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目的观察PPARγ激动剂吡格列酮对大鼠创伤性脑损伤的神经保护作用。方法将72只SD大鼠按随机数字表法分为假致伤组、对照组、吡格列酮治疗组,每组24只。采用改良的Feeney法制作脑创伤模型,治疗组采用吡格列酮(10 mg/kg)灌胃,假致伤组和对照组用等量生理盐水灌胃。致伤后在相应时相点行大鼠神经功能评分后,用干湿质量法进行脑组织含水量测定,进行HE、Nissl及TUNEL染色观察脑组织损伤、迟发性神经元死亡及神经细胞凋亡程度。结果①在伤后48 h、5 d,治疗组的神经功能评分[分别为(2.12±0.58)、(1.67±0.78)]好于对照组[(2.67±0.65)、(2.25±0.62),P<0.05];②伤后24 h治疗组与对照组脑组织含水量差异无统计学意义[分别为(78.84±1.92)%、(79.21±2.20)%,P>0.05];③伤后48 h,治疗组迟发性神经元死亡(38.59±1.97)%和神经细胞凋亡数(31.67±4.76)明显低于对照组[分别为(51.25±4.01)%、(45.33±4.68),P<0.05]。结论 PPARγ激动剂吡格列酮能抑制创伤性脑损伤后的神经细胞凋亡,保护神经元,从而发挥神经保护作用。
Objective To observe the neuroprotective effect of PPARγ agonist pioglitazone on traumatic brain injury in rats. Methods Seventy-two SD rats were randomly divided into sham injury group, control group and pioglitazone treatment group, 24 rats in each group. The model of traumatic brain injury was made by the modified Feeney method. The treatment group was given pioglitazone (10 mg / kg) orally, while the sham injury group and the control group were given orally by normal saline. After injury, the rats were sacrificed at the corresponding time point to evaluate the neurological function. The water content of brain tissue was determined by the wet and dry method. The damage of brain tissue, the death of delayed neurons and the neuronal apoptosis were observed by HE, Nissl and TUNEL staining Death degree. Results ① At 48 h and 5 d after injury, the scores of neurological function in the treatment group [(2.12 ± 0.58), (1.67 ± 0.78)] were significantly better than those in the control group [(2.67 ± 0.65), (2.25 ± 0.62), P <0.05]. ② There was no significant difference in brain water content between the treatment group and the control group 24 h after injury (78.84 ± 1.92%, (79.21 ± 2.20)%, P> 0.05] (38.59 ± 1.97%) and neuron apoptosis (31.67 ± 4.76) in the treatment group were significantly lower than those in the control group [(51.25 ± 4.01)%, (45.33 ± 4.68), P <0.05 ]. Conclusions Pioglitazone, a PPARγ agonist, can inhibit neuronal apoptosis after traumatic brain injury and protect neurons and thus play a neuroprotective role.