摘要
目的:考察NADPH氧化酶对门静脉海绵样变(cavernous transformation of portal vein,CTPV)大鼠体内氧化应激的影响.方法:将大鼠按随机抓取的方式分为假手术组、CTPV(门静脉海绵样变性)模型组.采用门脉部分结扎法复制CTPV大鼠动物模型;测定门静脉内血清超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活力及丙二醛(MDA)、门静脉组织一氧化氮(NO)、内皮型一氧化氮合酶(eNOS)的含量;采用实时荧光定量RT-PCR法测定门静脉组织NADPH氧化酶p22phox以及gp91phox亚基的mRNA表达.结果:与Sham组大鼠相比,CTPV组大鼠SOD、GSH-Px活性(酶活力单位)降低(93.79±8.87μU/L vs 103.05±8.07μU/L,157.44±26.46 vs 709.09+83.21,均P<0.05),而MDA含量增加(5.33±0.35μmol/L vs 3.59±0.44μmol/L,P<0.01);实时荧光定量RT-PCR显示门静脉NADPH氧化酶亚基gp91phox以及p22phox的mRNA表达增强(16.77±3.27 vs 1.31±0.95,11.64±7.34 vs 1.93±0.86,均P<0.01);门静脉组织NO含量及eNOS活性均降低(2.33±0.82μmol/L vs 85.00±3.16μmol/L,0.24±0.11U/mg prot vs 1.76±0.78U/mg prot,均P<0.01).结论:CTPV大鼠体内氧化应激状态与NADPH氧化酶亚基gp91phox以及p22phox mRNA过表达有关;NADPH氧化酶依赖的氧化应激可能与CTPV大鼠门静脉内皮功能障碍的发生发展密切相关.
AIM: To investigate the role of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in oxidative stress that is involved in cavernous transformation of the portal vein (CTPV) in rats. METHODS: CTPV was induced in rats by partial portal vein ligation. Antioxidant capacity was evaluated by assaying the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the portal vein blood. The content of malonaldehyde (MDA), a marker of lipid peroxidation, was assayed to assess oxidative stress level in the portal vein blood. The changes in endothelial function were evaluated by assaying nitric oxide (NO) and endothelial NO synthase in the portal vein. The mRNA expression of NADPH oxidase subunits gp91phox and p22phox was measured by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: Compared with sham-operated rats, the activities of SOD and GSH-Px significantly decreased (93.79 ± 8.87 μU/L vs 103.05 ± 8.07 μU/L and 157.44± 26.46 vs 709.09 ±83.21, respectively; both P 〈 0.05), the content of MDA increased (5.33± 0.35 μmol/L vs 3.59± 0.44 μmol/L, P 〈 0.01), the expression of NADPH oxidase subunits gp91phox and p22phox was significantly upregulated (16.77± 3.27 vs 1.31 ± 0.95 and 11.64 ±7.34 vs 1.93± 0.86, respectively; both P 〈 0.01), and the endothelial NO content and endothelial NO synthase activity in the portal vein were significantly reduced in CTPV rats (2.33 ± 0.82 μmol/L vs 85.00 ± 3.16μmol/L and 0.24 ± 0.11 U/mg prot vs 1.76 ±0.78 U/rag prot, respectively; both P 〈 0.01). CONCLUSION: The upregulation of NADPH oxidase subunits gp91phox and p22phox genes is correlated with the oxidative stress status in CTPV rats. NADPH oxidase-dependent oxidaive stress may contribute to endothelial dysfunction in CTPV rats.
出处
《世界华人消化杂志》
CAS
北大核心
2009年第35期3595-3600,共6页
World Chinese Journal of Digestology
基金
深圳市卫生局科技局基金资助项目
No.200650~~
关键词
NADPH氧化酶
门静脉海绵样变性
氧化应激
一氧化氮
Nicotinamide adenine dinucleotide phosphate oxidase
Cavernous transformation of the portal vein
Oxidative stress
Nitric oxide