目的:研究参麦注射液干预高血压心衰的生物学机制。方法:通过高盐饲料(含8%Nacl)喂养Dahl盐敏感大鼠20周建立高血压心衰大鼠模型,另以普通饲料(含0.3%Nacl)喂养建立正常大鼠(8只),成模大鼠分为模型组(8只)和参麦注射液组各8只。药物干预...目的:研究参麦注射液干预高血压心衰的生物学机制。方法:通过高盐饲料(含8%Nacl)喂养Dahl盐敏感大鼠20周建立高血压心衰大鼠模型,另以普通饲料(含0.3%Nacl)喂养建立正常大鼠(8只),成模大鼠分为模型组(8只)和参麦注射液组各8只。药物干预15 d后采集所有大鼠的血清样本,运用液相色谱-质谱(liquid chromatography mass spectrometry,LC-MS)联用的代谢组学技术筛选组间差异代谢产物,分析关联代谢通路。结果:3组大鼠的代谢轮廓具有差异,与模型组比较参麦注射液组的四氢嘧啶、谷氨酸、腺嘌呤、异柠檬酸、乙酰乙酸、尸胺、12,13-二氢乳清酸表达水平向正常方向显著回调,涉及丁酸代谢通路、酮体的合成与降解通路、D-谷氨酰胺和D-谷氨酸代谢通路、谷胱甘肽代谢通路等4条代谢路径。结论:参麦注射液可促使氨基酸、酮体等代谢产物水平趋于正常化,调控能量代谢相关路径,从而优化心脏能量供应。展开更多
Objective: To study effects of Shenmai Injection on hypertensive heart failure and its mechanism for inhibiting myocardial fibrosis. Methods: Salt-sensitive(Dahl/SS) rats were fed with normal diet(0.3% Na Cl) and the ...Objective: To study effects of Shenmai Injection on hypertensive heart failure and its mechanism for inhibiting myocardial fibrosis. Methods: Salt-sensitive(Dahl/SS) rats were fed with normal diet(0.3% Na Cl) and the high-salt diet(8% Na Cl) to observe the changes in blood pressure and heart function, as the control group and the model group. Salt-insensitive rats(SS-13BN) were fed with the high-salt diet(8% Na Cl) as the negative control group. After modeling, the model rats were randomly divided into heart failure(HF) group, Shenmai Injection(SMI) group and pirfenidone(PFD) group by a random number table, with 6 rats in each group. They were given sterilized water, SMI and pirfenidone, respectively. Blood pressure, cardiac function, fibrosis and related molecular expression were detected by sphygmomanometer, echocardiogram, enzyme linked immunosorbent assay(ELISA),hematoxylin-eosin staining, Masson staining, immunofluorescence and qPCR analysis. Results: After high-salt feeding, compared with the control and negative control group, in the model group the blood pressure increased significantly, the left ventricular ejection fraction(LVEF) and left ventricular fraction shortening(LVFS) were significantly reduced, and the serum NT-pro BNP concentration increased significantly(all P<0.05);furthermore,the arrangement of myocardial cells was disordered, the edema was severe, and the degree of myocardial fibrosis was also significantly increased(P<0.05);the protein and m RNA expressions of collagen type Ⅰ(Col Ⅰ) were up-regulated(P<0.05), and the mRNA expressions of transforming growth factor β1(TGF-β1), Smad2 and Smad3 were significantly up-regulated(P<0.05). Compared with HF group, after intervention of Shenmai Injection, LVEF and LVFS increased, myocardial morphology was improved, collagen volume fraction decreased significantly(P<0.05), and the mRNA expressions of Col Ⅰ, TGF-β1, Smad2 and Smad3, as well as Col Ⅰprotein expression, were all significantly down-regulated(all P<0.05). Conclusion: Myocardial fibrosis is the main pathological manifestation of hypertensive heart failure, and Shenmai Injection could inhibit myocardial fibrosis and effectively improve heart failure by regulating TGF-β1/Smad signaling pathway.展开更多
文摘目的:研究参麦注射液对高血压心衰大鼠粪便代谢组学的影响。方法:20只Dahl盐敏感大鼠随机分为正常组(6只)、模型组(7只)和参麦注射液组(7只),以高盐饲料(8%NaCl浓度)喂养模型组、参麦注射液组大鼠20周建立高血压心衰模型。给药15 d后收集各组粪便样本,运用基于液相色谱-质谱(liquid chromatography mass spectrometry,LC-MS)联用的代谢组学技术进行研究。结果:主成分分析、偏最小二乘判别分析得分图显示,3组大鼠的代谢模式存在显著差异,与模型组比较参麦注射液组神经氨酸、别石胆酸、丙氨酰色氨酸、3,9-十六碳二烯酸、N-棕榈酰酪氨酸、亚油基肉碱、3-羟基-顺式-5-十四碳酰肉碱表达水平回调。结论:参麦注射液干预高血压心衰的机制涉及优化氨基酸代谢、蛋白质代谢、肉碱代谢、胆汁酸代谢、脂质代谢等多个层面。
文摘目的:研究参麦注射液干预高血压心衰的生物学机制。方法:通过高盐饲料(含8%Nacl)喂养Dahl盐敏感大鼠20周建立高血压心衰大鼠模型,另以普通饲料(含0.3%Nacl)喂养建立正常大鼠(8只),成模大鼠分为模型组(8只)和参麦注射液组各8只。药物干预15 d后采集所有大鼠的血清样本,运用液相色谱-质谱(liquid chromatography mass spectrometry,LC-MS)联用的代谢组学技术筛选组间差异代谢产物,分析关联代谢通路。结果:3组大鼠的代谢轮廓具有差异,与模型组比较参麦注射液组的四氢嘧啶、谷氨酸、腺嘌呤、异柠檬酸、乙酰乙酸、尸胺、12,13-二氢乳清酸表达水平向正常方向显著回调,涉及丁酸代谢通路、酮体的合成与降解通路、D-谷氨酰胺和D-谷氨酸代谢通路、谷胱甘肽代谢通路等4条代谢路径。结论:参麦注射液可促使氨基酸、酮体等代谢产物水平趋于正常化,调控能量代谢相关路径,从而优化心脏能量供应。
文摘目的:研究高盐饮食对大鼠尿液代谢组学的影响,探讨咸味致病的潜在生物学机制。方法:将16只SD大鼠随机分为高盐饮食组和正常对照组各8只,高盐饮食组给予高盐饲料(8%Nacl浓度)饲养,正常对照组给予普通饲料(0.4%Nacl浓度)饲养,60 d后收集2组的尿液样本,运用基于气相色谱-质谱联用(gas chromatography mass spectrometer,GC-MS)的代谢组学技术进行研究。结果:PCA与OPLS-DA得分图显示,2组的代谢轮廓存在显著差异。与正常对照组比较,高盐饮食组中有28种代谢产物表达水平出现改变,差异代谢产物主要涉及半乳糖代谢、丙氨酸与天冬氨酸和谷氨酸代谢、嘧啶代谢、淀粉和蔗糖代谢、泛酸和辅酶A生物合成、三羧酸循环等6条代谢路径。结论:过食咸味影响机制涉及扰动机体的糖代谢、能量代谢、嘧啶代谢、脂质代谢等多个层面,是一个多因素、多层次的复杂过程。
基金Supported by Hunan Provincial Natural Science Foundation of China(No.2020JJ5408)Scientific Research Fund of Hunan Provincial Education Department(No.21B0361)+1 种基金Research Fund of Hunan University of Chinese Medicine(No.2019XJJJ012)Zhuzhou Second Batch of Science and Technology Guidance Projects(No.2017-17)。
文摘Objective: To study effects of Shenmai Injection on hypertensive heart failure and its mechanism for inhibiting myocardial fibrosis. Methods: Salt-sensitive(Dahl/SS) rats were fed with normal diet(0.3% Na Cl) and the high-salt diet(8% Na Cl) to observe the changes in blood pressure and heart function, as the control group and the model group. Salt-insensitive rats(SS-13BN) were fed with the high-salt diet(8% Na Cl) as the negative control group. After modeling, the model rats were randomly divided into heart failure(HF) group, Shenmai Injection(SMI) group and pirfenidone(PFD) group by a random number table, with 6 rats in each group. They were given sterilized water, SMI and pirfenidone, respectively. Blood pressure, cardiac function, fibrosis and related molecular expression were detected by sphygmomanometer, echocardiogram, enzyme linked immunosorbent assay(ELISA),hematoxylin-eosin staining, Masson staining, immunofluorescence and qPCR analysis. Results: After high-salt feeding, compared with the control and negative control group, in the model group the blood pressure increased significantly, the left ventricular ejection fraction(LVEF) and left ventricular fraction shortening(LVFS) were significantly reduced, and the serum NT-pro BNP concentration increased significantly(all P<0.05);furthermore,the arrangement of myocardial cells was disordered, the edema was severe, and the degree of myocardial fibrosis was also significantly increased(P<0.05);the protein and m RNA expressions of collagen type Ⅰ(Col Ⅰ) were up-regulated(P<0.05), and the mRNA expressions of transforming growth factor β1(TGF-β1), Smad2 and Smad3 were significantly up-regulated(P<0.05). Compared with HF group, after intervention of Shenmai Injection, LVEF and LVFS increased, myocardial morphology was improved, collagen volume fraction decreased significantly(P<0.05), and the mRNA expressions of Col Ⅰ, TGF-β1, Smad2 and Smad3, as well as Col Ⅰprotein expression, were all significantly down-regulated(all P<0.05). Conclusion: Myocardial fibrosis is the main pathological manifestation of hypertensive heart failure, and Shenmai Injection could inhibit myocardial fibrosis and effectively improve heart failure by regulating TGF-β1/Smad signaling pathway.
