The Effect Of Atorvastatin Calcium On Rats With Acute Lung Injury Induced By Lipopolysaccharides

Objective:To observe the effect of Atorvastatin Calcium on theexpression of the VEGF and Thromboxane B2(TXB2),andbronchoalveolar lavage fluid (BALF) protein content as well as theproportion of neutrophils (PMN) by lipopolysaccharide (LPS)-inducedacute lung injury (ALI) in lung tissue of rats. Explore the role ofatorvastatin calcium in rats with acute lung injury induced by LPS.Methods: healthy male SD rats90were randomly divided into normalsaline (NS) group, LPS group, the atorvastatin calcium small doses of (S)group, atorvastatin calcium in the middle dose (M) group, atorvastatincalcium high-dose (L) group, rats in each group18.NS group LPSgroup be NS gavage, the S group, M group and L group were to be theatorvastatin calcium5mg/Kg/d,10mg/Kg/d,20mg/Kg/d orally, in eachgroup are consecutive to drug for14days,15days after the four-grouptail vein injection of LPS (6mg/Kg) was diluted to1ml preparation ALIrat model, the NS group tail vein injection of1ml of NS. Were in the tailvein injection after2h,4h,8h rats were sacrificed6. Comparison of lunghistopathological changes and lung injury score; each group weredetected in rat lung wet/dry weight ratio (W/D); Coomassie brilliantblue method for the determination of protein content in BALF at thesame time monitoring in BALF PMN ratio. FQ RT-PCR,detection of lung tissue VEGF and TXB2mRNA expression; immunohistochemical methodfor the determination of lung tissue expression of VEGF and TXB2.Results:â‘ pathological changes: the NS group at each time point clearstructure of mouse lung tissue, alveolar wall integrity not found in theinfiltration of inflammatory cells and alveolar septa edema. LPS group atall time points alveolar wall rupture, alveolar collapse consolidation,alveolar septa and alveolar spaces bleeding, pulmonary interstitial edema,alveolar and interstitial large number of neutral inflammatory cellinfiltration. Pathological changes of the S group, M group, L groupranged between NS group and LPS group, the lightest injury in L group,M group followed by S group heavier. Each group4h heaviest damage,8hfollowed,2h lightest.â‘¡lung W/D, lung injury score: rats in eachgroup2h,4h,8h compared with NS group increased (P<0.05), S group,M group and L group at the same time point lower than the LPS group(P<0.05), M group at the same time point compared with S groupdecreased (P<0.05), L group reduced at the same time point comparedwith group M (P<0.05).â‘¢rats in each group2h,4h,8hBALF proteincontent and PMN proportion compared with the NS group increased(P<0.05), S group, M group and L group at the same time point lowerthan the LPS group (P<0.05), M group at the same time point comparedwith S group decreased (P<0.05), L group at the same time point than theM group lower (P<0.05).â‘£rats in each group2h,4h,8h lung of VEGF,TXB2mRNA expression compared with NS group increased (P<0.05), Sgroup, M group and L group at the same time point lower than the LPSgroup (P<0.05), the same point in time, M group compared with S groupdecreased (P<0.05), L group lower than the M group (P<0.05).Conclusions: atorvastatin calcium intragastric can reduce LPS-inducedALI in BALF protein content and the proportion of PMN, its mechanismmay be related to lung of VEGF and TXB2mRNA expression reducemicrovascular permeability to lower them, so as to achieve the protectionof lung injury.