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CMV感染激活mTOR/p70S6K信号通路促进脑梗死患者颈动脉粥样硬化的机制

Mechanism of CMV infection promoting carotid atherosclerosis by activating mTOR/p70S6K signaling pathway in patients with cerebral infarction
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摘要 目的 分析巨细胞病毒(CMV)感染激活哺乳动物雷帕霉素靶蛋白/70 kDa核糖体蛋白S6激酶(mTOR/p70S6K)信号通路促进脑梗死患者颈动脉粥样硬化形成和发展的机制。方法 选取2017年7月-2020年7月青岛市中医医院神经内科收治的脑梗死患者行颈动脉内膜剥脱术后的颈动脉粥样硬化斑块标本80例为研究组,另选择同期性别、年龄匹配的40例正常颈内动脉标本为对照组。统计不同病变支数的脑梗死患者各指标。结果研究组CMV DNA阳性率高于对照组(P<0.05),CMV DNA阳性者的血清总胆固醇(TC)、甘油三脂(TG)、低密度脂蛋白胆固醇(LDL-C)水平高于CMV DNA阴性者,高密度脂蛋白胆固醇(HDL-C)低于CMV DNA阴性者(P<0.05),CMV DNA阳性者颈动脉内膜中层厚度(IMT)较CMV DNA阴性者增厚(P<0.05);研究组组织mTOR mRNA、p70S6K mRNA表达水平均高于对照组(P<0.05);研究组中CMV DNA阳性者的mTOR mRNA、p70S6K mRNA表达水平高于CMV DNA阴性者(P<0.05);研究组中,单支病变者CMV DNA及mTOR mRNA、p70S6K mRNA低于多支病变者(P<0.05)。结论 CMV可能通过激活mTOR/p70S6K信号通路促进脑梗死患者颈动脉粥样硬化形成与发展。 OBJECTIVE To analyze the mechanism of cytomegalovirus(CMV) infection promoting the formation and development of carotid atherosclerosis in patients with cerebral infarction by activating mechanistic target of rapamycin/70 kDa ribosomal protein S6 kinase(mTOR/p70 S6 K) signaling pathway. METHODS Total of 80 cases of carotid atherosclerotic plaque specimens were collected from patients with cerebral infarction treated by carotid endarterectomy in the department of Neurology in Qingdao Hospital of Traditional Chinese Medicine from Jul 2017 to Jul 2020 were recruited in the study group. Another 40 cases of normal internal carotid artery specimens were collected from patients of matching gender and age during the same period were in the control group. Indicators in patients with different numbers of lesions were statistically analyzed. RESULTS The CMV DNA positive rate in study group was significantly higher than that in control group(P<0.05). The levels of serum total cholesterol(TC), triglyceride(TG) and low-density lipoprotein cholesterol(LDL-C) were significantly higher, and high-density lipoprotein cholesterol(HDL-C) was significantly lower in the CMV DNA-positive patients than that in the CMV DNA-negative ones(P<0.05). The carotid intima-media thickness(IMT) in the CMV DNA-positive patients was significantly larger than that in the CMV DNA-negative ones(P<0.05). The expression levels of mTOR mRNA and p70 S6 K mRNA in the study group were significantly higher than those in the control group(P<0.05). The expression levels of mTOR mRNA and p70 S6 K mRNA in CMV DNA-positive patients of the study group were significantly higher than those in CMV DNA-negative ones(P<0.05). Levels of CMV DNA, mTOR mRNA and p70 S6 K mRNA in patients with single-vessel lesions were significantly lower than those in patients with multi-vessel lesions(P<0.05). CONCLUSION CMV may promote the formation and development of carotid atherosclerosis in patients with cerebral infarction by activating mTOR/p70 S6 K signaling pathway.
作者 牛昱光 韩萍 孙杨 周喜燕 于淼 NIU Yu-guang;HAN Ping;SUN Yang;ZHOU Xi-yan;YU Miao(Qingdao Hospital of Traditional Chinese Medicine(Haici Hospital),Qingdao,Shandong 266000,China)
出处 《中华医院感染学杂志》 CAS CSCD 北大核心 2022年第7期985-989,共5页 Chinese Journal of Nosocomiology
基金 青岛市2018-2019年度中医药科研项目(2019-zyy08)。
关键词 巨细胞病毒 mTOR/p70S6K信号通路 脑梗死 颈动脉粥样硬化 形成机制 发展机制 Cytomegalovirus MTOR/p70S6K signaling pathway Cerebral infarction Carotid atherosclerosis Formation mechanism Development mechanism
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