphology were evaluated by H&E staining. The expression levels of nuclear factor (NF)-κB, cyclooxygenase-2 (COX‑2), interleukin (IL)-6 and tumor necrosis factor (TNF)-α in rat livers were assayed by reverse transcription‑polymerase chain reaction (RT-PCR) and immunohistochemistry. Both TARAP and PP attenuated hepatic steatosis induced by the high-fat diet. The modified high-fat diet caused a significant increase in ALT, AST, GGT, ALP, TG, TC, LDL-C levels and a decrease in HDL-C levels. TARAP and PP treatment abrogated the increase in the levels of liver enzymes and the levels of TG, TC, LDL-C, as well as suppressed the increase in HDL-C levels. The results of RT-PCR and immunohistochemical assay showed that PP and TARAP treatment decreased the expression of NF-κB, COX-2, IL-6 and TNF-α. In conclusion, these results suggest that TARAP may protect against NAFLD through regulation of the NF-κB pathway.

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