摘要
目的探讨熊果苷(AR)对乙酰胆碱-氯化钙(Ach-CaCl;)混合液诱导的心房颤动(AF)大鼠的心脏保护作用及其可能的机制。方法将30只健康雄性SD大鼠随机分为3组:正常对照组(Sham组)、AF模型组(AF组)与AR治疗组(AR+AF组),每组各10只。采用心电图及小动物超声心动图检测各组大鼠的心功能。采用Masson染色检测各组大鼠心房纤维化程度。通过酶联免疫吸附试验检测各组大鼠血清炎症因子。应用蛋白免疫印迹法检测各组大鼠炎症相关蛋白,并探讨AR对AF大鼠的保护作用及炎症相关作用机制。结果AF组大鼠AF持续时间显著多于Sham组、AR+AF组,差异均有统计学意义(P<0.05)。AF组大鼠左心房内径大于Sham组、AR+AF组,差异均有统计学意义(P<0.05)。与Sham组比较,AF组、AR+AF组的白细胞介素6(IL-6)、肿瘤坏死因子-α(TNF-α)水平明显升高,差异均有统计学意义(P<0.05)。与AF组比较,AR+AF组的IL-6、TNF-α水平明显降低,差异均有统计学意义(P<0.05)。与Sham组比较,AF组蛋白磷酸化磷脂酰肌醇3-激酶(p-PI3K)、磷酸化丝氨酸/苏氨酸激酶(p-AKT)、磷酸化哺乳动物雷帕霉素靶蛋白(p-mTOR)、TNF-α、IL-6表达显著增多,差异均有统计学意义(P<0.05);与AF组比较,AR+AF组蛋白p-PI3K、p-AKT、p-mTOR、TNF-α、IL-6表达明显降低,差异均有统计学意义(P<0.05)。结论AR可能通过抑制PI3K-AKT、mTOR通路减轻炎症反应,在大鼠阵发性AF模型中起到保护作用。
Objective To investigate the cardioprotective effect of arbutin(AR)on atrial fibrillation(AF)induced by acetylcholine chloride(Ach-CaCl;)mixture and its possible mechanism.Methods Thirty healthy male SD rats were randomly divided into 3 groups:normal control group(Sham group),AF model group(AF group)and AR treatment group(AR+AF group),with 10 rats in each group.Electrocardiogram and small animal echocardiography were used to detect the cardiac function of rats.Masson staining was used to detect the degree of atrial fibrosis in each group.Serum inflammatory factors were detected by enzyme-linked immunosorbent assay.Western blot was used to detect inflammation related proteins in each group,and the protective effect of AR on AF rats and the mechanism of inflammation related action were investigated.Results The duration of AF in AF group was significantly longer than that in Sham group and AR+AF group,with statistical significance(P<0.05).The inner diameter of left atrium in AF group was larger than that in Sham group and AR+AF group,with statistical significance(P<0.05).Compared with Sham group,the levels of interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α)in AF group and AR+AF group were significantly increased,with statistical significance(P<0.05).Compared with AF group,the levels of IL-6 and TNF-αin AR+AF group were significantly decreased,with statistical significance(P<0.05).Compared with Sham group,the expressions of phosphatidylinositol-3-kinase(p-PI3 K),phospho-protein kinase B(p-AKT),phospho-mammalian target of rapamycin(p-MTOR),TNF-αand IL-6 in AF group were significantly increased,and the differences were statistically significant(P<0.05).Compared with AF group,the expressions of p-PI3 K,p-AKT,P-MTOR,TNF-αand IL-6 in AR+AF group were significantly decreased,with statistical significance(P<0.05).Conclusion AR can reduce inflammation by inhibiting PI3 K-Akt and mTOR pathways,and play a protective role in the rat paroxysmal AF model.
作者
徐银丽
徐登月
于立明
赵继凯
黄涛
王辉山
XU Yin-li;XU Deng-yue;YU Li-ming;ZHAO Ji-kai;HUANG Tao;WANG Hui-shan(Department of Cardiovascular Surgery,General Hospital of Northern Theater Command,Shenyang 110016,China)
出处
《临床军医杂志》
CAS
2022年第4期350-354,共5页
Clinical Journal of Medical Officers
基金
国家自然科学基金(82070239)
作者简介
第一作者:徐银丽(1989-),女,云南腾冲人,主管技师,硕士;通信作者:王辉山,E-mail:huishanw@126.com
