ABSTRACT
Objective To investigate the effects of Lipo-PGE1 on the expression of T-bet and Gata-3,and its potential mechanisms causing the shift of T cells from Th1 to Th2 on Acute lung injury(ALI)induced by Lipopolysaccharide(LPS)in mice.Methods Sixty male BALB-C mice were randomly divided into three groups(n =20 in each group):(1)control group,mice were treated with intravenous injection of NS in dose of 10 ml/kg,(2)LPS group,mice were exposed to LPS with dosage of 5 mg/kg(0.5 g/ml diluted in saline),and(3)LPS + PGE1 group,mice were treated with Lipo-PGE1 in dose of 15μg/kg.Sixhours after injection,the lungs were removed for observing the histopathological changes and determination of wet/dry lung weight(W/D)ratio.The levels of Th1 and Th2 were determined by flow cytometry,and the expressions of T-bet and Gata-3 mRNA were detected by using RT-PCR.One-way ANOVA was used for comparing differences between groups,and all data were presented in((x)± s).Results The histological changes of lung injury were lessened by PGEC ompared with the W/D ratio(5.74 ± 0.31)in LPS group,the one(4.92 ±0.27)in LPS +PGE1 group was lower significantly(P ＜0.01).The levels of Th1 and Th2 and their ratio Were higher in LPS +PGE1 group[(20.31 ±2.20)％,(10.50±0.80)％,(1.93±0.05)]than in LPS group[(16.65 ±1.70)％,(9.40 ±1.25)％,(1.73 ±0.03)](P＜0.01).Compared with control group,the expressions ofT-bet mRNA(1.183 ±0.495),and Gata-3 mRNA(0.693±0.285),and their ratio(1.713 ± 0.131)were lower(P ＜0.01); compared with LPS group,PGE1 significantly increased the expressions of T-bet mRNA(1.827 ± 0.705)and the ratio of T-bet/Gata-3 (2.502 ±0.352)(P ＜0.01),while didn(t)increased the expressions of Gata-3 mRNA(0.7191 ±0.186)significantly(P ＞ 0.05).Conclusions Lipo-PGE1 may up-regulate transcription factor T-bet which participates in the Th1 differentiation ratio,and then improve the inflammatorv svmntom.
ABSTRACT
Intravenous injection of SPD 10 mg/kg could increase the tolerant dose of ouabain, and prevent the arrhythmias induced by acute myo-cardial ischemia in rats and that elicited by adrenaline-chloroform model in rabbits. SPD 60 mg/kg intraperitoneally could abolish the ventricular fibrillation produced by chloroform inhalation in mice. It inhibited the contractility, prolonged the functional refractory period and decreased the automaticity significantly of the isolated guinea pig papillary muscles, but no significant effect on excitability.