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Protective effects of prostaglandin E1 on human umbilical vein endothelial cell injury induced by hydrogen peroxide.

ABSTRACT: AIM: To investigate the protective effects of prostaglandin E(1) (PGE(1)) against H(2)O(2)-induced oxidative damage on human umbilical vein endothelial cells (HUVECs). METHODS: HUVECs were pretreated with PGE(1) (0.25, 0.50, and 1.00 micromol/L) for 24 h and exposed to H(2)O(2) (200 micromol/L) for 12 h, and cell viability was measured by the MTT assay. LDH, NO, SOD, GSH-Px, MDA, ROS, and apoptotic percentage were determined. eNOS expression was measured by Western blotting and real-time PCR. RESULTS: PGE(1) (0.25-1.00 micromol/L) was able to markedly restore the viability of HUVECs under oxidative stress, and scavenged intracellular reactive oxygen species induced by H(2)O(2). PGE(1) also suppressed the production of lipid peroxides, such as MDA, restored the activities of endogenous antioxidants including SOD and GSH-Px, and inhibited cell apoptosis. In addition, PGE(1) significantly increased NO content, eNOS protein, and mRNA expression. CONCLUSION: PGE(1) effectively protected endothelial cells against oxidative stress induced by H(2)O(2), an activity that might depend on the up-regulation of NO expression.

SUBMITTER: Fang WT

PROVIDER: S-EPMC4007667 | biostudies-other | 2010 Apr

REPOSITORIES: biostudies-other

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Pyomelanin produced by Streptomyces sp. ZL-24 and its protective effects against SH-SY5Y cells injury induced by hydrogen peroxide.

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Project description:Inflammation, which causes injury to vascular endothelial cells, is one of the major factors associated with atherosclerosis (AS); therefore, inhibition of endothelial inflammation is a key step toward preventing AS. The present study aimed to investigate the effects of bakkenolide‑IIIa (Bak‑IIIa), an important active component of bakkenolides, on endothelial inflammation, as well as the mechanisms underlying such effects. Lipopolysaccharide (LPS)‑damaged human umbilical vein endothelial cells (HUVECs) were treated with Bak‑IIIa. The results of the MTT assay and enzyme‑linked immunosorbent assay indicated that Bak‑IIIa significantly alleviated survival inhibition, and decreased the levels of LPS‑induced TNF‑α, interleukin (IL)‑1β, IL‑8, and IL‑6. Furthermore, long noncoding RNA (lncRNA) microarray analyses revealed 70 differentially expressed lncRNAs (DELs) in LPS‑damaged HUVECs treated with Bak‑IIIa. lncRNA target prediction results revealed that 44 DELs had 52 cis‑targets, whereas 12 DELs covered 386 trans‑targets. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes analyses of the trans‑targets indicated that three GO terms were associated with inflammation. Therefore, 17 targets involved in these GO terms and six relevant DELs were screened out. Validation via reverse transcription‑quantitative PCR indicated that the fold change of NR_015451 (LINC00294) was the highest among the six candidates and that overexpression of LINC00294 significantly alleviated LPS‑induced survival inhibition and inflammatory damage in HUVECs. In conclusion, Bak‑IIIa ameliorated LPS‑induced inflammatory damage in HUVECs by upregulating LINC00294. Thus, Bak‑IIIa exhibited potential for preventing vascular inflammation.

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The protective effect of thymoquinone on <i>tert</i>-butylhydroquinone induced cytotoxicity in human umbilical vein endothelial cells.

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