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目的:探讨地黄饮子孵育骨髓间充质干细胞(BMSCs)移植对鼠缺血性脑损伤的脑组织Bcl-2(B淋巴细胞性白血病-2)及Bax(Bcl-2相关X蛋白)表达的影响作用。方法:选用健康SPF级Wistar大鼠随机分为假手术组、模型组、BMSCs组、维甲酸组和地黄饮子组。用线栓法制成大鼠大脑中动脉缺血(MCAO)模型,术后24h,假手术、模型组大鼠尾静脉注射生理盐水,其余各组大鼠经尾静脉输入等量相应药物诱导后的BMSCs。移植7d和14d后断头取脑,用免疫组化法染色,分别观察大脑皮质每高倍镜视野Bcl-2、Bax的阳性表达情况。结果:与假手术组比较,模型组缺血性脑损伤时大脑皮层均有Bcl-2和Bax的表达明显增加(P<0.05);地黄饮子组、维甲酸组、BMSCs组与假手术组、模型组比较,缺血性脑损伤时皮层Bcl-2的表达均显著增高(P<0.05),Bax的表达均明显降低(P<0.05)。结论:Bcl-2和Bax在缺血性脑损伤过程中发挥重要作用,地黄饮子对缺血性脑损伤具有保护作用,其保护作用机制可能与提高Bcl-2表达、抑制Bax表达而减少细胞凋亡有关。
OBJECTIVE: To investigate the effects of Rehmannia glutinosa submerged coculture of bone marrow mesenchymal stem cells (BMSCs) on the expression of Bcl-2 (B lymphocyte leukemia-2) and Bax (Bcl-2 related protein X) Impact. Methods: Healthy SPF Wistar rats were randomly divided into sham operation group, model group, BMSCs group, retinoic acid group and Rehmanniae Decoction group. The rat middle cerebral artery occlusion (MCAO) model was established by thread occlusion method. At 24 hours after operation, the rats in the model group were injected with saline through the caudal vein and the rats in the other groups were injected with the same amount of corresponding drugs through tail vein BMSCs. The brain was decapitated 7d and 14d after transplantation, and immunohistochemical staining was used to observe the positive expression of Bcl-2 and Bax in each high magnification field of cerebral cortex. Results: Compared with the sham operation group, the expressions of Bcl-2 and Bax in the cerebral cortex of the model group were significantly increased (P <0.05). Compared with the sham-operation group, Compared with the model group, the expression of Bcl-2 in the cerebral cortex was significantly increased (P <0.05) and the expression of Bax was significantly decreased in the model group (P <0.05). CONCLUSION: Bcl-2 and Bax play an important role in the process of ischemic brain injury. Rehmanniae Decoction has a protective effect on ischemic brain injury, and its protective mechanism may be related to increasing the expression of Bcl-2, inhibiting the expression of Bax and decreasing the number of cells Apoptosis related.