【摘 要】
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Background Endogenous sulfur dioxide (SO2) is a novel gasotransmitter involved in the pathophysiologic process of pulmonary artery hypertension (PAH).However,the molecular pathways on which endogenous SO2 impact remains unclarified.Methods In the present
【机 构】
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Department of Intensive Care Unit of Cardiac Surgery,Guangdong Cardiovascular Institute,Guangdong Pr
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Background Endogenous sulfur dioxide (SO2) is a novel gasotransmitter involved in the pathophysiologic process of pulmonary artery hypertension (PAH).However,the molecular pathways on which endogenous SO2 impact remains unclarified.Methods In the present study,the regulatory role of endogenous SO2 in the patho-genesis of PAH and its associated molecular mechanisms were investigated.A Wistar rat model of PAH induced by hypoxic exposure was established.Endogenous SO2 content in rat plasma and rat lungs,mean PAH,ratio of right ventricular/(left ventricular+septum)[RV/(LV+SP)]and body weight of Wistar rats were examined.Protein expression of aspartate aminotransferase 1 (AAT1),endothelial nitric oxide synthase (eNOS) and Rho-associated coiled kinase (ROCK) in rat lung tissues were determined by western blot.Activation of AAT1 and Ras homolog gene family member A (RhoA) in rat lungs were detected by assay kits according to manufacturers\' instructions.The concentration of nitric oxide (NO),level of cyclic guanosine monophosphate (cGMP) and activity of protein kinase G (PKG) in rat lung tissues after exposure to hypoxic conditions or treatment with SO2 donor were also ex-amined using commercial kits.Results Our data showed that the endogenous SO2/AAT1 pathway was marked-ly downregulated in rats with PAH induced by hypoxic exposure.However,SO2 donor upregulated the endoge-nous SO2 pathway and attenuated PAH.Further investigation revealed that in the PAH model,the eNOS/cGMP/PKG cascade was downregulated and the RhoA/ROCK pathway was upregulated,which could be reversed by SO2 donor.Conclusions In conclusion,the endogenous SO2/AAT1 pathway might protect against the develop-ment of hypoxic exposure induced PAH by promoting the eNOS/cGMP/PKG cascade and downregulating RhoA/ROCK pathway.
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