In order to explore whether the member of Bcl-2 gene family, for example, Bcl-2 and Bax, are induced after cerebral ischemia, and whether expression of genes can be modulated by calcium-antagonist, the rat cerebral is...In order to explore whether the member of Bcl-2 gene family, for example, Bcl-2 and Bax, are induced after cerebral ischemia, and whether expression of genes can be modulated by calcium-antagonist, the rat cerebral ischemic models were made by occluding left middle cerebral artery. The expression of Bcl-2 and Bax mRNA was measured by RT-PCR method. After middle cerebral artery occlusion (MCAO), the expression of both Bcl-2 and Bax mRNA were induced. Level of Bcl-2 mRNA increased steadily and level of Bax mRNA increased gradually at first, reached a peak after 24 h, then decreased slowly. After administration of nimodipine, Bcl-2 mRNA was up-regulated in the hippocampus 6 and 24h after ischemia, while Bax mRNA was down-regulated 6 and 24 h after ischemia. Focal cerebral ischemia can induce proto-oncogenes to express, which was associated with apoptosis. Calcium-antagonist can up-regulate Bcl-2 mRNA and down-regulate Bax mRNA. The increased ratio of Bcl-2 and Bax mRNA may contribute to the anti-apoptic effect of nimodipine. The study indicates that pharmacological modulation of Bcl-2 family member expression could become a new strategy to manage neuronal damage.展开更多
目的通过研究溃疡性结肠炎(UC)模型大鼠结肠组织Bcl-2、Bax m RNA的变化,探讨香连丸对UC大鼠细胞凋亡的影响。方法将50只7周龄Wistar大鼠随机分为正常组、模型组(UC模型)、中药组(香连丸)、抑制剂组、中药+抑制剂组。采用经典三硝基苯...目的通过研究溃疡性结肠炎(UC)模型大鼠结肠组织Bcl-2、Bax m RNA的变化,探讨香连丸对UC大鼠细胞凋亡的影响。方法将50只7周龄Wistar大鼠随机分为正常组、模型组(UC模型)、中药组(香连丸)、抑制剂组、中药+抑制剂组。采用经典三硝基苯磺酸灌肠法复制UC模型大鼠;造模成功后光学显微镜下观察各组大鼠结肠黏膜组织损伤程度并评分,逆转录聚合酶链反应检测Bcl-2、Bax m RNA表达变化,原位末端凋亡法检测细胞凋亡情况。结果 UC模型大鼠肉眼及镜下可见结肠溃疡形成,可伴有炎症、充血、水肿等病理改变;与正常组相比,模型组Bcl-2 m RNA表达降低,Bax m RNA表达增高;香连丸干预后可改善结肠上皮细胞凋亡,降低Bax m RNA表达,Bcl-2 m RNA表达增加。结论 UC模型大鼠结肠黏膜损伤,与细胞凋亡因子Bcl-2、Bax的变化有关;香连丸可提高Bcl-2 m RNA、减少Bax m RNA的表达,改善结肠黏膜损伤,减少上皮细胞凋亡,改善细胞凋亡情况。展开更多
文摘In order to explore whether the member of Bcl-2 gene family, for example, Bcl-2 and Bax, are induced after cerebral ischemia, and whether expression of genes can be modulated by calcium-antagonist, the rat cerebral ischemic models were made by occluding left middle cerebral artery. The expression of Bcl-2 and Bax mRNA was measured by RT-PCR method. After middle cerebral artery occlusion (MCAO), the expression of both Bcl-2 and Bax mRNA were induced. Level of Bcl-2 mRNA increased steadily and level of Bax mRNA increased gradually at first, reached a peak after 24 h, then decreased slowly. After administration of nimodipine, Bcl-2 mRNA was up-regulated in the hippocampus 6 and 24h after ischemia, while Bax mRNA was down-regulated 6 and 24 h after ischemia. Focal cerebral ischemia can induce proto-oncogenes to express, which was associated with apoptosis. Calcium-antagonist can up-regulate Bcl-2 mRNA and down-regulate Bax mRNA. The increased ratio of Bcl-2 and Bax mRNA may contribute to the anti-apoptic effect of nimodipine. The study indicates that pharmacological modulation of Bcl-2 family member expression could become a new strategy to manage neuronal damage.
文摘目的通过研究溃疡性结肠炎(UC)模型大鼠结肠组织Bcl-2、Bax m RNA的变化,探讨香连丸对UC大鼠细胞凋亡的影响。方法将50只7周龄Wistar大鼠随机分为正常组、模型组(UC模型)、中药组(香连丸)、抑制剂组、中药+抑制剂组。采用经典三硝基苯磺酸灌肠法复制UC模型大鼠;造模成功后光学显微镜下观察各组大鼠结肠黏膜组织损伤程度并评分,逆转录聚合酶链反应检测Bcl-2、Bax m RNA表达变化,原位末端凋亡法检测细胞凋亡情况。结果 UC模型大鼠肉眼及镜下可见结肠溃疡形成,可伴有炎症、充血、水肿等病理改变;与正常组相比,模型组Bcl-2 m RNA表达降低,Bax m RNA表达增高;香连丸干预后可改善结肠上皮细胞凋亡,降低Bax m RNA表达,Bcl-2 m RNA表达增加。结论 UC模型大鼠结肠黏膜损伤,与细胞凋亡因子Bcl-2、Bax的变化有关;香连丸可提高Bcl-2 m RNA、减少Bax m RNA的表达,改善结肠黏膜损伤,减少上皮细胞凋亡,改善细胞凋亡情况。
