幽门螺杆菌感染对老年高血压颈动脉斑块易损性的影响

Influence of Helicobacter pylori infection on vulnerability of carotid plaques of elderly patients with hypertension

  • 摘要: 目的 探讨幽门螺杆菌(Hp)感染对老年高血压患者外周血核因子κB/NOD样受体热蛋白结构域相关蛋白3/半胱天冬酶-1(NF-κB/NLRP3/Caspase-1)炎症信号通路的激活状态及其与颈动脉粥样硬化斑块易损性的关联性。方法 选取2022年1月-2025年6月于广西医科大学第一附属医院就诊的老年高血压合并颈动脉粥样硬化斑块患者585例为研究对象,根据14C-尿素呼气试验结果分为Hp阳性组285例和Hp阴性组300例。检测患者外周血血脂谱、超敏C-反应蛋白(hs-CRP)、炎性因子[TNF-α/白细胞介素(IL)-1β/IL-18]、NF-κB/NLRP3/Caspase-1表达及颈动脉指标[内膜中层厚度(IMT)/斑块积分/性质],单因素和多因素分析斑块易损性的危险因素。结果 Hp阳性组患者血脂谱异常[总胆固醇(TC)和低密度脂蛋白胆固醇(LDL-C)升高,高密度脂蛋白胆固醇(HDL-C)降低]、炎症标志物升高、颈动脉粥样硬化加重(IMT增厚、斑块积分及易损斑块检出率增加)、NF-κB/NLRP3通路激活(mRNA/蛋白表达升高),均具有统计学意义(P<0.05)。多因素分析显示Hp感染(OR=2.850)、LDL-C(OR=1.920)及NLRP3表达(OR=2.850)是易损斑块的危险因素(P<0.05)。结论 Hp感染可能通过在转录和翻译水平上激活NF-κB/NLRP3/Caspase-1炎症信号通路,加剧机体系统性炎症反应和脂质代谢紊乱,促进高血压老年患者颈动脉粥样硬化斑块形成和不稳定性增加。

     

    Abstract: OBJECTIVE To explore the influence of Helicobacter pylori (Hp) infection on activation of peripheral blood inflammatory signaling pathways nuclear factor κB/NOD-like receptor thermal protein domain-related protein 3/Caspase-1 (NF-κB/NLRP3/Caspase-1) in the elderly patients with hypertension and observe its association with vulnerability of carotid atherosclerosis plaques. METHODS A total of 585 elderly patients with hypertension who were complicated with carotid atherosclerosis plaques and treated in the First Affiliated Hospital of Guangxi Medical University from Jan. 2022 to Jun. 2025 were recruited as the research subjects and were divided into the Hp-positive group with 285 cases and the Hp-negative group with 300 cases according to the result of 14C-urea breast test. The peripheral blood lipid profiles, high-sensitivity C-reactive protein (hs-CRP), inflammatory factors , NF-κB/NLRP3/Caspase-1 and carotid artery-related indicators were detected. Univariate analysis and multivariate analysis were performed for the risk factors for the vulnerability of plaques. RESULTS The patients of the Hp-positive group showed the abnormal blood lipid profiles rise of total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C), decline of high density lipoprotein cholesterol (HDL-C), rise of inflammatory markers, exacerbation of carotid artery atherosclerosis (increase of IMT, plaque score and detection rate of vulnerable plaques), and activation of NF-κB/NLRP3 pathways (rise of mRNA/protein expression level); there were significant differences(P<0.05). Multivariate analysis showed that H. pylori infection (OR=2.850), LDL-C(OR=1.920)and NLRP3(OR=2.850)expression levels were the risk factors for the vulnerable plaques(P<0.05). CONCLUSION The H. pylori infection may activate the NF-κB/NLRP3/Caspase-1 inflammatory signaling pathways on transcriptional and translational levels, exacerbates the systemic inflammatory response and lipid metabolism disorders of bodies, and accelerate the formation of carotid atherosclerosis plaques of the elderly patients with hypertension and increase the instability.

     

/

返回文章
返回