Title: Effect of NADPH Oxidase Inhibitor Apocynin on the Expression of Hypoxia-induced Factor-1a and Endothelin-1 in Rat Carotid Body Exposed to Chronic Intermittent Hypoxia
Abstract: The effects of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor apocynin on the enhanced hypoxia induced factor-1α (HIF-1α) and endothelin-1 (ET-1) expression,elevated systolic blood pressure under chronic intermittent hypoxia (CIH) condition and its action mechanism were investigated.Thirty healthy 8-week old Sprague-Dawley (SD) male rats were randomly divided into three groups (n=10 each): sham group,CIH group,and apocynin-treated CIH group.Tail artery systolic blood pressure was measured by tail-cuff method.Real-time fluorescence quantitative polymerase chain reaction (PCR) was used to detect the mRNA expression of HIF-1α and ET-1 in the carotid body,and the HIF-1α protein expression was examined by using Western blotting.The levels of malondialdehyde (MDA) and superoxide dismutase (SOD) were determined by using colorimetric method.In addition,the plasma ET-1 and HIF-1α levels were measured by using enzyme-linked immunosorbent assay.It was found that CIH exposure was associated with increased MDA levels,and apocynin-treated CIH animals showed reduction in MDA levels.Apocynin treatment prevented CIH-induced hypertension as well as CIH-induced decrease in SOD.The increases of HIF-1α and ET-1 mRNA along with HIF-1α protein expression in the carotid body,and elevated circulating HIF-1α and ET-1 levels were observed in CIH-exposed animals.Treatment with apocynin significantly decreased the ET-1 mRNA,HIF-1α protein expression and circulating HIF-1α level in CIH-exposed animals,and there was no statistically significant difference in the HIF-1α mRNA expression between CIH group and apocynin-treated group.These results indicated that apocynin alleviated CIH-induced hypertension by inhibiting NADPH oxidase,further leading to the reduced vasoconstrictor ET-1 level and oxidative stress.HIF-1α/ET-1 system signal pathway may interact with CIH-induced NADPH oxidase-dependent oxidative stress.Inhibition of NADPH oxidase activity may hopefully serve as a useful strategy for prevention and trea
Publication Year: 2013
Publication Date: 2013-01-01
Language: en
Type: article
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