目的 研究氯吡格雷联合低分子肝素对老年急性心肌梗死(acute myocardial infarction, AMI)患者血清中血脂及炎性因子的影响,为临床AMI的治疗提供参考依据。方法 选取新乡医学院第一附属医院于2016年10月—2019年11月期间收治的老年AMI患者112例,按照随机分配的原则分成两组,即对照组和观察组,每组病例各56例,治疗方式为对照组单给予口服氯吡格雷进行治疗,观察组给予口服氯吡格雷与皮下注射低分子肝素联合治疗,比较治疗前后两组患者血清中甘油三酯(triglyceride,TG)、总胆固醇(total cholesterol,TC)及低密度脂蛋白胆固醇(low-density lipoprotein cholesterol,LDH-C),炎性因子的水平变化及心功能的改变情况。结果 与治疗前相比较,治疗后对照组和观察组患者血清TG、TC及LDH-C水平均降低,炎性因子TNF-α,IL-1β,CRP,IL-6的水平均降低,患者的左心室后壁厚度、左心室舒张末期内径均有降低,射血分数升高;而与对照组治疗后相比较,治疗后观察组患者血清TG、TC及LDH-C水平进一步降低,炎性因子TNF-α,IL-1β,CRP,IL-6的水平进一步降低,患者的左心室后壁厚度、左心室舒张末期内径均降低,而射血分数升高,差异有统计学意义。结论 氯吡格雷联合低分子量肝素可通过降低血清中血脂的水平,抑制AMI过程中的炎症反应,减少炎性因子的释放,提高患者的心功能,改善患者的病情。

Objective To explore the effects of clopidogrel combined with low molecular weight heparin on serum lipids and inflammatory factors in elderly patients with acute myocardial infarction, and provide reference for clinical treatment of AMI. Methods 112 elderly patients with AMI admitted to the First Affiliated Hospital of Xinxiang Medical University from October 2016 to November 2019 were randomly divided into control group and observation group,56 cases in each group.The control group was treated with clopidogrel alone, and the observation group was treated with clopidogrel combined with low molecular weight heparin. The levels of serum TG, TC and LDH-C, inflammatory factors and cardiac function were compared between the two groups before and after treatment. Results Compared with before treatment, the levels of serum TG, TC and LDH-C decreased, and the levels of inflammatory factors TNF-α, IL-1β, CRP and IL-6 decreased in the observation group and the control group after treatment. The left ventricular posterior wall thickness and LVEDD decreased, but LVEF increased in the observation group and control group after treatment. Compared with control group after treatment, the levels of serum TG, TC and LDH-C decreased, and the levels of inflammatory factors TNF-α, IL-1β, CRP and IL-6 decreased, the left ventricular posterior wall thickness and LVEDD decreased, but LVEF increased further in observation group after treatment. Conclusion Clopidogrel combined with low molecular weight heparin may improve the patient's cardiac function, then improve the patient's condition through reducing the level of serum lipids, inhibit the inflammatory reaction in AMI, reduce the release of inflammatory factors.

目的 探讨miR-148a对大鼠急性胰腺炎细胞模型中细胞自噬的影响。方法 选取培养AR42J细胞,细胞分为4组,即正常对照组、模型组、miR-148a mimics组及miR-148a阴性对照组。利用Lipofectamine 2000转染miR-148a mimics及阴性对照miR-148a至AR42J细胞,继续培养48 h后,利用浓度为200 μmol的牛磺胆酸钠盐(TLCs)刺激以上两组及模型组AR42J细胞20 min,正常对照组不做处理,然后提取各组细胞蛋白及RNA。利用RT-qPCR检测各组细胞中miR-148a的表达;利用CCK8实验检测各组细胞的活性;利用ELISA法检测各组细胞培养液中炎性因子IL-6,IL-1β及TNF-α的含量;利用Western blot检测自噬相关的基因Beclin1、LC3Ⅰ、 LC3Ⅱ的表达。结果 RT-qPCR结果显示,与正常对照组相比较,模型组心肌细胞中miR-148a mRNA的表达降低,而miR-148a mimics组细胞中miR-148a mRNA的表达显著升高;CCK-8实验结果显示,转染miR-148a mimics至细胞后,可提高模型细胞的活性;ELISA实验结果显示,与模型组相比较,转染miR-148a mimics至细胞后,细胞培养液中炎性因子IL-6,IL-1β及TNF-α的含量显著降低;Western blot结果显示,与模型组相比较,转染miR-148a mimics至细胞后,可降低细胞中Beclin1的表达,降低LC3Ⅱ/LC3Ⅰ的比率。结论 利用miR-148a mimics提高TLCs刺激的细胞模型中的miR-148a表达后,细胞中Beclin1的表达降低,LC3Ⅱ/LC3Ⅰ的比率降低,抑制了细胞自噬,降低了炎性因子IL-6、IL-1β、TNF-α的释放,从而提高了细胞的活性,miR-148a可通过调节模型细胞的自噬而发挥细胞保护作用。

Objective To investigate the effect of miR-148a on autophagy in rat acute pancreatitis cell model. Methods AR42J cells were cultured and divided into 4 groups: normal control group, model group, miR-148a mimics group and miR-148a negative control group. miR-148a mimics and miR-148a negative control were transfected to AR42J cells with Lipofectamine 2 000, then cells were cultured for 48 h. The AR42J cells were stimulated with sodium taurocholate (TLCs) at a concentration of 200 μmol for 20 min, the normal control group was not treated, then the protein and RNA were extracted in each group. The expression of miR-148a was detected by RT-qPCR in each group. The activity of cells was detected by CCK8 assay in each group. The contents of IL-6, IL-1β and TNF-α in the cell culture medium were detected by ELISA. Western blot was used to detect the expression of autophagy related genes Beclin1, LC3Ⅰ and LC3Ⅱ. Results RT-qPCR results showed that the expression of miR-148a mRNA in model group was significantly lower than that in normal control group, while the expression of miR-148a mRNA in miR-148a mimics group was significantly higher than that in normal control group. The results of CCK-8 assay showed that miR-148a could significantly increase the activity of model cells stimulated by TLCs. The results of ELISA showed that the contents of IL-6, IL-1β and TNF-α in cell culture medium were significantly decreased after miR-148a mimics transfection, compared with the model group. Western blot showed that miR-148a mimics could significantly decrease the expression of Beclin1 and the ratio of LC3Ⅱ/LC3Ⅰ, compared with the model group. Conclusion miR-148a mimics was used to enhance the expression of miR-148a in cells model stimulated by TLCs, the expression of Beclin1 and the ratio of LC3Ⅱ/LC3Ⅰ were decreased, and the autophagy was inhibited. The release of IL-6, IL-1β and TNF-α was decreased and the activity of cells was increased. miR-148a plays a cellular protective role by regulating autophagy in model cells.