DETA-NONOate对卒中后大鼠NADPH氧化酶介导的氧化应激的影响
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摘要
目的：通过检测NO供体DETA-NONOate对大脑中动脉闭塞/再灌注(MCAO/再灌注)大鼠脑组织NADPH氧化酶活性的影响,探讨DETA-NONOate对缺血性脑卒中的治疗保护作用及其机制。方法：SD大鼠随机分为假手术组、MCAO/再灌注组和MCAO/再灌注+DETA-NONOate干预组。线栓法建立大鼠MCAO/再灌注模型,缺血1h后拔出线栓,进入再灌注期。干预组大鼠在再灌注后10-15min内尾静脉注射DETA-NONOate (0.4mg/kg)。部分MCAO大鼠在再灌注期进行神经功能缺损评分,24小时后断颈法牺牲大鼠,TTC染色评价大鼠脑梗死体积。其余大鼠在再灌注4小时后提取脑组织标本,测定脑组织脂质过氧化产物MDA含量,脑组织NO水平,以及NADPH氧化酶活性,Western blot测定NADPH氧化酶各亚基(p22phox,p47phox, Nox2/gp91phox, Nox和Rac-1)的表达。结果：1)DETA-NONOate可以降低1hMCAO/24h再灌注大鼠脑梗死的体积(P<0.01),改善卒中后大鼠12h、24h的神经功能缺损症状(P<0.05)；2)大鼠1hMCAO/4h再灌注后脑组织脂质过氧化产物MDA水平较假手术组升高(P<0.05),而经DETA-NONOate干预后脑组织MDA水平较对照组明显下降(P<0.05);3) 1hMCAO大鼠在再灌注初期静脉使用DETA-NONOate可以提高再灌注4h时脑组织NO水平(P<0.05)；4)DETA-NONOate降低1hMCAO/4h再灌注大鼠脑组织NADPH氧化酶活性(P<0.01)；5)DETA-NONOate使1hMCAO/4h再灌注大鼠脑组织NADPH氧化酶亚基p22phox, p47phox和Rac-1表达下降(P<0.05)。结论：NO供体DETA-NONOate可以改善缺血性卒中大鼠的神经功能缺损症状,抑制大鼠脑组织NADPH氧化酶活性及表达,对抗缺血性卒中的氧化应激效应,从而对脑组织缺血及继发的再灌注损伤发挥神经保护作用。
Objective:To determine the effect of NO donor DETA-NONOate on stroke rats after experimental MCAO and reperfusion injury, especially focus on the mechanisms concerning NADPH oxidase. Methods:A total of approximately 65 male Sprague-Dawley rats were used in this study. The animals were freely divided into three groups:(i) sham-operated group; (ii) control group:ischemia (60min) and reperfusion group (4h or 24h); (iii) ischemia (60min) and reperfusion (4h or 24h) with DETA-NONOate-treated group. Right MCA was occluded with a 4.0 monofilament nylon suture for an hour and then the nylon monofilament was withdrawn at the end of ischemic period for the beginning of reperfusion. DETA-NONOate-treated animals were treated with effective doses (0.4mg/kg) of NO donors DETA-NONOate in 250μl saline. The solution was slowly infused by tail vein at the time of reperfusion in 10-15 min. We evaluated the neuroprotective effect and antioxidant property of DETA-NONOate in rats after MCAO/reperfusion by ischemic infarct volume, neurological function score, MDA level, NO level, NADPH oxidase activities and the expressions of NADPH oxidase subunits (p22phox, p47phox, gp91phox, Nox4 and Rac-1). Results:1) DETA-NONOate improved neurological function by decreasing brain infarction volume and neurological function score in 60min MCAO/24h reperfusion rats compared to control group (P<0.05);2) The NO level of DETA-NONOate treated group was higher than control in 60min MCAO/4h reperfusion rats (P<0.05); 3) DETA-NONOate depressed MDA formation in brains of rats after 60min MACO and 4h reperfusion compared to control group (P <0.05); 4) NADPH oxidase activity and the expressions of NADPH oxidase subunit p22phox, p47phox, and Rac-1 in brains of 60min MCAO/4h reperfusion rats were significantly reduced by DETA-NONOate treatment compared to control (P<0.05). Conclusion:NO donor DETA-NONOate depressed the level of oxidative stress in the brains of MCAO/reperfusion rats by reducing the activity of NADPH oxidase, and thus played a protective role in ischemic stroke.
Objective:To determine the effect of NO donor DETA-NONOate on stroke rats after experimental MCAO and reperfusion injury, especially focus on the mechanisms concerning NADPH oxidase. Methods:A total of approximately 65 male Sprague-Dawley rats were used in this study. The animals were freely divided into three groups:(i) sham-operated group; (ii) control group:ischemia (60min) and reperfusion group (4h or 24h); (iii) ischemia (60min) and reperfusion (4h or 24h) with DETA-NONOate-treated group. Right MCA was occluded with a 4.0 monofilament nylon suture for an hour and then the nylon monofilament was withdrawn at the end of ischemic period for the beginning of reperfusion. DETA-NONOate-treated animals were treated with effective doses (0.4mg/kg) of NO donors DETA-NONOate in 250μl saline. The solution was slowly infused by tail vein at the time of reperfusion in 10-15 min. We evaluated the neuroprotective effect and antioxidant property of DETA-NONOate in rats after MCAO/reperfusion by ischemic infarct volume, neurological function score, MDA level, NO level, NADPH oxidase activities and the expressions of NADPH oxidase subunits (p22phox, p47phox, gp91phox, Nox4 and Rac-1). Results:1) DETA-NONOate improved neurological function by decreasing brain infarction volume and neurological function score in 60min MCAO/24h reperfusion rats compared to control group (P<0.05);2) The NO level of DETA-NONOate treated group was higher than control in 60min MCAO/4h reperfusion rats (P<0.05); 3) DETA-NONOate depressed MDA formation in brains of rats after 60min MACO and 4h reperfusion compared to control group (P <0.05); 4) NADPH oxidase activity and the expressions of NADPH oxidase subunit p22phox, p47phox, and Rac-1 in brains of 60min MCAO/4h reperfusion rats were significantly reduced by DETA-NONOate treatment compared to control (P<0.05). Conclusion:NO donor DETA-NONOate depressed the level of oxidative stress in the brains of MCAO/reperfusion rats by reducing the activity of NADPH oxidase, and thus played a protective role in ischemic stroke.
引文
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