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目的观察麝香酮鼻腔给药对创伤性脑损伤模型大鼠脑保护作用影响。方法 SD大鼠按随机数字法分为假手术组、模型组和治疗组,每组各50只,通过控制性皮层撞击制备创伤性脑损伤模型,假手术组只进行手术及麻醉程序,无冲击损伤过程。治疗组采用大鼠在体鼻腔循环灌流法将麝香酮(1.8 mg/kg)从鼻腔给药,30 min/次,2次/日,共7日。检测各组动物干预前(T1)、干预第3日(T2)、干预第5日(T3)、干预后(T4)脑组织含水量,干预结束后采用免疫组织化学方法分析检测脑源性神经营养因子(brain derived neurotrophic factor,BDNF)和神经生长因子(nerve growth factor,NGF)表达。结果与假手术组比较,模型组T1-4脑含水量升高(P<0.05),NGF、BDNF表达降低(P<0.01)。与模型组比较,治疗组T1-3脑含水量降低(P<0.05),NGF、BDNF表达升高(P<0.01)。结论创伤性脑损伤后鼻腔给予麝香酮可降低脑含水量,减轻脑水肿,促进嗅鞘细胞分泌BDNF和NGF。
Objective To observe the effect of intranasal administration of musk ketone on the neuroprotective effect of traumatic brain injury model rats. Methods SD rats were randomly divided into sham operation group, model group and treatment group, 50 rats in each group. Traumatic brain injury model was established by controlled cortical injection. Sham operation group received only operation and anesthesia procedure without impact Damage process. In the treatment group, musk ketone (1.8 mg / kg) was administered intranasally by the nasal circulation perfusion method in rats for 30 min, twice daily for 7 days. The brain water content was measured before intervention (T1), on the 3rd day (T2), on the 5th day (T3) and after the intervention (T4). After the intervention, the immunohistochemistry was used to detect the brain-derived nerve Brain derived neurotrophic factor (BDNF) and nerve growth factor (nerve growth factor, NGF) expression. Results Compared with the sham operation group, the brain water content in T1-4 model group increased (P <0.05) and the expression of NGF and BDNF decreased (P <0.01). Compared with the model group, the brain water content in T1-3 group decreased (P <0.05) and the expression of NGF and BDNF increased (P <0.01). Conclusions Musk ketone can reduce brain water content, reduce brain edema and promote the secretion of BDNF and NGF in olfactory ensheathing cells after traumatic brain injury.