Objective：To observe the effect of Chinese herbal medicine for calming Gan（肝） and suppressing hyperactive yang（平肝潜阳,CGSHY） on arterial elasticity function and the circadian rhythm of blood pressure in patients with essential hypertension（EH）.Methods：Adopting a parallel,randomized design,sixty-four patients with EH of stagesⅠandⅡwere randomly divided into two groups according to a random number table,with 32 in each group.The patients in the treatment group were treated with CGSHY and those in the control group were treated with Enalapril.All patients were given 24-h ambulatory blood pressure monitoring（ABPM） before and after a 12-week treatment.Trough/peak（T/P） ratios of systolic and diastolic blood pressure（SBP DBP） of each group were calculated.The circadian rhythm of their blood pressure was observed at the same time. The changes in elasticity of the carotid artery in the patients,including stiffness parameter（β）,pressure-strain elastic modulus（Ep）,arterial compliance（AC）,augmentation index（Al）,and pulse wave velocity（PVWβ） were determined by the echo-tracking technique before and after a 12-week treatment.In the meantime,their levels of nitric oxide（NO） and endothelin-1（ET-1） were measured respectively.Results：After treatment,all parameters in the 24-h ABPM and the elasticity of the carotid artery（β,Ep,AC and PVWβ） were markedly improved,the level of NO was increased,and ET-1 was decreased in both groups as compared with values before treatment （P0.05 or P0.01）.Further,the improvements in the ratio of T/P of SBP DBP and in the level of NO and ET-1 in the treatment group were more significant than those in the control group（P0.05）.There were no significant differences in all parameters in the ABPM monitoring and the elasticity of the carotid artery,the recovery of blood pressure circadian rhythm,and the therapeutic effect of antihypertension in EH patients between the two groups （P0.05）.Conclusions：Chinese herbal medi
目的:观察平肝潜阳方药对自发性高血压大鼠血管组织中蛋白质表达的影响,为深入研究平肝潜阳方药治疗高血压的作用机制奠定基础。方法:选择WKY大鼠10只作为正常对照,自发性高血压大鼠20只随机分为模型组和平肝潜阳方治疗组。治疗时间为4周,治疗期间每周监测大鼠血压和心率,并观察大鼠行为学指标;治疗结束后,采用双向凝胶电泳(two-di mensional gel electrophoresis,2-DE)结合质谱技术分离鉴定血管组织相关蛋白。结果:平肝潜阳方药不仅能够明显降低自发性高血压大鼠的血压,而且能够改善大鼠的心率、易激惹程度和旋转耐受时间。本实验建立了自发性高血压大鼠血管组织的2-DE图谱。与正常组比较,模型组蛋白质点表达上升2倍及以上的有12个,下降2倍及以上的有15个。治疗组与模型组比较发现,表达下调的15个蛋白质中有10个表达增强,而表达上调的12个蛋白质中有8个表达降低。共得到16个肽质量指纹图谱,3个无质谱结果,搜索到13个具有统计学意义的蛋白质。结论:平肝潜阳方药能够降低血压和改善大鼠的行为学指标,其机制可能与调节血管组织的蛋白质表达谱有关。
Background Increasing research suggests that mitochondrial defect plays a major role in pulmonary hypertension(PH) pathogenesis. Mitochondrial dynamics and quality control have a central role in the maintenance of the cell proliferation and apoptosis balance. However, the molecular mechanism underlying of this balance is still unknown. Methods To clarify the biological effects of hypoxic air exposure and hypoxia-inducible factor-1α(HIF-1α) on pulmonary arterial smooth muscle cell(PASMC) and pulmonary arterial hypertension rats, the cells were cultured in a hypoxic chamber under oxygen concentrations. Cell viability, reactive oxygen species level, cell death, mitochondrial morphology, mitochondrial membrane potential, mitochondrial function and mitochondrial biosynthesis, as well as fission-and fusion-related proteins, were measured under hypoxic conditions. In addition, rats were maintained under hypoxic conditions, and the right ventricular systolic pressure, right ventricular hypertrophy index and right ventricular weight/body weight ratio were examined and recorded. Further, we assessed the role of HIF-1α in the development and progression of PH using HIF-1α gene knockdown using small interfering RNA transfection. Mdivi-1 treatment was performed before hypoxia to inhibit dynamin-related protein 1(Drp1). Results We found that HIF-1α expression was increased during hypoxia, which was crucial for hypoxia-induced mitochondrial dysfunction and hypoxia-stimulated PASMCs proliferation and apoptosis. We also found that targeting mitochondrial fission Drp1 by mitochondrial division inhibitor Mdivi-1 was effective in PH model rats. The results showed that mitochondrial dynamics were involved in the pulmonary vascular remodeling under hypoxia in vivo and in vitro. Furthermore, HIF-1α also modulated mitochondrial dynamics in pulmonary vascular remodeling under hypoxia through directly regulating the expression of Drp1. Conclusions In conclusion, our data suggests that abnormal mitochondrial dynamics could be a marke
Xi CHENJia-Mei YAOXia FANGCui ZHANGYu-Shu YANGCheng-Ping HUQiong CHENGuang-Wei ZHONG
