Int. J. Mol. Sci. 2008, 9(4), 638-661; doi:10.3390/ijms9040638
Article

Specific siRNA Targeting the Receptor for Advanced Glycation End Products Inhibits Experimental Hepatic Fibrosis in Rats

Department of Gastroenterology, Zhong Da Hospital, Southeast University, Nanjing 210009, China
* Author to whom correspondence should be addressed.
Received: 13 January 2008; in revised form: 17 August 2008 / Accepted: 22 April 2008 / Published: 24 April 2008
(This article belongs to the Section Biochemistry, Molecular Biology and Biophysics)
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Abstract: Receptor for advanced glycation end products (RAGE) was studied in different stages of carbon tetrachloride induced hepatic fibrosis (HF), and effect of its gene silencing in the HF development was evaluated in rats. Silencing RAGE expression by specific siRNA effectively suppressed NF-κB activity, hepatic stellate cell activation, and accumulation of extracellular matrix proteins in the fibrotic liver, and also greatly improved the histopathology and the ultra-structure of liver cells. These effects may be partially mediated by the inhibition on IκBα degradation. RAGE gene silencing effectively prevented liver from fibrosis, therefore it offers a potential pharmacological tool for anti-HF gene therapy.
Keywords: Receptor for advanced glycation end products (RAGE); small interfering RNA (siRNA); hepatic stellate cells (HSCs); hepatic fibrosis (HF); gene therapy

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MDPI and ACS Style

Xia, J.-R.; Liu, N.-F.; Zhu, N.-X. Specific siRNA Targeting the Receptor for Advanced Glycation End Products Inhibits Experimental Hepatic Fibrosis in Rats. Int. J. Mol. Sci. 2008, 9, 638-661.

AMA Style

Xia J-R, Liu N-F, Zhu N-X. Specific siRNA Targeting the Receptor for Advanced Glycation End Products Inhibits Experimental Hepatic Fibrosis in Rats. International Journal of Molecular Sciences. 2008; 9(4):638-661.

Chicago/Turabian Style

Xia, Jin-Rong; Liu, Nai-Feng; Zhu, Nai-Xun. 2008. "Specific siRNA Targeting the Receptor for Advanced Glycation End Products Inhibits Experimental Hepatic Fibrosis in Rats." Int. J. Mol. Sci. 9, no. 4: 638-661.

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