首页|期刊导航|检验医学与临床|葱白提取物通过PPARγ/HO-1途径对动脉粥样硬化大鼠血脂异常和炎症反应的调节作用

葱白提取物通过PPARγ/HO-1途径对动脉粥样硬化大鼠血脂异常和炎症反应的调节作用OACSTPCD

Regulatory effect of fistular onion bulb extract on dyslipidemia and inflammatory response in atherosclerotic rats via PPARγ/HO-1 pathway

中文摘要英文摘要

目的 探讨葱白提取物(FOB)通过调控过氧化物酶体增殖物激活受体γ(PPARγ)/血红素氧合酶1(HO-1)途径对动脉粥样硬化(AS)大鼠血脂异常和炎症反应的影响.方法 40 只 SD大鼠随机分为对照组、模型组(AS组)、FOB组和FOB+ GW9662 组,每组 10 只.对照组大鼠给予正常饲料喂养,其余 3 组大鼠均建立AS模型.各组大鼠连续给药 4 周.采用苏木精-伊红(HE)染色与油红 O 染色观察主动脉病变和脂质沉积情况;采用全自动分析仪检测总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)和高密度脂蛋白胆固醇(HDL-C)水平,并计算动脉粥样硬化指数(AI);采用酶联免疫吸附试验(ELISA)检测白细胞介素-6(IL-6)、白细胞介素-1β(IL-1β)和肿瘤坏死因子-α(TNF-α)水平;采用实时定量聚合酶链反应(qRT-PCR)法和West-ern blot法分别检测大鼠胸主动脉组织中PPARγ和HO-1 的mRNA和蛋白表达水平.结果 与对照组相比,AS组大鼠胸主动脉管壁明显增厚,内膜下可见炎症细胞浸润和泡沫细胞堆积,脂质斑块形成;FOB组大鼠胸主动脉组织病理变化及脂质斑块较AS组明显改善;FOB+GW9662 组大鼠胸主动脉组织病理变化及脂质斑块较FOB组明显加重.与对照组相比,AS组大鼠血清 TC、TG、LDL-C、IL-6、IL-1β、TNF-α水平及 AI 均显著升高(P<0.05),HDL-C 水平及胸主动脉组织中 PPARγ和 HO-1 的 mRNA、蛋白表达水平均显著降低(P<0.05).与 AS 组相比,FOB 组大鼠血清 TC、TG、LDL-C、IL-6、IL-1β、TNF-α水平及 AI 均显著降低(P<0.05),HDL-C水平及胸主动脉组织中PPARγ和 HO-1 的 mRNA、蛋白表达水平均显著升高(P<0.05).与FOB组相比,FOB+GW9662 组大鼠血清 TC、TG、LDL-C、IL-6、IL-1β、TNF-α水平及 AI 均显著升高(P<0.05),HDL-C水平及胸主动脉组织中PPARγ和 HO-1 的 mRNA、蛋白表达水平均显著降低(P<0.05).结论 FOB可能通过激活PPARγ/H O-1 信号通路调节血脂异常和炎症反应,缓解大鼠AS进展.

Objective To explore the regulatory effect of fistular onion bulb extract(FOB)via peroxisome proliferators activated receptor γ (PPAR γ )/heme oxygenase-1(HO-1)pathway on dyslipidemia and inflam-matory reaction in atherosclerosis(AS)rats.Methods Forty SD rats were randomly divided into control group,model group(AS group),FOB group and FOB+GW9662 group,with 10 rats in each group.The con-trol group rats were fed with normal feed,while the other three groups of rats established AS models.The rats in each group were treated with drugs for 4 weeks.The aortic lesions and lipid deposition were observed by HE staining and oil red O staining.The levels of total cholesterol(TC),triacylglycerol(TG),low-density lip-oprotein cholesterol(LDL-C)and high-density lipoprotein cholesterol(HDL-C)were detected by automatic analyzer,and the atherosclerosis index(AI)were calculated.The levels of interleukin-6(IL-6),interleukin-1β(IL-1β),tumor necrosis factor-α(TNF-α)were detected by ELISA assay.The mRNA and protein expression levels of PPAR γ and HO-1 were detected by qRT-PCR and Western blot.Results Compared with the control group,the aortic wall in the AS group was significantly thickened,inflammatory cell infiltration and foam cell accumulation were seen under the intima,and lipid plaque was formed;the pathological changes and lipid plaques in the thoracic aorta of rats in the FOB group were significantly improved compared to those in the AS group.The pathological changes and lipid plaques in the thoracic aorta tissue of rats in the FOB+GW9662 group were obviously worse than those in the FOB group.Compared with the Control group,the serum TC,TG,LDL-C,IL-6,IL-1β,TNF-α levels and AI in the AS group were significantly increased(P<0.05),while the serum HDL-C level,mRNA and protein expression levels of PPAR γ and HO-1 in thoracic aortic tissue were significantly decreased(P<0.05).Compared with the AS group,the serum TC,TG,LDL-C,IL-6,IL-1β,TNF-α levels and AI in the FOB group rats were significantly decreased(P<0.05),while the serum HDL-C level,mRNA and protein expression levels of PPAR γ and HO-1 in thoracic aortic tissue were significantly increased(P<0.05).Compared with the FOB group,the serum TC,TG,LDL-C,IL-6,IL-1β,TNF-α levels and AI in the FOB+GW9662 group were significantly increased(P<0.05),while the serum HDL-C level,mRNA and protein expression levels of PPAR γ and HO-1 in thoracic aortic tissue were significantly decreased(P<0.05).Conclusion FOB may modulate dyslipidemia and inflammatory response by activating PPARγ/HO-1 signaling pathway to alleviate the progression of AS disease in rats.

范鸿儒;王栋;张帆;杨力;易春峰;贺立群

湖北省武汉市第一医院/武汉市中西医结合医院心血管内科,湖北武汉 430022

中医学

葱白提取物动脉粥样硬化脂质代谢炎症反应PPARγ/HO-1信号通路

fistular onion bulb extractarteriosclerosislipid metabolisminflammatory reactionPPARγ/HO-1 signaling pathway

《检验医学与临床》 2024 (009)

1208-1213 / 6

湖北省知识创新专项(自然科学基金项目)(2019CFB405).

10.3969/j.issn.1672-9455.2024.09.005

评论