Department of Traditional Chinese Medicine, People's Hospital of Ningxia Hui Autonomous Region, the First Affiliated Hospital of Northwest University for Nationalities, Yinchuan, 750000, Ningxia, China.
Department of Emergency, People's Hospital of Ningxia Hui Autonomous Region, the First Affiliated Hospital of Northwest University for Nationalities, No.301 Zhengyuan North Street, Yinchuan, 750000, Ningxia, China.
Inflammation. 2019 Apr;42(2):731-739. doi: 10.1007/s10753-018-0931-3.
To investigate the mechanism of Schisandrin B (Sch B) on the inflammation in LPS-induced sepsis. Sepsis mouse model was established by injecting LPS. qRT-PCR and western blot were used to measure the expression of miR-17-5p and TLR4. ELISA was used to test the concentrations of IL-1β and TNF-α. Sch B could increase miR-17-5p expression, promote inflammation, and decrease TLR4 expression in sepsis mice and LPS-induced macrophages. Moreover, miR-17-5p could negatively regulate TLR4. Overexpression of miR-17-5p suppressed the concentrations of inflammatory factors (IL-1β and TNF-α) in LPS induced-macrophages, while pcDNA-TLR4 could change the inhibition effect. Additionally, miR-17-5p inhibitor changed the inhibitory effects of Sch B on TLR4 expression and the concentrations of IL-1β and TNF-α in LPS induced-macrophages. Sch B could attenuate inflammation in LPS-induced sepsis through miR-17-5p downregulating TLR4.
探讨五味子乙素（Sch B）对脂多糖（LPS）诱导脓毒症炎症反应的作用机制。
通过注射 LPS 建立脓毒症小鼠模型。采用 qRT-PCR 和 Western blot 检测 miR-17-5p 和 TLR4 的表达。ELISA 检测 IL-1β 和 TNF-α 的浓度。
Sch B 可增加 miR-17-5p 的表达，促进脓毒症小鼠和 LPS 诱导的巨噬细胞中的炎症反应，并降低 TLR4 的表达。此外，miR-17-5p 可负调控 TLR4。过表达 miR-17-5p 可抑制 LPS 诱导的巨噬细胞中炎症因子（IL-1β 和 TNF-α）的浓度，而 pcDNA-TLR4 可改变这种抑制作用。此外，miR-17-5p 抑制剂改变了 Sch B 对 LPS 诱导的巨噬细胞中 TLR4 表达和 IL-1β 和 TNF-α 浓度的抑制作用。
Sch B 通过下调 TLR4 减轻 LPS 诱导的脓毒症中的炎症反应。
