Dihydromyricetin alleviates endothelial inflammatory response through IRE1α/NF-κB signaling pathway in sepsis

Introduction The high mortality of sepsis is closely related to disorder coagulation induced by endothelial inflammatory response. Our aim investigate the protective effects Dihydromyricetin (DHM) on cells in and endoplasmic reticulum (ER) stress mechanism. Material methods In vivo, we conducted an animal study for which fifty male Wistar rats were randomly equally divided into five groups: sham group, cecal ligation puncture (CLP) group three CLP+ DHM (50, 100, 150 mg/kg) groups, was orally administered 2 h after CLP 3 days (once per day). vitro, human umbilical vein (HUVECs) treated with (50μmol) 24 stimulation lipopolysaccharide (LPS). inhibition reactive oxygen species (ROS) inhibitor N-acetylcysteine (NAC, mmol) (STF-083010, 10 μmol) incubated prior LPS. Results results indicated that (150 alleviated histopathological injury endothelium, decreased release cytokines adhesion molecules such as interleukin-1β (IL-1β), interleukin-6 (IL-6) , tumor necrosis factor alpha (TNF-α), vascular cell molecule 1 (VCAM-1) endothelin-1 (ET-1), inhibited production ROS production. addition, found ameliorated ER damage, significantly protein expressions IRE1α/NF-κB signaling pathway. Conclusions treatment response through pathway triggered oxidative stress. This provided experimental rationale therapy sepsis.