Tang Ling-Ling, Zheng Jie-Sheng
First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Neurol Res. 2011 Dec;33(10):1064-7. doi: 10.1179/016164110X12700393823651. Epub 2010 May 19.
The present study investigated the effects of tetrahydrobiopterin (BH4) on cerebral infarction after transient focal ischemia in rats.
Focal ischemia (1·5 hours) was created in male Sprague-Dawley rats (250-280 g) by middle cerebral artery occlusion. Some rats were treated with 20 mg/kg tetrahydrobiopterin by intraperitoneal injection 30 minutes before reperfusion. At 2, 6, and 12 hours of reperfusion, the brains were harvested for the nitric oxide synthase (NOS) activity and nitric oxide (NO) level assays. At 12 hours of reperfusion, the brains were harvested for infarct size measurement.
NOS activity and NO level were all augmented after reperfusion. BH4 treatment significantly further increased NOS activity and NO level. Cerebral infarct size was significantly bigger in BH4 treatment group compared to that in no treatment group.
The data indicate that BH4 enhances cerebral infarction after transient focal ischemia in rats, through NOS and NO pathway.
本研究探讨四氢生物蝶呤（BH4）对大鼠短暂局灶性缺血后脑梗死的影响。
采用大脑中动脉闭塞法，在雄性Sprague-Dawley大鼠（250 - 280 g）中制造局灶性缺血（1.5小时）。部分大鼠在再灌注前30分钟腹腔注射20 mg/kg四氢生物蝶呤。在再灌注2、6和12小时时，取脑进行一氧化氮合酶（NOS）活性和一氧化氮（NO）水平检测。在再灌注12小时时，取脑测量梗死面积。
再灌注后NOS活性和NO水平均升高。BH4治疗显著进一步提高了NOS活性和NO水平。与未治疗组相比，BH4治疗组的脑梗死面积明显更大。
数据表明，BH4通过NOS和NO途径加重大鼠短暂局灶性缺血后的脑梗死。
