中成药治疗室性早搏的临床研究证据图

该研究运用证据图系统梳理中成药治疗室性早搏的临床研究,了解该领域的证据分布。通过检索PubMed、Cochrane Library、Web of Science、中国知网(CNKI)、万方(Wanfang)、维普(VIP)数据库中关于中成药治疗室性早搏的文献,检索日期为2016年1月至2022年12月。采用图表结合文字的方式对证据进行分析与展示。最终纳入文献164篇,包括干预性研究147篇、观察性研究4篇、系统评价13篇。结果共获得27种中成药,其中参松养心胶囊和稳心颗粒报告频次较高;临床用药存在超适应证使用现象;近年来国内外该领域发文量呈下降趋势;干预性研究的结局指标有8类,动态心电图、临床有效率、安全性、超声心动图报告频次较高,缺乏对β受体阻滞剂减停率、主要心血管事件和药物经济学指标的报告,评价维度单一;纳入文献整体质量较低,降低了研究结论的可信度。未来需更加规范临床用药,提高临床研究质量,开展临床综合评价,为中成药治疗室性早搏提供更健全的科学依据。

Panax Notoginseng Saponins Inhibits Ventricular Remodeling after Myocardial Infarction in Rats Through Regulating ATF3/MAP2K3/p38 MAPK and NFκB Pathway

Objective:To explore whether Panax notoginseng saponins(PNS)exhibits heart protective effect in myocardial infarction(MI)rats and to identify the potential signaling pathways involved.Methods:MI rats induced by ligating the left anterior descending(LAD)coronary artery were assigned to sham coronary artery ligation or coronary artery ligation.Totally 36 Sprague-Dawley rats were randomly divided into sham group(distilled water,n=9),MI group(distilled water,n=9),PNS group(PNS,40 mg/kg daily,n=9)and fosinopril group(FIP,1.2 mg/kg daily,n=9)according to a random number table.The left ventricular morphology and function were conducted by echocardiography.Histological alterations were evaluated by the stainings of HE and Masson.The serum levels of C reactive protein(CRP),tumor necrosis factorα(TNF-α),growth differentiation factor-15(GDF-15)and the ratio of metalloproteinase-9(MMP-9)and tissue inhibitor of MMP-9(TIMP-1)were determined by ELISA.The levels of activating transcription factor 3(ATF3),mitogen-activated protein kinase kinase 3(MAP2 K3),p38 mitogen-activated protein kinase(p38 MAPK),phosphorylation of p38 MAPK(p-p38 MAPK),transforming growth factor-β(TGF-β1),collagenⅠ,nuclear factor kappa B p65(NFκB p65),phosphorylation of NFκB p65(p-NFκB p65),and phosphorylation of inhibitory kappa Bα(p-IκBα)in hearts were measured by Western blot and immunohistochemical staining,respectively.Results:PNS improved cardiac function and fibrosis in MI rats(P<0.05).The serum levels of CRP,TNF-α,GDF-15 and the ratio of MMP9/TIMP1 were reversed by PNS in MI rats.The expressions of TGF-β1,collagenⅠ,MAP2 K3,p38 MAPK,p-p38 MAPK,NFκB p65,p-NFκB p65,and p-IκBαwere down-regulated,while ATF3 increased with the treatment of PNS(P<0.05).Conclusions:PNS may improve cardiac function and fibrosis in MI rats via regulating ATF3/MAP2 K3/p38 MAPK and NFκB signaling pathways.These results suggest the potential of PNS in preventing the development of ventricular remodeling in MI rats.