Department of Neurology, The First Affiliated Hospital, Chongqing Medical University, Chongqing 400016, China.
Brain Res. 2012 Aug 27;1470:111-8. doi: 10.1016/j.brainres.2012.06.026. Epub 2012 Jul 11.
The pathophysiological mechanism of global ischemia damage is complex. Recent studies indicate that the excessive inflammatory response induced by cerebral ischemia/reperfusion plays an important role in ischemic damage. Baicalin (5,6-dihydroxy-7-O-glucuronide flavonoid glycosides) is extracted from the dry dicotyledonous skullcap root, and belongs to one of the flavonoid compounds. Baicalin has a neuroprotective effect in a variety of brain injury animal models, although the mechanism remains unclear. We suggest that baicalin prevents deterioration in rats' spatial learning abilities associated with acute global cerebral ischemia by inhibiting the inflammatory reaction and reducing apoptosis.
Forty-two Sprague Dawley rats were divided into three groups: 14 rats in a sham (S) group; 14 in a global cerebral ischemia/reperfusion (I/R) group; and 14 in a global cerebral ischemia/reperfusion+baicalin treatment (I/RB) group. A Morris water maze test was used to assess learning and memory, HE staining was conducted for pathomorphology, a terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay was used to determine neuronal apoptosis, and Western blot for cyclooxygenase-2 (COX-2) expression in the hippocampus CA1 region.
Compared to the I/R group, Baicalin improved the learning and memory of I/RB rats. There was decreased hippocampal apoptosis and a reduction in the level of COX-2 expression in the I/RB group. In addition, the pathomorphological changes were worse in the I/R than in the I/RB group.
Baicalin improved the detrimental effects on spatial memory associated with global cerebral ischemia by reducing hippocampal apoptosis via the inhibition of COX-2 expression.
全脑缺血损伤的病理生理机制较为复杂。最近的研究表明，脑缺血/再灌注引起的过度炎症反应在缺血性损伤中起重要作用。黄芩苷（5,6-二羟基-7-O-葡萄糖醛酸黄酮苷）是从干燥的双子叶黄芩根中提取的，属于黄酮类化合物之一。黄芩苷在多种脑损伤动物模型中具有神经保护作用，但其机制尚不清楚。我们推测，黄芩苷通过抑制炎症反应和减少细胞凋亡，防止急性全脑缺血大鼠空间学习能力的恶化。
42 只 Sprague Dawley 大鼠分为三组：假手术（S）组 14 只，全脑缺血/再灌注（I/R）组 14 只，全脑缺血/再灌注+黄芩苷治疗（I/RB）组 14 只。采用 Morris 水迷宫试验评估学习记忆能力，HE 染色进行病理形态学观察，末端脱氧核苷酸转移酶 dUTP 缺口末端标记（TUNEL）法检测神经元凋亡，Western blot 检测海马 CA1 区环氧化酶-2（COX-2）表达。
与 I/R 组相比，黄芩苷改善了 I/RB 大鼠的学习记忆能力。I/RB 组海马凋亡减少，COX-2 表达水平降低。此外，I/R 组的病理形态学变化比 I/RB 组更严重。
黄芩苷通过抑制 COX-2 表达，减少海马凋亡，改善全脑缺血所致空间记忆损伤。
