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电针“内关”对心肌肥厚模型大鼠p38丝裂原激活蛋白激酶信号通路的影响 被引量:15

Effects of electroacupuncture at "Neiguan"(PC 6) on p38 MAPK signaling pathway in rats with cardiac hypertrophy
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摘要 目的:探讨电针"内关"穴治疗心肌肥厚的作用机制。方法:SD大鼠40只用随机数字表法分为正常组、模型组、模型+p38抑制剂组、模型+电针组,每组10只。采用皮下注射盐酸异丙肾上腺素3mg/(kg.d)建立心肌肥厚大鼠模型,模型+p38抑制剂组在造模基础上每日皮下注射0.3mg/kg p38丝裂原激活蛋白激酶(p38MAPK)特异性抑制剂SB 203580;模型+电针组电针"内关"穴,采用连续波,频率2Hz,强度1mA,通电20min,1次/d,共14d。其他两组不予治疗干预。放射免疫法技术检测心肌组织肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)含量,免疫印迹法检测p38MAPK、磷酸化p38MAPK(p-p38MAPK)含量。观察电针"内关"穴对TNF-α和IL-1β、p38MAPK、p-p38MAPK的影响。结果:与正常组大鼠比较,模型组大鼠TNF-α和IL-1β、p38MAPK、p-p38MAPK均显著升高(均P<0.01);经抑制剂和电针处理后,模型+p38抑制剂组和模型+电针组大鼠TNF-α、IL-1β、p38MAPK、p-p38MAPK均明显降低,与模型组比较差异有统计学意义(均P<0.05),与正常组比较差异亦有统计学意义(P<0.05,P<0.01);模型+p38抑制剂组和模型+电针组之间比较差异无统计学意义(P>0.05)。结论:电针"内关"可以明显抑制心肌肥厚p38MAPK的磷酸化,这种保护作用可能通过抑制TNF-α、IL-1β等炎性因子的表达实现对p38MAPK信号通路调节。 Objective To discuss the mechanisms of electroacupuncture at "Neiguan"(PC 6) on p38 MAPK signaling pathway in rats with cardiac hypertrophy.Methods Forty SD rats were randomly divided into four groups: a normal group,a model group,a model plus p38 MAPK inhibitor group,a model plus electroacupuncture group,ten rats in each group.The model rats were established by subcutaneous injection 3 mg/(kg·d) of Isoprenaline Hydrochloride;model plus p38 MAPK inhibitor group were injected 0.3 mg/(kg·d) of specific inhibitor SB 203580;model plus electroacupuncture group was treated by electroacupuncture at "Neiguan"(PC 6) with continuous-wave,2 Hz and 1 mA for 20 minutes,once a day for 14 days.There was no treatment in other two groups.The contents of TNF-α and IL-1β in heart tissue were detected by radioimmunoassay and the p38 MAPK、p-p38 MAPK by western blot.Results Compared with normal group,the contents of TNF-α,IL-1β,p38 MAPK,p-p38 MAPK were significantly increased in model group(all P0.01).The contents of TNF-α,IL-1β,p38 MAPK,p-p38 MAPK were significantly decreased in model plus p38 MAPK inhibitor group and model plus electroacupuncture group,compared with model group,all P0.05;compared with normal group,P0.05,P0.01;but no significant difference between model plus p38 MAPK inhibitor group and model plus electroacupuncture group(P0.05).Conclusion Electroacupuncture at "Neiguan"(PC 6) can prevent the phosphorylation of p38 MAPK of myocardial hypertrophy,and the mechanism maybe adjust p38 MAPK signaling pathway by inhibiting the expression of TNF-α and IL-1β.
出处 《中国针灸》 CAS CSCD 北大核心 2012年第2期145-148,共4页 Chinese Acupuncture & Moxibustion
基金 国家自然科学基金项目:30973786 湖北省教育厅项目:Q 20101810
关键词 心肌肥厚 电针 内关 P38丝裂原激活蛋白激酶 肿瘤坏死因子-α 白细胞介素-1Β Cardiac Hypertrophy Electroacupuncture Point PC6(Neiguan) p38 MAPK TNF-α IL-1β
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