Dynamic changes of TGF-α and TGF-β1 in rats with liver cirrhosis induced by multiple pathogenic factors / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To explore the dynamic changes of transforming growth factor-α (TGF-α) and transforming growth factor-β1 (TGF-β1) of liver cirrhosis induced by multiple pathogenic factors in rats.</p><p><b>METHODS</b>Animals in the cirrhosis group were fed a mixture of maize flour, lard, cholesterol and alcohol plus subcutaneously injection with carbon tetrachloride (CCl₄), the CCl₄(0.5 ml/100 g · w) was injected at the first day of experiment and the 40% CCl₄oil solution (0.3 ml /100 g · w) was injected at an interval of three days. The thirty-six male SD rats were randomly divided into liver cirrhosis group of the 4th, 6th and 8 th week, and normal control group of the 4th, 6th and 8th week. The contents of alanine transferase (ALT), endotoxin, tumor necrosis factor-α (TNF-α) and homocysteine (Hcy) in plasma were evaluated. Histopathological changes of the liver were observed under microscope with the staining of HE. The expressions of TGF-α and TGF-β1 were analyzed by the method of immunohistochemistry.</p><p><b>RESULTS</b>Compared with the corresponding normal control group, the levels of ALT, endotoxin, TNF-α and Hcy in plasma were gradually significantly increased in liver cirrhosis group of the 4th, 6th and 8th week (P < 0.05); the expression of TGF-α in the liver tissues was significantly increased at the 4th week (P < 0.05); the expression of TGF-β1 in the liver tissues was gradually significantly increased in every model group (P < 0.05).</p><p><b>CONCLUSION</b>In the formation process of cirrhosis, the expression of TGF-α was increased in liver of cirrhosis group at the 4th week, and later it was suppressed; the expression of TGF-β1 was continuously increased. The characteristic dynamic changes of TGF-α and TGF-β1 might be related to sustained endotoxemia, the high level of TNF-α and hyperhomocysteinemia.</p>

Effect of ischemic postconditioning on the expression of myocardium matrix metalloproteinase-2 induced by ischemia/reperfusion in rats / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate the effect of ischemic postconditioning on the expression of rat myocardium matris metalloproteinase-2 (MMP-2) induced by ischemia/reperfusion (I/R) and relationship between its expression and interstitium and the effect on left ventricular function.</p><p><b>METHODS</b>Twenty-four rats were randomly divided into 3 groups (n = 8): sham control (SC) group, ischemic/reperfusion (I/R) group and ischemic postconditioning (IPTC) group. The left ventricular peak systolic pressure and its derivate (+/- dp/dt) were calculated; The amount of myocardium collagenous were determined; The vitality of superoxide dismutase (SOD) and content of malondialdehyde (MDA) of plasma were detected; The activity of myocardium MMP-2 was measured by Western blot and RT-PCR.</p><p><b>RESULTS</b>As compared with I/R group, IPTC could lower the expression of MMP-2, ameliorate left ventricular function and increase the content of myocardium collagenous. In the meantime, the vitality of superoxide dismutase (SOD) of plasma were greatly enhanced and the content of malondialdehyde (MDA) of plasma were reduced in IFC group.</p><p><b>CONCLUSION</b>Protective effect of IPIC on myocardium may be due to reduce free radical, lower expression of MMP-2 and protect myocardial interstitium. MMPs plays an important role in the myocardial protection provided by IPTC.</p>

Protective effect of tanshinol on the hepatopulmonary syndrome in rat / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To explore the mechanism of tanshinol on alleviate the inflammatory injury of lung tissue in rat hepatopulmonary syndrome (HPS).</p><p><b>METHODS</b>SD rats were randomly divided into normal control group (n = 8), hepatopulmonary syndrome (HPS) group (n = 11) and tanshinol intervention group (n = 9). HE staining was used to observe the histopathology changes of pulmonary and hepatic tissues, and to count the number of macrophages in lung tissues. The activity of alanine transferase (ALT) and concentrations of endotoxin, tumor necrosis factor-a (TNF-alpha) and homocystein (Hcy) in plasma were detected. The concentrations of TNF-alpha, nitric oxide (NO) and malondialdehyde (MDA) and the activity of inducible nitric oxide synthase (iNOS) in the lung tissues were measured, respectively.</p><p><b>RESULTS</b>Thickened alveolar septum and increased macrophages were observed in lungs in HPS rat. After administered with tanshinol, the pulmonary pathological changes were alleviated and the number of macrophages in lung tissue was decreased compared with HPS group. The activity of ALT and the concentrations of endotoxin, TNF-alpha and Hcy in plasma ,and TNF-alpha, iNOS, NO and MDA in lung tissue in HPS group were higher than those of normal control group; meanwhile, those tanshinol group were less those that of HPS group.</p><p><b>CONCLUSION</b>Tanshinol may play an important role in delaying the development of HPS through protecting liver or directly antagonizing the effect of intestinal endotoxemia so as to alleviate the inflammatory reaction in lung tissue.</p>