Background： Current knowledge indicates that oxidative damage and the following inflammation is pivotal pathway for myocardial cell death. In recent decades, hydrogen sulfide （H2S） has been identified as a novel en...Background： Current knowledge indicates that oxidative damage and the following inflammation is pivotal pathway for myocardial cell death. In recent decades, hydrogen sulfide （H2S） has been identified as a novel endogenous vasodilator and neuromodulator due to its antioxidation capacity. However, whether H2S pretreatment in neonatal mouse cardiomyocytes is a protection effect against oxidative stress remains elusive. Methods： Primary neonatal mouse cardiomyocytes were isolated and cultured, subsequently, pretreated with the H2S donor, sodium hydrosulfide （NaHS）. Cell viability, lactate dehydrogenase （LDH） release, and reactive oxygen species （ROS） production are evaluated. The levels of superoxide dismutase （Sod2） and Sirtuin 1 （Sirt1）, a deacetylation enzyme, were detected by Western blotting. The statistics was performed using independent＇sample t-test. Results： NaHS （100 μmol/L） had no toxicity to primary neonatal mouse cardiomyocytes. Furthermore, NaHS pretreatment significantly improved neonatal mouse cardiomyocytes survival after H2O2-induced cell death, indicated by the decrease in LDH release （40.00 ± 2.65%vs. 65.33 ± 4.33%, P 〈 0.01） and ROS production （1.90 ±0.33 vs. 4.56 ± 0.56, P 〈 0.05）, and that the salubrious effect was accompanied by the upregulation of Sod2 expression. In addition, the study showed that NaHS pretreatment improved mitochondrial DNA number in neonatal mouse cardiomyocyte. Furthermore, the result demonstrated NaHS increased the expression of Sirt1 in neonatal mouse cardiomyocyte. Ex 527, an inhibitor of Sirt1, could attenuate these effects of NaHS-nduced Sod2 expression and mtDNAnumber increase, furthermore, abrogate the cytoprotective effects of NaHS for neonatal mouse cardiomyocytes. Conclusion： Sirt1 mediated H2S-induced cytoprotection effects in neonatal mouse cardiomyocytes.展开更多
Congenital heart disease(CHD)has become the leading mortal cause for an infant from congenital abnormalities.Pulmonary artery hypertension(PAH)is one of the complications of CHD.[1]It has also been reported that upreg...Congenital heart disease(CHD)has become the leading mortal cause for an infant from congenital abnormalities.Pulmonary artery hypertension(PAH)is one of the complications of CHD.[1]It has also been reported that upregulation of microRNA-98(miR-98)could mediate the suppression of cardiac hypertrophy,which implies that miR-98 might play an important role in CHD.[2]In this study,the clinical data from hospitalized patients were retrospectively analyzed to identify if there is any evidence of diagnosis of circulating miR-98 on CHD patients with PAH.展开更多
文摘Background： Current knowledge indicates that oxidative damage and the following inflammation is pivotal pathway for myocardial cell death. In recent decades, hydrogen sulfide （H2S） has been identified as a novel endogenous vasodilator and neuromodulator due to its antioxidation capacity. However, whether H2S pretreatment in neonatal mouse cardiomyocytes is a protection effect against oxidative stress remains elusive. Methods： Primary neonatal mouse cardiomyocytes were isolated and cultured, subsequently, pretreated with the H2S donor, sodium hydrosulfide （NaHS）. Cell viability, lactate dehydrogenase （LDH） release, and reactive oxygen species （ROS） production are evaluated. The levels of superoxide dismutase （Sod2） and Sirtuin 1 （Sirt1）, a deacetylation enzyme, were detected by Western blotting. The statistics was performed using independent＇sample t-test. Results： NaHS （100 μmol/L） had no toxicity to primary neonatal mouse cardiomyocytes. Furthermore, NaHS pretreatment significantly improved neonatal mouse cardiomyocytes survival after H2O2-induced cell death, indicated by the decrease in LDH release （40.00 ± 2.65%vs. 65.33 ± 4.33%, P 〈 0.01） and ROS production （1.90 ±0.33 vs. 4.56 ± 0.56, P 〈 0.05）, and that the salubrious effect was accompanied by the upregulation of Sod2 expression. In addition, the study showed that NaHS pretreatment improved mitochondrial DNA number in neonatal mouse cardiomyocyte. Furthermore, the result demonstrated NaHS increased the expression of Sirt1 in neonatal mouse cardiomyocyte. Ex 527, an inhibitor of Sirt1, could attenuate these effects of NaHS-nduced Sod2 expression and mtDNAnumber increase, furthermore, abrogate the cytoprotective effects of NaHS for neonatal mouse cardiomyocytes. Conclusion： Sirt1 mediated H2S-induced cytoprotection effects in neonatal mouse cardiomyocytes.
文摘Congenital heart disease(CHD)has become the leading mortal cause for an infant from congenital abnormalities.Pulmonary artery hypertension(PAH)is one of the complications of CHD.[1]It has also been reported that upregulation of microRNA-98(miR-98)could mediate the suppression of cardiac hypertrophy,which implies that miR-98 might play an important role in CHD.[2]In this study,the clinical data from hospitalized patients were retrospectively analyzed to identify if there is any evidence of diagnosis of circulating miR-98 on CHD patients with PAH.
