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首页> 外文期刊>American Journal of Physiology >Role of AT1 receptors and NAD(P)H oxidase in diabetes-aggravated ischemic brain injury.
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Role of AT1 receptors and NAD(P)H oxidase in diabetes-aggravated ischemic brain injury.

机译：AT1受体和NAD（P）H氧化酶在糖尿病加重性缺血性脑损伤中的作用。

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The objective of the present study was to examine the role of the angiotensin II type 1 receptor (AT(1)-R) in the diabetes-aggravated oxidative stress and brain injury observed in a rat model of combined diabetes and focal cerebral ischemia. Diabetes was induced by an injection of streptozotoxin (STZ; 55 mg/kg iv) at 8 wk of age. Two weeks after the induction of diabetes, some animals received continuous subcutaneous infusion of the AT(1)-R antagonist candesartan (0.5 mg.kg(-1).day(-1)) for 14 days. Focal cerebral ischemia, induced by middle cerebral artery occlusion/reperfusion (MCAO), was conducted at 4 wk after STZ injection. Male Sprague-Dawley rats (n = 189) were divided into five groups: normal control, diabetes, MCAO, diabetes + MCAO, and diabetes + MCAO + candesartan. The major observations were that 1) MCAO produced typical cerebral infarction and neurological deficits at 24 h that were accompanied by elevation of NAD(P)H oxidase gp91(phox) and p22(phox) mRNAs, and lipid hydroperoxide production in the ipsilateral hemisphere; 2) diabetes enhanced NAD(P)H oxidase gp91(phox) and p22(phox) mRNA expression, potentiated lipid peroxidation, aggravated neurological deficits, and enlarged cerebral infarction; and 3) candesartan reduced the expression of gp91(phox) and p22(phox), decreased lipid peroxidation, lessened cerebral infarction, and improved the neurological outcome. We conclude that diabetes exaggerates the oxidative stress, NAD(P)H oxidase induction, and brain injury induced by focal cerebral ischemia. The diabetes-aggravated brain injury involves AT(1)-Rs. We have shown for the first time that candesartan reduces brain injury in a combined model of diabetes and cerebral ischemia.
机译：本研究的目的是检查在合并糖尿病和局灶性脑缺血的大鼠模型中观察到的糖尿病加重氧化应激和脑损伤中血管紧张素II 1型受体（AT（1）-R）的作用。在年龄8周龄时注射链脲佐菌素（STZ; 55 mg / kg iv）诱发糖尿病。诱发糖尿病后两周，一些动物接受了皮下输注AT（1）-R拮抗剂坎地沙坦（0.5 mg.kg（-1）.day（-1））的治疗，持续14天。注射STZ后第4周，由大脑中动脉闭塞/再灌注（MCAO）诱发局灶性脑缺血。将雄性Sprague-Dawley大鼠（n = 189）分为五组：正常对照组，糖尿病，MCAO，糖尿病+ MCAO和糖尿病+ MCAO +坎地沙坦。主要观察结果是：1）MCAO在24 h产生典型的脑梗塞和神经功能缺损，并伴有NAD（P）H氧化酶gp91（phox）和p22（phox）mRNA的升高，以及同侧半球脂质过氧化氢的产生; 2）糖尿病会增强NAD（P）H氧化酶gp91（phox）和p22（phox）mRNA的表达，增强脂质过氧化作用，加剧神经功能缺损，并扩大脑梗塞;和3）坎地沙坦可降低gp91（phox）和p22（phox）的表达，减少脂质过氧化，减轻脑梗塞，并改善神经功能。我们得出的结论是，糖尿病会夸大氧化应激，NAD（P）H氧化酶的诱导作用以及局灶性脑缺血所致的脑损伤。糖尿病加重的脑损伤涉及AT（1）-Rs。我们首次证明坎地沙坦在糖尿病和脑缺血的联合模型中可减轻脑损伤。

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