海南师范大学学报（自然科学版）2026，Vol.39Issue(2)：192-199,8.DOI:10.12051/j.issn.1674-4942.2026.02.010
岩藻聚糖硫酸酯联合吲哚布芬经TLR4/NF-κB/NLRP3通路改善高脂诱导冠心病的机制
Fucoidan Sulfate and Indobufen Ameliorate High-Fat-Induced CAD via TLR4/NF-κB/NLRP3 Pathway
摘要
Abstract
This study investigated the mechanism by which fucoidan sulfate combined with indobutfen improved hyperlipidemia-induced coronary artery disease(CAD)by inhibiting cell pyroptosis mediated through the TLR4/NF-κB/NLRP3 signaling pathway,providing a theoretical basis for marine-based therapeutic interventions in CAD.A rat CAD model was established using a high-fat diet combined with pituitrin administration,while an in vitro inflammatory model was induced in human coronary artery endothelial cells(HCAEC)with LPS.Rats were randomly divided into a control group,a hyperlipidemia+coronary artery disease group,and a fucoidan sulfate+indobutafen group(n=8).Drug efficacy was evaluated by measuring lipid parameters(TC,TG,HDL-C,LDL-C),cellular viability(MTT assay),nitric oxide(NO)levels,lipid droplet formation(oil red O staining),and protein expression levels of TLR4,NLRP3,and p-p65 via Western blot.The results demonstrated that,compared with the control group,the hyperlipidemia+coronary artery disease(CAD)group exhibited significantly elevated serum levels of total cholesterol(TC),triglycerides(TG),and low-density lipoprotein cholesterol(LDL-C)(P<0.05),decreased high-density lipoprotein cholesterol(HDL-C)(P<0.05),and increased nitric oxide(NO)concentration(P<0.05),along with marked cellular morphological changes(curved and annular shapes)and lipid droplet accumulation.Compared with the hyperlipidemia+CAD group,the combined drug therapy group showed significantly reduced serum TC[(2.81±1.310)vs.(3.86±0.92)mmol/L],TG[(1.57±0.59)vs.(2.13±1.09)mmol/L],and LDL-C[(1.13±0.95)vs.(1.80±1.06)mmol/L](P<0.05),elevated HDL-C[(1.11±0.72)vs.(0.97±1.04)mmol/L,P<0.05],decreased NO concentration(P<0.05),restored cellular morphology(elongated spindle-shaped),and reduced lipid droplet accumulation.Additionally,protein expression of TLR4,NLRP3,and p-p65 was significantly inhibited(P<0.05).Fucoidan sulfate(1 mg/mL)combined with indobutfen(10 μmol/L)effectively improved hyperlipidemia-induced CAD by inhibiting cell pyroptosis mediated through the TLR4/NF-κB/NLRP3 signaling pathway,providing a novel approach for marine-based therapeutic interventions in cardiovascular diseases.关键词
岩藻聚糖硫酸酯/吲哚布芬/冠状动脉粥样硬化性心脏病/TLR4/NF-κB/NLRP3信号通路/细胞焦亡Key words
fucoidan/indobufen/coronary atherosclerotic heart disease/TLR4/NF-κB/NLRP3 signaling pathway/pyroptosis分类
医药卫生引用本文复制引用
谢伟,方超华,陈枫楠,沈凯,关丽萍..岩藻聚糖硫酸酯联合吲哚布芬经TLR4/NF-κB/NLRP3通路改善高脂诱导冠心病的机制[J].海南师范大学学报（自然科学版）,2026,39(2):192-199,8.基金项目
浙江省医学会临床医学科研专项资金项目(2023ZYC-A65) （2023ZYC-A65）
舟山市医药卫生科技计划项目(2023YA10) （2023YA10）
