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目的观察Ⅱ组代谢型谷氨酸受体阻断剂对大鼠海马神经元凋亡的影响。方法 SD大鼠24只随机分为假手术组、痴呆组和阻断剂组,每组8只。大鼠脑室注射凝聚肽Aβ_(25-35)5建立痴呆大鼠模型,阻断剂组1周后行阻断剂脑室注射,另2组等量注射人工脑脊液4周行Morris水迷宫测试;测试1周后取材行病理观察,采用TUNEL法检测海马CA1区锥体细胞凋亡情况。结果与假手术组比较,痴呆组大鼠平均潜伏期明显延长,平台象限滞留时间明显缩短(P<0.05);与痴呆组比较,阻断剂组大鼠上述指标明显提高(P<0.05)。与假手术组比较,痴呆组大鼠海马CA1区可见大量的凋亡锥体细胞,阳性锥体细胞数、总面积、平均吸光度(A)值明显升高(P<0.05);与痴呆组比较,阻断剂组大鼠海马CA1区可见明显的阳性细胞和核固缩,但其阳性染色锥体细胞数、总面积、平均A值明显降低(P<0.05)。结论Ⅱ组代谢型谷氨酸受体阻断剂可明显抑制痴呆引起的海马CA1区锥体细胞的凋亡,提示其可能通过影响细胞凋亡,参与痴呆的发病过程。
Objective To investigate the effect of metabotropic glutamate receptor blocker Ⅱ on apoptosis of hippocampal neurons in rats. Methods Twenty-four SD rats were randomly divided into sham-operation group, dementia group and blocker group, with 8 rats in each group. The rats were injected intracerebroventricularly with the agglutinated peptide Aβ_ (25-35) 5 to establish a rat model of dementia. The rats in the blocker group were injected intraventricular blockade one week later and the other two groups were injected with artificial cerebrospinal fluid for 4 weeks for Morris water maze test. After the pathological observation, the apoptosis of hippocampal CA1 pyramidal cells was detected by TUNEL method. Results Compared with the sham operation group, the average latency of rats in dementia group was significantly prolonged, and the retention time in platform quadrant was significantly shorter (P <0.05). Compared with the dementia group, the above indexes in the blocking group were significantly increased (P <0.05). Compared with the sham operation group, a large number of apoptotic pyramidal cells were found in CA1 area of hippocampus in dementia group, and the number of pyramidal neurons, total area and mean absorbance (A) were significantly increased (P <0.05); compared with dementia group (P <0.05). The number of positive staining pyramidal cells, total area and average A value were significantly decreased (P <0.05). Conclusions Group Ⅱ metabotropic glutamate receptor blocker can obviously inhibit the apoptosis of pyramidal cells in hippocampal CA1 region induced by dementia, suggesting that it may participate in the pathogenesis of dementia by affecting apoptosis.