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目的:探讨地塞米松(DEX)对大鼠中央髓鞘溶解症(CPM)的预防作用及机理。方法:通过皮下注射长效尿崩停针和腹腔注射2.5%葡萄糖液诱导大鼠低钠血症3 d,第4天腹腔注射1 m o l/L氯化钠液(高渗盐水)快速补钠的方法诱导大鼠CPM模型。DEX早期治疗组大鼠在注射高渗盐水同时肌注5 m g/kg DEX;DEX延迟治疗组大鼠在注射高渗盐水后24 h肌注5 m g/kg DEX;生理盐水治疗组大鼠在注射高渗盐水同时肌注生理盐水;另设正常对照组。观察大鼠脑组织脱髓鞘病变发生情况;测定脑内伊文思兰(EB)的含量变化;W estern b lot印迹法测定脑内一氧化氮合酶(iN-OS)的表达变化。结果:通过诱导低钠血症、快速补钠的方法成功建立了大鼠CPM模型。DEX早期治疗组、DEX延迟治疗组、生理盐水治疗组3组大鼠在快速补钠后0 h时点,脑内EB含量与正常对照组无明显差异(P>0.05)。生理盐水治疗组大鼠在快速补钠后6 h,脑内EB含量比0 h时点明显增加(P<0.05),24 h达高峰,同时脑内iNOS在快速补钠后3 h开始表达增强,36 h仍呈较强表达,脱髓鞘发生率为66.7%。DEX早期治疗组大鼠快速补钠后脑内EB含量及iNOS表达,均较同时点生理盐水治疗组明显下降,未见明显脱髓鞘病变。DEX延迟治疗组脱髓鞘病变发生率为75%,与生理盐水治疗组无明显差异(P>0.05)。结论:早期应用DEX能够通过保护血脑屏障和抑制脑内iN-OS表达,起到预防CPM的作用。
Objective: To investigate the preventive effect and mechanism of dexamethasone (DEX) on central myelinolysis (CPM) in rats. Methods: Hyponatremia was induced by hypodermic injection of 2.5% dextrose and intraperitoneal injection of 3% dextrose for 3 d. The rats were infused with 1 mol / L sodium chloride solution (hypertonic saline) Methods Induction of rat CPM model. Rats in DEX treated group were injected intraperitoneally with 5 mg / kg DEX at the same time, while rats in DEX treated group were intramuscularly injected with 5 mg / kg DEX at 24 h after injection of hypertonic saline. Hypertonic saline at the same time intramuscular saline; another normal control group. The occurrence of demyelinating lesions in rat brain was observed. The content of Evans blue (EB) in brain was measured. The expression of iNOS in brain was measured by Western blot. Results: Rat model of CPM was successfully established by inducing hyponatremia and rapidly supplementing sodium. Compared with the normal control group, there was no significant difference in brain EB content between the DEX early treatment group, the DEX delayed treatment group and the saline treatment group at 0 h after rapid sodium supplementation (P> 0.05). The content of EB in brain of rats in NS group was significantly higher than that of 0 h group (P <0.05) at 6 h after sodium supplementation, and peaked at 24 h, while iNOS expression increased at 3 h , 36 h still showed strong expression of demyelination was 66.7%. The content of EB and the expression of iNOS in brain of rats in DEX treatment group were significantly lower than those in saline treatment group at the same time point, and no obvious demyelinating disease was found. DEX delayed treatment group, the incidence of demyelination was 75%, no significant difference with the saline treatment group (P> 0.05). Conclusion: Early application of DEX can prevent CPM by protecting the blood-brain barrier and inhibiting the expression of iN-OS in the brain.