甲基泼尼松龙冲击疗法对大鼠脊髓损伤后细胞凋亡的影响

Effect of methylprednisolone on apoptosis following acute spinal cord injury in rats

目的观察甲基泼尼松龙（MP）对脊髓损伤大鼠脊髓胶质细胞、神经元凋亡的影响。方法将72只健康成年大鼠随机分为单纯损伤组及MP组各36只，制成脊髓损伤动物模型。MP组经大鼠尾静脉给予MP冲击治疗，单纯损伤组经大鼠尾静脉每日注射生理盐水0．2mL。2组大鼠分批于1，3，5，8，14，21d各处死6只，常规制成脊髓切片，行Bcl-2检测，TUNEL原位末端标记，检测大鼠脊髓损伤后细胞凋亡的情况。结果单纯损伤组Bcl-2高峰发生在损伤后3d，而MP组于伤后1d达到高峰。此时Bcl-2蛋白在神经细胞中表达，在胶质细胞中大量表达，且一直维持到伤后14d才开始下降，伤后21d仅少量表达（P〈0．05）。TUNEL原位标记检测单纯损伤组24h已出现不少阳性细胞，以胶质细胞为主，3～8d达到高峰，此后逐渐回落，但21d时仍有阳性细胞；MP组凋亡细胞明显减少（P〈0．05）。结论MP在脊髓损伤中通过改善微循环，促进Bcl-2蛋白表达，清除氧自由基，抑制脊髓损伤早期神经细胞和胶质细胞的凋亡，从而减轻脊髓继发性损伤，促进脊髓神经功能的恢复。

Objective It is to observe the influence of methylprednisolone （MP） in rats with apoptosis following spinal cord injury in different time. Methods 72 healthy rats were divided into control group and MP group with 36 cases each other, and the rat spinal cord injury models were established. MP was injected in MP group through rat vena caudalis; and physiological saline was injected in every day in control group. After spinal cord injury 1 d, 3 d, 5 d, 8 d, 14d, 21d, 6 rats were sacrificed respectively each group in batch, and the spinal cord slices＇ were prepared. The apoptosis following spinal cord injury was detected by bcl - 2 detection and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling （TUNEL）. Results The expression of bcl - 2 protein in the spinal cord tissue was reached the peak on the third day after spinal cord injury in control group and on the first day in MP group. Bcl - 2 protein was more in glial cells than those in nerve cells, and began to decrease after the fourteenth day of spinal cord injury （P〈 0.05）. There were many positive cells after 24 hours in control group, most of them are glial cells, it reached the peak after 3 - 8 day, and then, they were decreased gradually. The positive cells were obviously less than those of control group in MP group （ P 〈 0.05 ） . Conclusion MP can improve the microcirculation, promote protein expression, get rid of oxygen free radical, restrain the apoptosis of nerve cell and glial cell, so as to reduce secondary spinal cord injury, improve spinal nerve recovery.