Jiang Zhu-chang, Bi Gui-nan, Shi Sheng-liang
Department of Neurology, The Third Affiliated Hospital, Guangxi Traditional Chinese Medical University, Liuzhou 545001, Guangxi, China.
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2005 May;17(5):289-92.
To observe the effect and mechanism of clausenamide on the expression of Bcl-2 and apoptosis after focal cerebral ischemia/reperfusion in renovascular hypertensive rats.
Seventy-five renovascular hypertensive rats were randomly divided into three groups (25 in each group): clausenamide intervention group, single ischemia/reperfusion model group and sham-operated group. Focal cerebral ischemia was reproduced by ligature for 2 hours and loosening of the ligature in the rats. No arterial ligature was applied in sham-operated group. Computerized pathological image analyzer was used to determine the number of cells positive for Bcl-2 by immunohistochemical staining, and also the counts of apoptotic cells after TdT-mediated dUTP nick end labeling (TUNEL) staining respectively in coronal sections of brain after reperfusion (6, 12, 24, 48 and 72 hours).
(1) The expression of Bcl-2 protein was detected 6 hours after reperfusion, peaking at 24 hours, then declined gradually. The Bcl-2 protein positive cell counts at every time point in clausenamide intervention group were significantly higher than simple ischemia/reperfusion model group (all P<0.01). (2) The number of apoptotic cells was increased with reperfusion, reaching its peak at 72 hours. The apoptosis counts in clausenamide intervention group were significantly lower than single ischemia/reperfusion model group (all P<0.01). At all time points, except at 48 hours after reperfusion, as there was no significant difference (all P>0.05). No Bcl-2 positive cells and only 0-2 apoptotic cells could be discernible in brain sections from sham-operated animals or in the contralateral side of ischemia in animals of the other groups.
Expression of Bcl-2 protein is enhanced and apoptosis appears after focal cerebral ischemia/reperfusion in rat brain. Clausenamide can enhance the expression of Bcl-2 protein and inhibit apoptosis remarkably. Clausenamide may coordinate with Bcl-2 in inhibiting apoptosis. This may be the mechanism of protection of brain cells from ischemic damage of clausenamide treatment.
观察黄皮酰胺对肾血管性高血压大鼠局灶性脑缺血/再灌注后Bcl-2表达及细胞凋亡的影响及其机制。
将75只肾血管性高血压大鼠随机分为三组（每组25只）：黄皮酰胺干预组、单纯缺血/再灌注模型组和假手术组。采用结扎大鼠动脉2小时并松开结扎线的方法复制局灶性脑缺血模型。假手术组不进行动脉结扎。再灌注后（6、12、24、48和72小时），分别用计算机病理图像分析仪通过免疫组化染色检测Bcl-2阳性细胞数，并用TdT介导的dUTP缺口末端标记（TUNEL）染色检测脑冠状切片中的凋亡细胞数。
（1）再灌注6小时后检测到Bcl-2蛋白表达，24小时达到峰值，随后逐渐下降。黄皮酰胺干预组各时间点Bcl-2蛋白阳性细胞数均显著高于单纯缺血/再灌注模型组（均P<0.01）。（2）凋亡细胞数随再灌注时间增加，72小时达到峰值。黄皮酰胺干预组凋亡细胞数显著低于单纯缺血/再灌注模型组（均P<0.01）。在所有时间点，除再灌注48小时外，差异均无统计学意义（均P>0.05）。假手术组动物脑切片或其他组动物缺血对侧脑切片中未见Bcl-2阳性细胞，仅见0~2个凋亡细胞。
大鼠脑局灶性脑缺血/再灌注后Bcl-2蛋白表达增强，出现细胞凋亡。黄皮酰胺可显著增强Bcl-2蛋白表达并抑制细胞凋亡。黄皮酰胺可能与Bcl-2协同抑制细胞凋亡。这可能是黄皮酰胺治疗保护脑细胞免受缺血损伤的机制。
