首页|圣草酚改善自发性高血压大鼠血管重构的机制研究

圣草酚改善自发性高血压大鼠血管重构的机制研究

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目的:观察圣草酚能否改善自发性高血压大鼠(SHRs)的血管重构,并探讨其可能机制。方法:设置WKY正常对照、SHRs模型及圣草酚给药(EDT 120 mg/kg,SHRs+EDT)组,连续给药 20 周。尾袖法测量血压[收缩压(SBP)、舒张压(DBP)及平均血压(MBP)],超声检测脉搏波速度(PWV),HE染色观察主动脉中膜厚度(MT),MASSON染色观察主动脉胶原百分比(VFC)变化,ELISA检测血清TNF-α、IL-6及IL-10含量,q-PCR检测主动脉中TNF-α、IL-6及IL-10 mRNA变化,免疫组化观察主动脉 Collagen Ⅰ 和 Collagen Ⅲ 表达,Western blotting 检测主动脉 TGF-β1、MMP-2、MMP-9、Toll样受体4(TLR4)、p-IκBa、IKBa、p-p65 及 p65 表达。结果:圣草酚给药20周后,SHRs的SBP、DBP、MBP及PWV显著下降(P<0。05或P<0。01),主动脉的MT和 VFC显著减少(P<0。05),Collagen Ⅰ、Collagen Ⅲ、TGF-β1、MMP-2、MMP-9、TLR4、p-lκBa、p-p65 蛋白表达显著减少(P<0。05或P<0。01)。结论:圣草酚长期给药后,可抑制TLR4、NF-κB表达发挥抗炎作用,从而减少TGF-β1、MMP-2、MMP-9表达,使胶原含量下降,改善SHRs的主动脉重构和硬化。
Eriodictyol resists vascular remodeling in spontaneously hyperten-sive rats by inhibiting TLR4/NF-κB signaling
AIM:To observe the vascular remodel-ing of eriodictyol(EDT)in spontaneously hyperten-sive rats(SHRs)by inhibiting TLR4/NF-kB signaling and to investigate the potential mechanism of ac-tion.METHODS:WKY normal control,SHRs model and EDT administration(EDT 120 mg/kg,SHRs+EDT)group were set for 20 weeks.Tail cuff method for blood BP measurement(SBP,DBP and MBP).Ul-trasonic detection of pulse wave velocity(PWV).The aortic media membrane thickness(MT)was vi-sualized by HE staining.The percentage of aortic collagen(VFC)changes were observed by MASSON staining,Serum content of TNF-α,IL-6,and IL-10 was measured by ELISA.The TNF-α,IL-6,and IL-10 mRNA changes in the aorta were detected by q-PCR.The aortic Collagen Ⅰ and Collagen Ⅲ expres-sion was observed by immunohistochemistry,WB measured the expression of aortic TGF-β1,MMP-2,MMP-9,TLR4,p-IκBa,IκBa,p-p65 and p65.RE-SULTS:After 20 weeks of EDT administration,SBP,DBP,MBP and PWV of SHRs were significantly de-creased,MT and VFC of aorta were significantly de-creased,and protein expressions of Collagen Ⅰ,Col-lagen Ⅲ,TGF-β1,MMP-2,MMP-9,TLR4,p-l Camba and p-p65 were significantly decreased.CONCLU-SION:After long-term administration of EDT could inhibit TLR4/NF-κB signaling and exert anti-inflam-matory effects,thus reducing TGF-β1,MMP-2 and MMP-9 expression,decreasing collagen content,and finally improving aortic remodeling and sclero-sis of SHRs.

hypertensionvascular remodelinginflammationTLR4NF-κB

王欢、张俊秀、张雅、戎浩、王友娣、汪五三、马同军

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皖南医学院药学院,芜湖 241002,安徽

皖南医学院公共卫生学院,芜湖 241002,安徽

皖南医学院基础医学院,芜湖 241002,安徽

高血压 血管重构 炎症 Toll样受体4 核转录因子κB

安徽省高校科研计划项目安徽省高校科研计划项目安徽省高等学校省级质量工程项目芜湖市科技局项目皖南医学院校级科研项目

2023AH0301052023AH0517742018xfsyxm0732022jc311WK202204

2024

中国临床药理学与治疗学
中国药理学会

中国临床药理学与治疗学

CSTPCD北大核心
影响因子:0.97
ISSN:1009-2501
年,卷(期):2024.29(9)