The Investigation Of The Differential MRNA Expressions Of KLF2and ENOS In The Acute Hypoxia Exposed Atherosclerosis Rats

Objective: Atherosclerosis(AS）was one commonly occurred arterial sclerosis disease,the AS lesions mainly involved in the systemic circulation system of large andmedium-sized type muscle elastic artery, and it’s effecting lesions mainly initiatedfrom the vascular endometrium, and the pathophysiological process includinglipidosis, thrombosis, fibrous tissue hyperplasia and calcification etc. Throughartificial established the atherosclerosis rats models as well as exposed them in thehypobaric oxygen chamber to simulation the acute hypoxia environment, this studywe try to discuss the difference of KLF2and endothelial nitric oxide synthase (eNOS)genes mRNA levels various expressions and their influential effects during the acutehypoxic exposures.Method: Healthy male Wistar rats were divided into model group (n=24) and controlgroup (n=23). After the AS model was build，we recapitalized the head and take outthe aorta to collected samples into frozen. The total RNA extracted from the aortatissues, and the RT-PCR reaction preformed to detect the expression of KLF2,endothelial nitric oxide synthase (eNOS) and GAPDH also used as the internalreference. And the residual tissue was used to observe the tissue morphology underoptical microscope after H&E staining.Result:1. After acute hypoxia4and8hours of treatment, the expression of KLF2inmodel group were significantly higher than the same acute hypoxia time controlgroup（P<0.05）; After12hours with acute hypoxia, the expression of KLF2inmodel group was significantly lower than that of chronic hypoxia model group andacute hypoxia4hours model group（P<0.05）; The expression of KLF2in Chronichypoxia group was higher than the chronic hypoxic control group（P<0.05）; Acutehypoxia12hours model group had no difference compared with acute hypoxia12hours control group（P>0.05）;2. The expression of eNOS in Chronic hypoxia modelgroup was significantly higher than chronic hypoxia control group（P<0.05）;.Afteracute hypoxia4hours treatment, the expression of eNOS in model group were significantly higher than chronic hypoxia group and acute hypoxia4hours controlgroup（P<0.05）;3. The expression of KLF2in model group was negative correlationwith acute hypoxia time（P<0.05）. The expression of eNOS in model group wasnegative correlation with acute hypoxia time（P<0.05).Conclusion: Acute hypoxia condition can inhibit the expression of KLF2inatherosclerosis rats aorta tissue; Prolonged the time of exposing in acute hypoxia, theexpression of KLF2and eNOS in aorta tissue of atherosclerosis rats were graduallyreduced; Acute hypoxia conditions may increase the severity of the rat aorticatherosclerotic lesions.