The Protective Effect Of EOFAZ On Vascular Endothelial Cells’Inflammatory Injury Induced By LPS Relying On NF-κB And COX-2in Vivo

Objective To investigate the protective effects of essential oil fromFructus Alpinia zerumbet (EOFAZ) regulation on lipopolysaccharide (LPS)-inducedendothelial dysfunction of cultured human aortic endothelial cells (HAEC) and on theregulation of NF-κB and COX-2Signaling. Methods HAECs were obtained fromSciencell, which was cultured in accordance with the manufacturer’s instructions ofSciencell. The passage4or5cell was used in the present experiments. CulturedHAECs were treated with LPS alone (1g/mL) or in the presence of different dosagesof EOFAZ (50,100ng/mL), aspirin (Asp,2mM), atorvastatin (Atv,5M) for up to12h. Cell pathological morphology was observed by Giemsa/HE staining. MTT/LDHassays were assayed the cell viability/toxicity. Apoptosis was evaluated by Tunelassay.The reverse transcription PCR was used to determine the mRNA expression ofICAM-1and COX-2mRNA. The western blotting was assayed the protein expressionof Iκ Bα, NF-κB, ICAM-1and COX-2in HAECs injury induced by LPS. ResultsExposure HAECs to LPS(1g/mL)12h, the MTT volume decrease and LDHreleasing ratio increase that confirmed HAECs injury. Further research indicatedHAECs apoptosis increase, up-regulation the mRNA and protein expression ofICAM-1/COX-2after incubated with LPS. NF-κB p65phosphorylation was increasedand IκB α degradation was decreased in LPS-treated HAECs as well. Thepre-incubated with EOFAZ(50ng/mL,100ng/mL), Atv(5μM), and Asp(2mM)protected against the HAECs injury induced by LPS in some degree as following:①ameliorated the cell viability, and decreased the apoptosis;②inhibited the ICAM-1mRNA and protein expression,③decreased COX-2mRNA and protein expression pretreated with EOFAZ and Asp;④Inhibited the NF-κ B activation and stabilizedIκ B α. The present results indicated that there was positive relation dose with effectof EOFAZ. Conclusion The LPS-induced HAECs injury was involving in the NF-κBand COX-2; EOFAZ protected against the HAECs injury induced by LPS, themechanism may be stabilized the Iκ B α, inhibited NF-κ B p65phosphorylation andCOX-2expression.