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目的研究姜黄素预处理对小鼠急性脊髓损伤后神经功能的保护作用及其可能机制。方法小鼠按体重随机分为假手术组、模型组、3个剂量(姜黄素,50,100,200 mg·kg~(-1))实验组,造模前30 min,分别腹腔注射生理盐水或相应药物,用改良的Allen’s法建立急性脊髓损伤模型后,作行为学评价,免疫印迹法测脊髓转化生长因子激酶1(TAK1)、p-TAK1、丝裂原蛋白激酶激酶6(MKK6)、p-MKK6、p38和p-p38蛋白表达。结果实验组,脊髓损伤48 h后旷场实验(BMS)评分由低到高依次为(0.80±0.79),(1.20±0.63),(1.60±0.52),较模型组的(0.70±0.48)均有不同程度改善;且实验组显著抑制了TAK1、MKK6和p-38的磷酸化,且呈现浓度依赖性。结论预防性应用姜黄素,可能通过抑制TAK1通路起到神经功能保护作用。
Objective To investigate the neuroprotective effect of curcumin pretreatment on acute spinal cord injury in mice and its possible mechanism. Methods The mice were randomly divided into sham-operation group, model group, three doses of curcumin (50, 100, 200 mg · kg -1) Acute spinal cord injury model was established by modified Allen’s method. Behavioral evaluation was made. Western blotting was used to detect the expression of transforming growth factor-kappa 1 (TAK1), p-TAK1, mitogen-activated protein kinase kinase 6 (MKK6) p38 and p-p38 protein expression. Results In the experimental group, the score of open field test (BMS) in experimental group was (0.80 ± 0.79), (1.20 ± 0.63) and (1.60 ± 0.52), respectively, compared with that of model group (0.70 ± 0.48) The experimental groups significantly inhibited the phosphorylation of TAK1, MKK6 and p-38 in a concentration-dependent manner. Conclusion The preventive application of curcumin may play a neuroprotective role through the inhibition of TAK1 pathway.