目的探讨针药结合对心肌梗死大鼠内向整流钾离子通道(inwardly rectifying K channel,Kir)相关蛋白表达的影响。方法63只大鼠采用随机数字表法随机抽取8只大鼠作为对照组,其余55只建立模型。对照组给予基础饲料,其余大鼠给予高脂喂饲。...目的探讨针药结合对心肌梗死大鼠内向整流钾离子通道(inwardly rectifying K channel,Kir)相关蛋白表达的影响。方法63只大鼠采用随机数字表法随机抽取8只大鼠作为对照组,其余55只建立模型。对照组给予基础饲料,其余大鼠给予高脂喂饲。3周后对55只造模大鼠采用一次性多点位注射盐酸异丙肾上腺素溶液建立动物模型。将造模成功的40只大鼠按照随机数字表法分为模型组、针刺组、中药组、针药结合组、西药组,每组8只,分别给予相应干预。15 d后观察大鼠心电图变化,采用全自动生化分析仪检测各组大鼠血清血脂水平,HE染色观察各组大鼠心脏组织形态学变化,ELISA法检测大鼠血清中血清超敏C反应蛋白(serum high sensitivity C-reactive protein,hs-CRP)、非对环二甲基精氨(ADMA)含量,Western Blot法检测大鼠Kir2.1、Kir2.2、Kir2.3蛋白表达。结果与对照组相比,模型组大鼠血清hs-CRP、ADMA含量均呈上升趋势(P<0.05),Kir2.1、Kir2.2、Kir2.3的蛋白表达量均呈下降趋势(P<0.05);与模型组相比,针刺组、中药组、针药结合组与西药组hs-CRP、ADMA含量均呈下降趋势(P<0.05),中药组、针药结合组与西药组Kir2.1的表达量均呈上升趋势(P<0.05),针刺组、中药组、针药结合组与西药组Kir2.2、Kir2.3的表达量均呈上升趋势(P<0.05);针刺组、中药组、西药组hs-CRP、ADMA含量均高于针药结合组(P<0.05),针刺组、中药组、西药组Kir2.1、Kir2.3表达量均低于针药结合组,针刺组、中药组Kir2.2表达量低于针药结合组(P<0.05)。结论针药结合可能通过调节内向整流钾离子通道,实现对心肌梗死大鼠的治疗改善作用,为日后针药结合治疗本病提供参考和思路。展开更多
OBJECTIVE:To investiage the possible mechanism underlying the effect of the Jianpi Qutan Fang(健脾祛痰方,JPQT)on Atherosclerosis(AS)which is the main pathological process of most cardiovascular diseases that affect mi...OBJECTIVE:To investiage the possible mechanism underlying the effect of the Jianpi Qutan Fang(健脾祛痰方,JPQT)on Atherosclerosis(AS)which is the main pathological process of most cardiovascular diseases that affect millions of adults worldwide.METHODS:In the present study,rats were fed with a high-fat-diet(HFD)with vitamin D3 for 16 weeks and were orally administered atorvastatin treatment and different doses of JPQT.Histopathological changes and ultrastructural changes in the aorta were evaluated through hematoxylin-eosin staining and transmission electron microscopy(TEM),respectively.Suppressor of cytokine signaling 1(SOCS1)/Janus kinase 1(JAK1)/signal transducer and activator of transcription 1(STAT1)signaling pathways were detected through Western blotting.RESULTS:JPQT treatment decreased the lipid levels of triglyceride,low-density lipoprotein,and cholesterol,the inflammatory cytokine levels of interleukin 1 beta(IL-1β),IL-6 and IL-8 in rat serum,but increased high-density lipoprotein and IL-10 serum levels.JPQT treatment ameliorated pathological changes in the aorta of AS model rats.Moreover,JPQT upregulated SOCS1 protein expression and down-regulated phosphorylated protein expression levels of p-JAK1 and p-STAT1.CONCLUSION:These results suggest that JPQT induces anti-atherosclerosis effects through anti-inflammatory and inhibiting JAK/STAT signaling pathways in HFD fed rats.展开更多
文摘目的探讨针药结合对心肌梗死大鼠内向整流钾离子通道(inwardly rectifying K channel,Kir)相关蛋白表达的影响。方法63只大鼠采用随机数字表法随机抽取8只大鼠作为对照组,其余55只建立模型。对照组给予基础饲料,其余大鼠给予高脂喂饲。3周后对55只造模大鼠采用一次性多点位注射盐酸异丙肾上腺素溶液建立动物模型。将造模成功的40只大鼠按照随机数字表法分为模型组、针刺组、中药组、针药结合组、西药组,每组8只,分别给予相应干预。15 d后观察大鼠心电图变化,采用全自动生化分析仪检测各组大鼠血清血脂水平,HE染色观察各组大鼠心脏组织形态学变化,ELISA法检测大鼠血清中血清超敏C反应蛋白(serum high sensitivity C-reactive protein,hs-CRP)、非对环二甲基精氨(ADMA)含量,Western Blot法检测大鼠Kir2.1、Kir2.2、Kir2.3蛋白表达。结果与对照组相比,模型组大鼠血清hs-CRP、ADMA含量均呈上升趋势(P<0.05),Kir2.1、Kir2.2、Kir2.3的蛋白表达量均呈下降趋势(P<0.05);与模型组相比,针刺组、中药组、针药结合组与西药组hs-CRP、ADMA含量均呈下降趋势(P<0.05),中药组、针药结合组与西药组Kir2.1的表达量均呈上升趋势(P<0.05),针刺组、中药组、针药结合组与西药组Kir2.2、Kir2.3的表达量均呈上升趋势(P<0.05);针刺组、中药组、西药组hs-CRP、ADMA含量均高于针药结合组(P<0.05),针刺组、中药组、西药组Kir2.1、Kir2.3表达量均低于针药结合组,针刺组、中药组Kir2.2表达量低于针药结合组(P<0.05)。结论针药结合可能通过调节内向整流钾离子通道,实现对心肌梗死大鼠的治疗改善作用,为日后针药结合治疗本病提供参考和思路。
基金the National Natural Science Foundation of China:Explore the Regulatory Mechanism of Coronary Endothelial Immune Inflammation Mediated by Micro RNA155-SOCS1 Axis in Bama Pigs based on “Xin Shou Qi Yu Pi”(No.81703970)the National 973 Program on Key Basic Research Project:Study on the Therapeutic Mechanism and Rule of Treating Angina Pectoris based on “Cong Pi Lun Zhi”(No.2013CB531704)
文摘OBJECTIVE:To investiage the possible mechanism underlying the effect of the Jianpi Qutan Fang(健脾祛痰方,JPQT)on Atherosclerosis(AS)which is the main pathological process of most cardiovascular diseases that affect millions of adults worldwide.METHODS:In the present study,rats were fed with a high-fat-diet(HFD)with vitamin D3 for 16 weeks and were orally administered atorvastatin treatment and different doses of JPQT.Histopathological changes and ultrastructural changes in the aorta were evaluated through hematoxylin-eosin staining and transmission electron microscopy(TEM),respectively.Suppressor of cytokine signaling 1(SOCS1)/Janus kinase 1(JAK1)/signal transducer and activator of transcription 1(STAT1)signaling pathways were detected through Western blotting.RESULTS:JPQT treatment decreased the lipid levels of triglyceride,low-density lipoprotein,and cholesterol,the inflammatory cytokine levels of interleukin 1 beta(IL-1β),IL-6 and IL-8 in rat serum,but increased high-density lipoprotein and IL-10 serum levels.JPQT treatment ameliorated pathological changes in the aorta of AS model rats.Moreover,JPQT upregulated SOCS1 protein expression and down-regulated phosphorylated protein expression levels of p-JAK1 and p-STAT1.CONCLUSION:These results suggest that JPQT induces anti-atherosclerosis effects through anti-inflammatory and inhibiting JAK/STAT signaling pathways in HFD fed rats.
