Modulation Effects And Mechanisms Of Parecoxib On Inflammatory Reaction Of Acute Lung Injury

Objective: To explore the modulate effects possible mechanisms of parecoxib sodiumonacute lung injury induced by LPS.Methods:48male-SD rats were divided randomly into4groups,①The control group,②L PS group,③p arecoxib sodium group,④parecoxib sodium with LPS group.Parecoxibsodium was intraperitoneally injected2mg/kg twice a day for one week in parecoxibsodium group and parecoxib sodium with LPS group. LPS5mg/kg was injectediutrpvenously in the other two groups on the eight day.Rats were sacrificed after2h,4h,6h,and8h respectively. Pathology changes of lung tissue were observed. The levels of TNF-α,IL-1β,IL-10and neutrophils from bronchoalveolar lavage fluid were also detected byElisa.Western blot and RT-PCR was used to detect the expression of COX-2protein andiNOSmRNA respectively.Result: ALI was observed in LPS group and parecoxib sodium with LPS group comparedwith control group.The pathology changes of lung tissue showed: amount of exudate in thealveolar cavity, interstitial hyperemia, edema, amount of inflammatory cells, swelling andnecrosis of alveolar epithelial cells,PaO2obviously decline(P﹤0.05).TNF-α，IL-1β，IL-10and neutrophils were significantly increased in bronchoalveolar lavage fluid comparedwith those in parecoxib sodium with LPS group(P﹤0.05). iNOSmRNA in control groupwas significantly up-regulated than other groups(P﹤0.05). The protein of COX-2incontrol group was significantly reduced than those in LPS group and parecoxib sodiumwith LPS group(P﹤0.05). Conclusion:①T he protein of COX-2was increased in acute lung injury induced by LPSin rats.②T he degree of acute lung injury less severe due to the low levels of COX-2, thepossible mechanisms is that parecoxib sodium down-regulated the expression of COX-2inlung tissues, and further down-regulated the expression of iNOS.