PMID- 31106593 OWN - NLM STAT- MEDLINE DCOM- 20191104 LR - 20191104 IS - 2169-141X (Electronic) IS - 2169-1401 (Linking) VI - 47 IP - 1 DP - 2019 Dec TI - Vascular protection of salicin on IL-1beta-induced endothelial inflammatory response and damages in retinal endothelial cells. PG - 1995-2002 LID - 10.1080/21691401.2019.1608220 [doi] AB - Retinal endothelial cells (RECs) are involved in many ocular diseases such as age-related macular degeneration (AMD) and diabetic retinopathy. Salicin is the major ingredient of willow bark extract, and it has been shown to be a potent anti-inflammatory agent. We aim to explore whether salicin has a vascular protective effect in RECs. Our data indicate that the presence of salicin in RECs culture media ameliorates interleukin-1beta (IL-1beta)-induced cellular reactive oxygen species (ROS) production and NADPH oxidase 4 (NOX-4) expression. At the cellular level, salicin attenuates IL-1beta-induced mitochondrial injury as revealed by its preservation on mitochondrial membrane potential (MMP). Furthermore, salicin inhibits IL-1beta-induced production of pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1), vascular adhesion molecules such as intercellular cell adhesion molecule-1 (iCAM-1) and vascular cell adhesion molecule 1 (VCAM-1), and high-mobility group protein 1 (HMGB-1). On the other hand, salicin recovers IL-1beta-induced reduction of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) release. The presence of salicin significantly reduces the IL-1beta-induced release of lactate dehydrogenase (LDH), indicating that it mitigates cytokine caused cytotoxicity. Mechanistically, we show that salicin suppresses IL-1beta-induced activation of the nuclear factor-kappa B (NF-kappaB) signaling as revealed by its suppression on nuclear p65 protein and transfected NF-kappaB promoter. Collectively, our study demonstrates by multiple facets of its mechanisms that salicin is a protective agent in retinal endothelial cells. These results imply its potential use in therapeutic usage of retinal disease. FAU - Song, Yu AU - Song Y AD - a Department of ophthalmology, Weihai Central hospital , Weihai , China. FAU - Tian, Xia AU - Tian X AD - a Department of ophthalmology, Weihai Central hospital , Weihai , China. FAU - Wang, Xuehong AU - Wang X AD - a Department of ophthalmology, Weihai Central hospital , Weihai , China. FAU - Feng, Hui AU - Feng H AD - a Department of ophthalmology, Weihai Central hospital , Weihai , China. LA - eng PT - Journal Article PL - England TA - Artif Cells Nanomed Biotechnol JT - Artificial cells, nanomedicine, and biotechnology JID - 101594777 RN - 0 (Benzyl Alcohols) RN - 0 (Glucosides) RN - 0 (HMGB1 Protein) RN - 0 (Interleukin-1beta) RN - 0 (NF-kappa B) RN - 0 (Reactive Oxygen Species) RN - 0 (Vascular Cell Adhesion Molecule-1) RN - 126547-89-5 (Intercellular Adhesion Molecule-1) RN - 31C4KY9ESH (Nitric Oxide) RN - 4649620TBZ (salicin) RN - EC 1.1.1.27 (L-Lactate Dehydrogenase) RN - EC 1.14.13.39 (Nitric Oxide Synthase Type III) SB - IM MH - Benzyl Alcohols/*pharmacology MH - Blood Vessels/cytology/*drug effects MH - Cell Line MH - Endothelial Cells/cytology/*drug effects/metabolism MH - Gene Expression Regulation/drug effects MH - Glucosides/*pharmacology MH - HMGB1 Protein/biosynthesis MH - Humans MH - Inflammation/chemically induced/pathology MH - Intercellular Adhesion Molecule-1/metabolism MH - Interleukin-1beta/*pharmacology MH - Intracellular Space/drug effects/metabolism MH - L-Lactate Dehydrogenase/metabolism MH - Mitochondria/drug effects/metabolism MH - NF-kappa B/metabolism MH - Nitric Oxide/metabolism MH - Nitric Oxide Synthase Type III/metabolism MH - Oxidative Stress/drug effects MH - Reactive Oxygen Species/metabolism MH - Retina/*cytology MH - Vascular Cell Adhesion Molecule-1/metabolism OTO - NOTNLM OT - IL-1beta OT - NF-kappaB OT - Retinal endothelial cell (RECs) OT - inflammation OT - reactive oxygen species (ROS) OT - salicin EDAT- 2019/05/21 06:00 MHDA- 2019/11/05 06:00 CRDT- 2019/05/21 06:00 PHST- 2019/05/21 06:00 [entrez] PHST- 2019/05/21 06:00 [pubmed] PHST- 2019/11/05 06:00 [medline] AID - 10.1080/21691401.2019.1608220 [doi] PST - ppublish SO - Artif Cells Nanomed Biotechnol. 2019 Dec;47(1):1995-2002. doi: 10.1080/21691401.2019.1608220.