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    徐庆梅, 莫辰, 朱飞宇, 张恒, 王洪巨, 高琴, 康品方, 唐碧. 二十二碳六烯酸介导MAPK途径抗房颤的作用及机制研究[J]. 蚌埠医科大学学报, 2021, 46(1): 1-5. DOI: 10.13898/j.cnki.issn.1000-2200.2021.01.001
    引用本文: 徐庆梅, 莫辰, 朱飞宇, 张恒, 王洪巨, 高琴, 康品方, 唐碧. 二十二碳六烯酸介导MAPK途径抗房颤的作用及机制研究[J]. 蚌埠医科大学学报, 2021, 46(1): 1-5. DOI: 10.13898/j.cnki.issn.1000-2200.2021.01.001
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    XU Qing-mei, MO Chen, ZHU Fei-yu, ZHANG Heng, WANG Hong-ju, GAO Qin, KANG Pin-fang, TANG Bi. Study on the effects and mechanism of MAPK pathway mediated by docosahexaenoic acid against atrial fibrillation[J]. Journal of Bengbu Medical University, 2021, 46(1): 1-5. DOI: 10.13898/j.cnki.issn.1000-2200.2021.01.001
    Citation: XU Qing-mei, MO Chen, ZHU Fei-yu, ZHANG Heng, WANG Hong-ju, GAO Qin, KANG Pin-fang, TANG Bi. Study on the effects and mechanism of MAPK pathway mediated by docosahexaenoic acid against atrial fibrillation[J]. Journal of Bengbu Medical University, 2021, 46(1): 1-5. DOI: 10.13898/j.cnki.issn.1000-2200.2021.01.001
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    二十二碳六烯酸介导MAPK途径抗房颤的作用及机制研究

    Study on the effects and mechanism of MAPK pathway mediated by docosahexaenoic acid against atrial fibrillation

      摘要
    • 摘要:
      目的探讨二十二碳六烯酸（DHA）通过影响P38 MAPK途径调控胶原表达发挥抗房颤作用可能的机制。
      方法将80只对乙酰胆碱（66 μg/mL）-氯化钙（50 mg/mL）混合液敏感的SD大鼠随机分为对照组（CON组）、对照DHA处理组（DHA组）、房颤组（AF组）和房颤DHA处理组（DHA+AF组），每组20只复制大鼠房颤模型。BL-420F描记心电图、连续双刺激法测定心房有效不应期（effective refractory period，ERP）、全细胞膜片钳技术记录心房肌细胞动作电位时程（action potential duration，APD）变化，酶免疫吸附法（ELISA）检测大鼠心房肌组织Ⅰ型、Ⅲ型胶原表达情况，蛋白印迹检测P38、P-P38及MKP-1表达情况。
      结果大鼠房颤持续时间随实验时间增加而逐渐延长，而DHA可以缩短房颤持续时间（P < 0.05~P < 0.01）。AF组大鼠心房ERP、APD明显缩短、DHA可明显延长大鼠心房ERP、APD（P < 0.01）；各组P38表达无明显变化，与CON组相比，AF组大鼠P-P38表达水平明显升高，MKP-1表达明显下降（P < 0.01）；与AF组相比，DHA+AF组P-P38表达水平明显降低，MKP-1表达明显增加（P < 0.01）。ELISA结果证实，DHA可明显下调大鼠心房肌组织Ⅰ型、Ⅲ型胶原表达（P < 0.01）。
      结论DHA可能通过调控P38 MAPK信号转导通路介导胶原表达发挥抗房颤作用。

       

      Abstract:
      ObjectiveTo investigate the possible mechanism of docosahexaenoic acid(DHA) regulating collagen expression by affecting the P38 MAPK pathway to play an anti-atrial fibrillation.
      MethodsEighty SD rats sensitive to acetylcholine(66 μg/mL)-calcium chloride(50 mg/mL) mixture were randomly divided into the control group(CON group), control DHA treatment group(DHA group), atrial fibrillation group(AF group) and atrial fibrillation DHA treatment group(DHA+AF group)(20 rats in each group model of atrial fibrillation).The BL-420F tractive electrocardiogram and continuous double stimulation method were used to detect the atrial effective refractory period(ERP), the whole cell patch clamp technique was used to record the atrial muscle cell action potential duration(APD) change, the enzyme immunosorbent assay(ELISA) was used to detect the typeⅠ, Ⅲ collagen expression in atrial muscle tissue of rats, and the expression levels of P38 and P-PP38 and MKP 1 protein were detected using Western blotting.
      ResultsThe duration of atrial fibrillation in rats prolonged with the increasing of experimental time, while DHA could shorten the duration of atrial fibrillation(P < 0.05 to P < 0.01).The ERP and APD significantly shortened, while DHA could significantly prolong the atrial ERP and APD in AF group(P < 0.01).There was no significant change in P38 protein among each group.Compared with the CON group, the expression level of P-P38 significantly increased, while the expression level of MKP-1 decreased in AF group(P < 0.01). Compared with the AF group, the expression level of P-P38 significantly decreased, while the expression level of MKP-1 increased in the DHA+AF group(P < 0.01).The results of ELISA showed that DHA could obviously down-regulate the typeⅠand Ⅲ collagen expression(P < 0.01).
      ConclusionsDHA may play an anti-atrial fibrillation role by regulating P38 MAPK signal transduction pathway mediating collagen expression.

       

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