Paeoniflorin regulates macrophage activation in dimethylnitrosamine-induced liver fibrosis in rats

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• 作者：Xiaorong Chen (1) (2)
  Cheng Liu (1) (2) (3)
  Yunfei Lu (1) (2)
  Zongguo Yang (1)
  Zhen Lv (1)
  Qingnian Xu (1) (2)
  Qi Pan (1) (2)
  Lingqing Lu (1)
  
• 关键词：Liver fibrosis ; Macrophage ; Paeoniflorin
• 刊名：BMC Complementary and Alternative Medicine
• 出版年：2012
• 出版时间：December 2012
• 年：2012
• 卷：12
• 期：1
• 全文大小：1712KB
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  35. The pre-publication history for this paper can be accessed here:http://www.biomedcentral.com/1472-6882/12/254/prepub
  
• 作者单位：Xiaorong Chen (1) (2)
  Cheng Liu (1) (2) (3)
  Yunfei Lu (1) (2)
  Zongguo Yang (1)
  Zhen Lv (1)
  Qingnian Xu (1) (2)
  Qi Pan (1) (2)
  Lingqing Lu (1)
  
  1. Department of Traditional Chinese Medicine, Shanghai Public Health Clinical Center, 2901 Caolang Road, Jin Shan District, Shanghai, 201508, China
  2. Key Laboratory of Infectious Diseases of State Administration of Traditional Chinese Medicine (clinical base), Shanghai, 201508, China
  3. Scientific Research Center, Shanghai Public Health Clinical Center, Shanghai, 201508, China
  

文摘

Background Macrophages in other organs (e.g. kidneys, lungs, and spleen, et. al) have rarely been reported in the development of liver fibrosis. Therefore, it is important to investigate macrophage activation in the main organs in liver fibrosis. We investigated the potential antifibrogenic effects of paeoniflorin (PF) in a dimethylnitrosamine (DMN)-induced rat model with special focus on inhibiting macrophage activation in the main organs. Methods Rat hepatic fibrosis was induced by treatment with DMN three times weekly over a 4-week period. DMN rats were treated with water, PF, or gadolinium chloride (GdCl3) from the beginning of the 3rd week. The expression of CD68, marker of macrophage, was investigated using immunohistochemical, real-time PCR, and western blot analysis. Results Hepatic hydroxyproline content markedly decreased and histopathology improved in the DMN-PF rats. Expression of desmin and collagen 1 decreased notably in DMN-PF liver. CD68 expression in the liver, spleen and kidney increased markedly after 2 weeks but decreased in DMN-water rats. PF and GdCl3 decreased CD68 expression in the liver and spleen and there was no effect on kidney. CD68 expression in the lung increased gradually during the course of DMN-induced liver fibrosis, and PF inhibited CD68 expression in the lung significantly while GdCl3 increased CD68 markedly. Expression of tumor necrosis factor (TNF-α) was decreased significantly by GdCl3 in the liver, as revealed by real-time PCR analysis. However, GdCl3 could not decrease TNF-α level in the serum by enzyme linked immunosorbent assay (ELISA). Conclusions Macrophage activation was disrupted in the liver, spleen, lung and kidney during development of DMN-induced liver fibrosis. PF administration attenuated DMN-induced liver fibrosis at least in part by regulating macrophage disruption in the main organs.