Therapeutic Sesamol Attenuates Monocrotaline-Induced Sinusoidal Obstruction Syndrome in Rats by Inhibiting Matrix Metalloproteinase-9

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• 作者：Srinivasan Periasamy (1)
  Dur-Zong Hsu (1)
  Shin-Yi Chen (1)
  Shan-Shan Yang (1)
  Victor Raj Mohan Chandrasekaran (1)
  Ming-Yie Liu (1) (2)
  
• 关键词：Sinusoidal obstruction syndrome ; Monocrotaline ; Mast cell ; Kupffer cell ; Neutrophil ; Matrix metalloproteinase ; 9 ; Laminin
• 刊名：Cell Biochemistry and Biophysics
• 出版年：2011
• 出版时间：November 2011
• 年：2011
• 卷：61
• 期：2
• 页码：327-336
• 全文大小：2081KB
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• 作者单位：Srinivasan Periasamy (1)
  Dur-Zong Hsu (1)
  Shin-Yi Chen (1)
  Shan-Shan Yang (1)
  Victor Raj Mohan Chandrasekaran (1)
  Ming-Yie Liu (1) (2)
  
  1. Department of Environmental and Occupational Health, National Cheng Kung University Medical College, 138 Sheng-Li Road, Tainan, 70428, Taiwan
  2. Research Center for Environmental and Occupational Health and Preventive Medicine, National Cheng Kung University Medical College, Tainan, 70428, Taiwan
  

文摘

We investigated the therapeutic effect of sesamol against monocrotaline-induced sinusoidal obstruction syndrome (SOS) in rats. Male Sprague–Dawley rats were gavaged with a single dose of monocrotaline (90?mg/kg) to induce SOS. Sesamol (5, 10, 20, and 40?mg/kg) was subcutaneously injected 24?h after monocrotaline treatment. Control rats were given saline only. Aspartate transaminase, alanine transaminase, mast cells, CD 68+ Kupffer cells, neutrophils, myeloperoxidase, matrix metalloproteinase-9 (MMP-9), tissue inhibitor of matrix metalloproteinase-1 (TIMP-1), laminin, and collagen were assessed 48?h after monocrotaline treatment. All tested parameters, except for TIMP-1, laminin, and collagen, were significantly higher in monocrotaline-treated rats than in control rats, and, except for TIMP-1, laminin, and collagen, significantly lower in sesamol-treated rats than in monocrotaline-treated rats. In addition, liver pathology revealed that sesamol offered significant protection against SOS. We conclude that a single dose of sesamol therapeutically attenuated SOS by decreasing the recruitment of inflammatory cells, downregulating MMP-9, and upregulating TIMP-1 expression.