Zhang Jian-xin, Li Lan-fang, Zhang Hui-xin, Li Yong-hui
Department of Pharmacology, Hebei Academy of Medical Sciences, Shijiazhuang 050021, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2007 Nov;23(4):446-9.
To evaluate the effect of NG-nitro-L-arginine (L-NA) on inflammatory factor and neuronal apoptosis after focal cerebral ischemic injury in rats and the possible mechanism of protective effect of L-NA against cerebral ischemic injury.
Thirty male SD rats weighing 250-280 g were randomly divided into three groups (n=10): (1) Sham operated group (SH), (2) Ischemic group (IS), (3) L-NA group. In L-NA group L-NA 20 mg/kg was given intraperitoneally twice a day for 3 consecutive days. In IS group normal saline was given instead of L-NA. Focal cerebral ischemia was produced by middle cerebral artery occlusion (MCAO) for 12 h. A nylon thread with rounded tip which was inserted into left internal carotid artery cranially until resistance was felt. The distance from bifurcation of common carotid artery to the tip of the thread was about 18-19 mm. Focal cerebral ischemia was confirmed by left Horner's syndrome and right side hemiplegia. In SH group the carotid artery was exposed but no thread was inserted. The expression of TNF-alpha was determined by immunochemistry and the content of IL-1beta was measured by radio immunity. The Bcl-2 and Bax protein expression were detected by flow cytometry.
The expression of TNF-alpha and the content of IL-1 beta were markedly increased after MCAO. Significantly increased DNA fragmentation indication of apoptosis was detected after MCAO. The expression of TNF-alpha and the content of IL-1 beta was significantly lower in L-NA group than in IS group. The percentage of apoptosis cells and expression of Bax protein were markedly lower in L-NA group than in IS group but still significantly higher than in SH group. The expression of Bcl-2 protein was markedly higher in L-NA group than in IS group. There was no significant difference in the expression of Bcl-2 protein between IS and SH group.
L-NA could inhibit the increase in the expression of TNF-alpha and the content of IL-1beta, and protect neurons from apoptosis induced by focal cerebral ischemia through increasing the Bcl-2 protein expression and inhibiting the Bax protein expression.
评估NG-硝基-L-精氨酸（L-NA）对大鼠局灶性脑缺血损伤后炎症因子及神经元凋亡的影响，以及L-NA对脑缺血损伤保护作用的可能机制。
将30只体重250 - 280 g的雄性SD大鼠随机分为三组（n = 10）：（1）假手术组（SH），（2）缺血组（IS），（3）L-NA组。L-NA组腹腔注射L-NA 20 mg/kg，每天2次，连续3天。IS组给予生理盐水代替L-NA。采用大脑中动脉闭塞（MCAO）法制造局灶性脑缺血12小时。将尖端圆润的尼龙线经颅插入左颈内动脉直至感觉到阻力。从颈总动脉分叉处到线尖端的距离约为18 - 19 mm。通过左侧霍纳综合征和右侧偏瘫确认局灶性脑缺血。SH组暴露颈动脉但不插入线。采用免疫化学法测定肿瘤坏死因子-α（TNF-α）的表达，采用放射免疫法测定白细胞介素-1β（IL-1β）的含量。通过流式细胞术检测Bcl-2和Bax蛋白表达。
MCAO后TNF-α表达及IL-1β含量显著增加。MCAO后检测到明显增加的凋亡DNA片段化迹象。L-NA组TNF-α表达及IL-1β含量显著低于IS组。L-NA组凋亡细胞百分比及Bax蛋白表达显著低于IS组，但仍显著高于SH组。L-NA组Bcl-2蛋白表达显著高于IS组。IS组和SH组Bcl-2蛋白表达无显著差异。
L-NA可抑制TNF-α表达增加及IL-1β含量升高，并通过增加Bcl-2蛋白表达和抑制Bax蛋白表达保护神经元免受局灶性脑缺血诱导的凋亡。
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