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Antioxidation And Signal Mechanism Of Resveratrol In The Acrolein-stimulated Rats With Chronic Obstructive Pulmonary Disease

Posted on:2014-05-14Degree:MasterType:Thesis
Country:ChinaCandidate:S C LiuFull Text:PDF
GTID:2254330401963745Subject:Human Anatomy and Embryology
Abstract/Summary:PDF Full Text Request
Objective:Objective:The study was to investigate the antioxidation and signal mechanism of resveratrol in the acrolein-stimulated rats with chronic obstructive pulmonary disease (COPD)Methods:rats were cultured and treated differently in vivo. During the experiments, rats were randomly divided into four groups, including the blank control group, the acrolein-stimulated (6.87ug/L) group, resveratrol (5,15, and45mg/Kg.d) was added1h before acrolein treatment group. Pulmonary function indicators were determined involving in lung compliance (CL),0.3seconds forced expiratory volume (FEV0.3)/forced vital capacity(FVC), peak expiratory flow(PEF), maximal mid-expiratory flow (MMF). Prostaglandin E2(PGE2) were measured by Griess reagent and ELISA; The mRNA and protein levels of proinflammatory enzymes cyclooxygenase-2(COX-2), and Nuclear transcription factor-κB/p65(NF-κB/p65) were analysed by RT-PCR. Phosphorylation levels of p38,ERK,JNK MAPK were measured by western blotting.Results:Resveratrol significantly increased the lever of CL and ratio of FEV0.3/FVC compared with the model group. Resveratrol significantly attenuated the acrolein-induced expression of prostaglandin E2(PGE2), COX-2.. NF-κB/p65in a dose-dependent manner. Resveratrol attenuated p38, ERK,JNK MAPK phosphorylation in rats.Conclusions:This investigation demonstrates that the mechanism of intervention effect of resveratrol on rat COPD may be associated with reduced expression of NF-kappaB subunit RelA/P65play an anti-inflammatory effect and lowered p38, ERK and JNK MAPK phosphorylation level thereby inhibiting the release of inflammatory proteases.
Keywords/Search Tags:resveratrol, Sprague-Dawley rat, Chronic obstructive pulmonary disease, PGE2, COX-2, NF-κB, p38, ERK, JNK
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