首页|丹皮酚抑制TLR4/NF-KB信号通路对子痫前期大鼠的治疗作用及机制研究

丹皮酚抑制TLR4/NF-KB信号通路对子痫前期大鼠的治疗作用及机制研究

扫码查看
目的 探讨丹皮酚通过抑制TLR4/NF-κB信号通路对子痫前期大鼠的治疗作用及机制.方法 建立PE大鼠模型,分为Control组,Model组,丹皮酚低、中、高剂量组(Pae-L、Pae-M、Pae-H组)和丹皮酚高剂量+脂多糖组(Pae-H+LPS组).尾带血压计检测大鼠收缩压;记录胚胎存活数、胎儿与胎盘质量;ELISA检测尿蛋白质(UP)、胎盘生长因子(PLGF)、可溶性酪氨酸激酶受体.1(sFlt-1)和血管内皮生长因子(VEGF)水平、炎症因子及氧化应激相关指标;H-E染色观察胎盘组织病理学变化;TUNEL检测胎盘组织细胞凋亡;Western blot检测凋亡和TLR4/NF-κB信号通路相关蛋白水平.结果 与Control组相比,Model组大鼠胎盘组织细胞肿胀和空泡化增加,炎症细胞浸润及纤维样坏死增加;SBP、UP、sFlt-1、TNF-α、IL-6、IFN-γ、ROS 和 MDA 水平、细胞凋亡率及 Bax、Caspase-3、TLR4 和NF-κB p65蛋白表达显著增加(P<0.05),胎儿质量、PLGF、VEGF和SOD水平及Bcl-2蛋白表达显著降低(P<0.05).与Model组相比,Pae-L组、Pae-M组和Pae-H组大鼠胎盘组织炎症浸润减轻,新生血管增多;SBP、UP、sFlt-1、TNF-α、IL-6、IFN-γ、ROS和MDA水平、细胞凋亡率及Bax、Caspase-3、TLR4和NF-κB p65蛋白表达显著降低(P<0.05),胎儿质量、PLGF、VEGF和SOD水平及Bcl-2蛋白表达显著增加(P<0.05).TLR4通路抑制剂LPS逆转了丹皮酚对PE大鼠的保护作用.结论 丹皮酚对子痫前期大鼠的治疗作用可能与抑制TLR4/NF-KB信号通路有关.
Therapeutic effect and mechanism of paeonol on preeclampsia rats by inhibiting TLR4/NF-κB signaling pathway
Objective To investigate the therapeutic effect and mechanism of paeonol on preeclampsia rats by inhib-iting TLR4/NF-κB signaling pathway.Methods PE rat models were established and separated into Control group,Model group,paeonol low,medium and high dose groups(Pae-L,Pae-M and Pae-H groups),and paeonol high dose+lipopolysaccharide group(Pae-H+LPS group).Caudal sphygmomanometer was applied to measure the systolic blood pressure of rats.The number of embryos surviving,fetal and placental weights were recorded.ELISA was applied to detect the levels of urinary protein(UP),placental growth factor(PLGF),soluble fms-like tyrosine kinase-1(sFlt-1),and vascular endothelial growth factor(VEGF)levels,inflammatory factors,and oxidative stress-related indicators.H-E staining was applied to observe pathological changes in placental tissue.TUNEL was used to detect apoptosis in placental tissue cells.Western blot was used to detect apoptosis and TLR4/NF-κB signaling pathway related protein levels.Results Compared with the Control group,the placental tissue cells in the Model group showed increased swelling and vacuolization,and the infiltration of inflammatory cells and fibroid necrosis increased.The levels of SBP,UP,sFlt-1,TNF-α,IL-6,IFN-γ,ROS and MDA,cell apoptosis rate,and the expression of Bax,Caspase-3,TLR4,and NF-κB p65 proteins were obviously increased(P<0.05),the fetal weight,the levels of PLGF,VEGF,SOD,and the expression of Bcl-2 protein were obviously reduced(P<0.05).Compared with the Model group,the inflamma-tory infiltration of placental tissue in rats in the Pae-L group,Pae-M group,and Pae-H group decreased,and the number of new blood vessels increased;the levels of SBP,UP,sFlt-1,TNF-α,IL-6,IFN-γ,ROS and MDA,cell apoptosis rate,and the ex-pression of Bax,Caspase-3,TLR4,and NF-κB p65 proteins were obviously reduced(P<0.05),the fetal weight,the levels of PLGF,VEGF,SOD and the expression of Bcl-2 protein were obviously increased(P<0.05),and were dose-dependent.The TLR4 pathway inhibitor LPS reversed the protective effect of paeonol on PE rats.Conclusion The therapeutic effect of paeonol on preeclampsia rats may be related to the inhibition of TLR4/NF-κB signaling pathway.

paeonolcell surface receptor Toll like receptor 4/nuclear factor-κB signaling pathwaypreeclampsia

王守燕、李洁

展开 >

潍坊医学院附属医院产一科,山东潍坊 261000

丹皮酚 细胞表面受体Toll样受体4/核因子-κB信号通路 子痫前期

2024

中国优生与遗传杂志
中国优生科学协会

中国优生与遗传杂志

CSTPCD
影响因子:0.527
ISSN:1006-9534
年,卷(期):2024.32(1)
  • 22