Degradation and inhibition of extracellular matrix
"From the point of view by promotion of degradation and inhibition of synthesis of hepatic extracellular matrix (ECM) to proceed with gene therapy of experimental hepatic fibrosis, it is possible to a certain extent to result in reversion of the pathologic changes of hepatic fibrosis". This was the information conveyed from the Shanghai International Seminar of Liver Cirrhosis and its Complications concluded not long ago.
Hepatic fibrosis is the pathological background and character of multiple chronic hepatic diseases, manifesting with increased synthesis of various components in the ECM. A relatively inadequate degradation resulted in over intra-hepatic deposition of these components. The final outcome will be liver cirrhosis following with further reconstruction of hepatic lobules and the formation of pseudo-lobules and nodules. Eventually, it is of significant importance to inhibit synthesis of ECM and promote ECM degradation for actively searching a new method for the management of liver fibrosis.
The rat interstitial collagenase mammals expression plasmid and tissue inhibitive factor (TIM-1) of metallo-proteinases (MMPs), type I receptor (TβR-1) eukaryotic cell anti-sense expression vector, composed with the technique of DNA recombination by Professor Wang Jiyao et al. of the department of digestive disease, Zhongshan Hospital, Fudan University, and the animal model of hepatic fibrosis with liver orientation of invivo transgene research showed that collagenase activity could be released by increasing the expression of hepatic interstitial collagenase and inhibition of high expression of TIMP-1 in the process of hepatic fibrosis. Also the ECM degradation could be promoted to inhibit the expression of TβR-1 and block the signal transmission of TGF-β1, to eliminate their biological action and then inhibit the synthesis of ECM., 百拇医药
Hepatic fibrosis is the pathological background and character of multiple chronic hepatic diseases, manifesting with increased synthesis of various components in the ECM. A relatively inadequate degradation resulted in over intra-hepatic deposition of these components. The final outcome will be liver cirrhosis following with further reconstruction of hepatic lobules and the formation of pseudo-lobules and nodules. Eventually, it is of significant importance to inhibit synthesis of ECM and promote ECM degradation for actively searching a new method for the management of liver fibrosis.
The rat interstitial collagenase mammals expression plasmid and tissue inhibitive factor (TIM-1) of metallo-proteinases (MMPs), type I receptor (TβR-1) eukaryotic cell anti-sense expression vector, composed with the technique of DNA recombination by Professor Wang Jiyao et al. of the department of digestive disease, Zhongshan Hospital, Fudan University, and the animal model of hepatic fibrosis with liver orientation of invivo transgene research showed that collagenase activity could be released by increasing the expression of hepatic interstitial collagenase and inhibition of high expression of TIMP-1 in the process of hepatic fibrosis. Also the ECM degradation could be promoted to inhibit the expression of TβR-1 and block the signal transmission of TGF-β1, to eliminate their biological action and then inhibit the synthesis of ECM., 百拇医药