过氧化物酶体增殖物激活受体γ激动剂吡格列酮对大鼠创伤性脑损伤的影响

Effect of pioglitazone on nerves of rats following traumatic brain injury

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 study the neural protective effect of pioglitazone, a peroxisome proliferatoractivated receptor gamma （PFARγ） agonist, on nerves of rats following traumatic brain injury （TBI）. Methods Seventy-two male Sprague-Dawley rats were randomly divided into pioglitazone treatment group, sham operation group, and control group （ n = 24 rats in each group）. Rats in pioglitazone treatment received pioglitazone gastric perfusion （10 mg/kg） while rats in sham operation group underwent normal saline gastric perfusion （10 mg/kg）. A rat model of brain injury was established with the Feeney＇ s free falling method. After neural function of rats was scored, water content in brain tissue was measured with the dry-wet weighing method. Injury of brain tissue, delayed death of neurons and apoptosis of nerve cells were observed with HE, TUNEL and Nissl＇ s staining, respectively. Results The neural function score was higher in pioglitazone treatment group than in control group in 48 h and 5 d after TBI （P 〈 0.05 ）. No significant difference was found in cantly lesser in pioglitazone treatment group than in control group in 48 h after TBI （P 〈 0.05 ）. Conclusion Pioglitazone can effectively inhibit the apoptosis of nerve cells, thus playing a role in protecting nerve cells of rats following TBI.