To investigate the reversing effects of DDPH on cardiac hypertrophy and increased collagen content in left ventricle tissue of rats, cardiac hypertrophy of rats were induced by partial narrowing of abdominal aorta. 4 ...To investigate the reversing effects of DDPH on cardiac hypertrophy and increased collagen content in left ventricle tissue of rats, cardiac hypertrophy of rats were induced by partial narrowing of abdominal aorta. 4 weeks after operation, the rats were given DDPH for 8 weeks. 12 weeks later, it was found that in model group, LVW/WHW and WHW/BW increased by 39. 0 % and 36. 9 % than those in control group; collagen content increased by 1. 5 times. I/E, LS decreased (P<0. 01), MMW/E. WZ increased (P<0. 01). The above-mentioned changes in two DDPH groups could be partly or completely reversed. It is concluded that DDPH could reverse cardiac hypertrophy of rats induced by partial narrowing of abdominal aorta and reduce collagen content in left ventricle tissue.展开更多
Objective： Endothelial nitric oxide synthase （eNOS） and nitric oxide （NO） have been implicated in protection against myocardial ischemia injury. This study was designed to explore a new method of therapy for myoc...Objective： Endothelial nitric oxide synthase （eNOS） and nitric oxide （NO） have been implicated in protection against myocardial ischemia injury. This study was designed to explore a new method of therapy for myocardial injury by eNOS gene transfection. Methods： A rat model of myocardial infarction （MI） was established by left anterior descending （LAD） coronary artery ligation, eNOS gene in an adenovirus vector was delivered locally into the rat heart and hemodynamic parameters were examined after 3 weeks, Matrix metalloproteinase-2 and 9 （MMP-2, MMP-9） mRNA were measured by reverse transcription polymerase chain reaction （RT-PCR）, and the protein levels of eNOS, caspase-3, and transforming grouth factor 131 （TGF-131） were determined by western blot assay. Results： eNOS gene transfer significantly reduced cardiomyocyte apoptosis and improved cardiac function. In addition, eNOS significantly reduced the mRNA levels of MMP-2 and MMP-9. In the eNOS gene transfected group, the activation of caspase-3 and TGF-β1 were decreased. However, the protection was reversed by administration of the NOS inhibitor, N（o））-nitro-l-arginine methyl ester （L-NAME）. Conclusion： These results demonstrate that the eNOS provides cardiac protection after myocardial infarction injury through inhibition of cardiac apoptosis and collagen deposition, and suppression of TGF-β1.展开更多
目的探讨氧化低密度脂蛋白(oxidized low density lipoprotein,ox-LDL)对大鼠心肌成纤维细胞胶原合成的影响。方法体外培养乳鼠心肌成纤维细胞,加入ox-LDL(10、20、50、100μg/ml)干预24h,3H-胸腺嘧啶核苷掺入法观察细胞DNA合成,3H-脯...目的探讨氧化低密度脂蛋白(oxidized low density lipoprotein,ox-LDL)对大鼠心肌成纤维细胞胶原合成的影响。方法体外培养乳鼠心肌成纤维细胞,加入ox-LDL(10、20、50、100μg/ml)干预24h,3H-胸腺嘧啶核苷掺入法观察细胞DNA合成,3H-脯氨酸掺入法观察胶原的合成,酶谱法测定基质金属蛋白酶MMP-2、MMP-9活性,Western blot检测MMP-2和MMP-9蛋白表达水平,RT-PCR检测MMP-2、MMP-9的mRNA表达。结果和对照组比较,ox-LDL作用于心肌成纤维细胞24h后,呈浓度依赖性促进细胞DNA合成,同时抑制细胞胶原合成。ox-LDL显著增加MMP-2和MMP-9活性,但各组间作用无明显区别;同时MMP-2和MMP-9蛋白表达也显著性增加,以100μg/ml组作用最强。50μg/ml ox-LDL能显著增加MMP-2和MMP-9的mRNA表达,100μg/ml组作用更强。结论ox-LDL作用于心肌成纤维细胞能减少胶原的合成并增加胶原的降解,提示其在心肌重构过程中起一定的作用。展开更多
文摘To investigate the reversing effects of DDPH on cardiac hypertrophy and increased collagen content in left ventricle tissue of rats, cardiac hypertrophy of rats were induced by partial narrowing of abdominal aorta. 4 weeks after operation, the rats were given DDPH for 8 weeks. 12 weeks later, it was found that in model group, LVW/WHW and WHW/BW increased by 39. 0 % and 36. 9 % than those in control group; collagen content increased by 1. 5 times. I/E, LS decreased (P<0. 01), MMW/E. WZ increased (P<0. 01). The above-mentioned changes in two DDPH groups could be partly or completely reversed. It is concluded that DDPH could reverse cardiac hypertrophy of rats induced by partial narrowing of abdominal aorta and reduce collagen content in left ventricle tissue.
文摘Objective： Endothelial nitric oxide synthase （eNOS） and nitric oxide （NO） have been implicated in protection against myocardial ischemia injury. This study was designed to explore a new method of therapy for myocardial injury by eNOS gene transfection. Methods： A rat model of myocardial infarction （MI） was established by left anterior descending （LAD） coronary artery ligation, eNOS gene in an adenovirus vector was delivered locally into the rat heart and hemodynamic parameters were examined after 3 weeks, Matrix metalloproteinase-2 and 9 （MMP-2, MMP-9） mRNA were measured by reverse transcription polymerase chain reaction （RT-PCR）, and the protein levels of eNOS, caspase-3, and transforming grouth factor 131 （TGF-131） were determined by western blot assay. Results： eNOS gene transfer significantly reduced cardiomyocyte apoptosis and improved cardiac function. In addition, eNOS significantly reduced the mRNA levels of MMP-2 and MMP-9. In the eNOS gene transfected group, the activation of caspase-3 and TGF-β1 were decreased. However, the protection was reversed by administration of the NOS inhibitor, N（o））-nitro-l-arginine methyl ester （L-NAME）. Conclusion： These results demonstrate that the eNOS provides cardiac protection after myocardial infarction injury through inhibition of cardiac apoptosis and collagen deposition, and suppression of TGF-β1.
