Cardiotrophin-1 （CT-1） activates a distinct form of cardiac muscle cell hypertrophy in which the sarcomeric units are assembled in series. The aim of the study was to determine the expres- sion pattern of sarcomeric...Cardiotrophin-1 （CT-1） activates a distinct form of cardiac muscle cell hypertrophy in which the sarcomeric units are assembled in series. The aim of the study was to determine the expres- sion pattern of sarcomeric contractile protein α-actin, specialized eytoskeletal protein α-actinin and mitochondrial uncoupling protein-2 （UCP2） in myocardial remodeling induced by chronic exposure to CT-1. Kunming mice were intraperitoneally injected with carboxy-terminal polypeptide （CP） of CT-1 （CT-1-CP, 500 μg·kg-1·day^-1） for 1, 2, 3 and 4 week （s）, respectively （4 groups obtained according to the injection time, n=10 each, with 5 males and 5 females in each group）, Those injected with physiological saline for 4 weeks served as controls （n=10, with 5 males and 5 females）. The heart tissues of mice were harvested at 1, 2, 3 or 4 week （s）. Immunohistochemistry （IHC） and Western blotting （WB） were used to detect the distribution and expression of sarcomeric α-actin, α-aetinin and mitoehondrial UCP2 in myocardial tissues. IHC showed that α-actin was mainly distributed around the nuclei of cardiomyo- cytes, α-actinin concentrated around the striae and UCP2 scattered rather evenly in the plasma. The ex- pression of α-actin was slightly greater than that of α-actinin and UCP2 in the control group （IHC： χ^2=6.125; WB： F=0.249, P〉0.05） and it gradually decreased after exposure to CT-1-CP. There was no significant difference in the expression of α-actin between the control group and the CT-1-CP-treated groups （χ^2=7.386, P〉0.05）. But Western blotting revealed significant difference in the expression of α-actin between the control group and the 4-week CT-1-CP-treated group （F=2.912; q=4.203, P〈0.05）. Moreover, it was found that the expression of α-actinin increased stepwise with the exposure time in CT-1-CP-treated groups and differed significantly between CT-1-CP-treated groups and the control group （ICH： χ^2=21.977; WB： F=50.388; P〈0.01）. The expression of UCP2 was initially increased （WB： control group vs. 1- or 2-week group, q values： 5.603 and 9.995, respectively, P〈0.01） and then de- creased （WB： control group vs. 3-week group, q=4.742, P〈0.01; control group vs. 4-week group, q=0.558, P〉0.05）. It was suggested that long-term exposure to CT-1-CP could lead to the alteration in the expression of sarcomeric α-actin, α-actinin and mitochonclrial UCP2. The different expressions of sarcomeric structure proteins and mitochondrial UCP2 may be involved in myocardial remodeling.展开更多
Atfer examining 88 gastropathic patieiits with Spleen deficiency syndrome by iJsing transmis-sion electron microscope, X-ray energy disperse analysis system, histochemical staining and radioimmunomethods, the authors ...Atfer examining 88 gastropathic patieiits with Spleen deficiency syndrome by iJsing transmis-sion electron microscope, X-ray energy disperse analysis system, histochemical staining and radioimmunomethods, the authors found that the gastric mucosa cyclic adenosine monophosphate, superoxide dismutaselevel, quantity of mitochondria and its crista, the ratio of diameter between ventricle and cavity of mitochon-dria aiid the conteiit ot zinc (Zn) , copper (Cu) of mitochondria were decreasing to certain extent which tendsto get lower and lower with different groups in the order of health coritrol group, Spleen Qi deficiency groupaiid SPIeen deficiency with Qi stagnation group; chronic superficial gastritis group, chronic atrophic gastritisgroup and gastric cancor group , complete small intestinal metaplasia (IM) group, incomplete small iM group,complete colonic iM groiJp and incomplete colonic iM group (P< 0 . 05￣0 . 001 ) . While tlie degeiieratiori rateof mitochondria, Cu/Zn ratio, metaplasia rate of gastric mucosa, rate of incomplete colonic IM and content ofIipid peroxide were increasing in the above order (P < 0 . 05 ￣0 . 001 ) . It is suggested that tlie comprehensiveeffect ot the degeneration of mitochoridria and the quantitative changes of its correlative factors is the phys-iopathologic base for indecing SPIeen deficiency disease, gastric mucosa iM and canceration.展开更多
文摘Cardiotrophin-1 （CT-1） activates a distinct form of cardiac muscle cell hypertrophy in which the sarcomeric units are assembled in series. The aim of the study was to determine the expres- sion pattern of sarcomeric contractile protein α-actin, specialized eytoskeletal protein α-actinin and mitochondrial uncoupling protein-2 （UCP2） in myocardial remodeling induced by chronic exposure to CT-1. Kunming mice were intraperitoneally injected with carboxy-terminal polypeptide （CP） of CT-1 （CT-1-CP, 500 μg·kg-1·day^-1） for 1, 2, 3 and 4 week （s）, respectively （4 groups obtained according to the injection time, n=10 each, with 5 males and 5 females in each group）, Those injected with physiological saline for 4 weeks served as controls （n=10, with 5 males and 5 females）. The heart tissues of mice were harvested at 1, 2, 3 or 4 week （s）. Immunohistochemistry （IHC） and Western blotting （WB） were used to detect the distribution and expression of sarcomeric α-actin, α-aetinin and mitoehondrial UCP2 in myocardial tissues. IHC showed that α-actin was mainly distributed around the nuclei of cardiomyo- cytes, α-actinin concentrated around the striae and UCP2 scattered rather evenly in the plasma. The ex- pression of α-actin was slightly greater than that of α-actinin and UCP2 in the control group （IHC： χ^2=6.125; WB： F=0.249, P〉0.05） and it gradually decreased after exposure to CT-1-CP. There was no significant difference in the expression of α-actin between the control group and the CT-1-CP-treated groups （χ^2=7.386, P〉0.05）. But Western blotting revealed significant difference in the expression of α-actin between the control group and the 4-week CT-1-CP-treated group （F=2.912; q=4.203, P〈0.05）. Moreover, it was found that the expression of α-actinin increased stepwise with the exposure time in CT-1-CP-treated groups and differed significantly between CT-1-CP-treated groups and the control group （ICH： χ^2=21.977; WB： F=50.388; P〈0.01）. The expression of UCP2 was initially increased （WB： control group vs. 1- or 2-week group, q values： 5.603 and 9.995, respectively, P〈0.01） and then de- creased （WB： control group vs. 3-week group, q=4.742, P〈0.01; control group vs. 4-week group, q=0.558, P〉0.05）. It was suggested that long-term exposure to CT-1-CP could lead to the alteration in the expression of sarcomeric α-actin, α-actinin and mitochonclrial UCP2. The different expressions of sarcomeric structure proteins and mitochondrial UCP2 may be involved in myocardial remodeling.
文摘Atfer examining 88 gastropathic patieiits with Spleen deficiency syndrome by iJsing transmis-sion electron microscope, X-ray energy disperse analysis system, histochemical staining and radioimmunomethods, the authors found that the gastric mucosa cyclic adenosine monophosphate, superoxide dismutaselevel, quantity of mitochondria and its crista, the ratio of diameter between ventricle and cavity of mitochon-dria aiid the conteiit ot zinc (Zn) , copper (Cu) of mitochondria were decreasing to certain extent which tendsto get lower and lower with different groups in the order of health coritrol group, Spleen Qi deficiency groupaiid SPIeen deficiency with Qi stagnation group; chronic superficial gastritis group, chronic atrophic gastritisgroup and gastric cancor group , complete small intestinal metaplasia (IM) group, incomplete small iM group,complete colonic iM groiJp and incomplete colonic iM group (P< 0 . 05￣0 . 001 ) . While tlie degeiieratiori rateof mitochondria, Cu/Zn ratio, metaplasia rate of gastric mucosa, rate of incomplete colonic IM and content ofIipid peroxide were increasing in the above order (P < 0 . 05 ￣0 . 001 ) . It is suggested that tlie comprehensiveeffect ot the degeneration of mitochoridria and the quantitative changes of its correlative factors is the phys-iopathologic base for indecing SPIeen deficiency disease, gastric mucosa iM and canceration.
