Research Article

洛哌丁胺诱导的便秘通过补体C3及其受体激活SD大鼠中结肠炎症信号通路

卷 22, 期 5, 2022

发表于: 24 August, 2021

页: [458 - 469] 页: 12

弟呕挨: 10.2174/1566524021666210618124220

open access plus

摘要

背景:补体成分3(C3)受体在先天免疫系统中作为炎症介质发挥着重要作用,尽管其在便秘中的作用机制尚未得到充分研究。 目的:本研究旨在探讨C3及其受体下游信号在便秘中的调节作用。 方法:测定洛哌丁胺(Lop)治疗的SD大鼠结肠中部C3、C3a受体(C3aR)和C3b受体(C3bR)表达、PI3K/AKT途径、RhoA/MLC途径、MAP激酶途径和炎性细胞因子表达的变化。 结果:Lop治疗成功诱导便秘表型,包括粪便参数下降和组织结构改变。在Lop诱导的便秘过程中,C3的表达水平显著升高,而C3aR和C3bR的表达降低。此外,Lop处理的SD大鼠结肠中部PI3K、AKT和GSK3β的磷酸化水平显著上调。Lop处理组中RhoA的表达和MLC的磷酸化也增强。此外,在MAP激酶途径和炎性细胞因子表达中也检测到类似的情况。经Lop治疗后,中结肠ERK和p38的磷酸化以及NF-κB、TNF-α、IL-6和IL-1α的mRNA水平显著升高。 结论:Lop诱导的便秘与SD大鼠中结肠C3aR和C3bR表达下调、C3和C3Rs下游信号通路上调密切相关,包括PI3K/AKT、RhoA/MLC、MAP激酶途径以及炎症细胞因子表达。

关键词: 补体C3、便秘、C3a受体、C3b受体、PI3K/AKT途径、洛哌丁胺

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