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目的探讨吡格列酮(PGZ)干预对大鼠颅脑损伤后脑组织中核转录因子NF-B、肿瘤坏死因子-(TNF-)和细胞凋亡的变化及其可能机制。方法 84只健康雄性SD大鼠随机分为PGZ组(=42)及对照组(=42),前者通过改良Feeney法建立颅脑损伤模型后立即予以腹腔注射PGZ10mg/kg,对照组则建立模型后予腹腔静脉注射0.9%氯化钠注射液2 ml/kg,以后各组分别每24小时腹腔注射一次等量PGZ或0.9%氯化钠注射液,直至动物被处死,根据伤后处死时间随机分为1h、3h、6h、12h、24h、3d和7d共7个亚组,每亚组各6只。取损伤灶周围组织采用免疫组织化学方法检测并比较挫伤灶周围脑组织中NF-B及TNF-蛋白表达情况,同时采用TUNEL法观察并比较脑挫伤灶周围细胞凋亡情况。结果 PGZ组NF-B及TNF-蛋白表达水平较对照组均明显下降(均<0.05)。以NF-B含量水平为自变量,TNF-含量水平为应变量,回归方程Y(PGZ组)=-0.432+0.271X,2=0.947(<0.01);Y(对照组)=-4.168+0.748X,2=0.961(<0.01)。结论颅脑损伤后PGZ可能通过降低NF-B活性,控制炎症反应,减少细胞凋亡,从而发挥对颅脑损伤后的神经细胞发挥保护作用。
Objective To investigate the effects of pioglitazone (PGZ) on nuclear factor-kappa B (NF-B), tumor necrosis factor- (TNF-) and apoptosis in brain tissue after traumatic brain injury in rats and its possible mechanism. Methods Eighty-four healthy male Sprague-Dawley rats were randomly divided into PGZ group (n = 42) and control group (n = 42). The former was given intraperitoneal injection of PGZ 10 mg / kg after the brain injury model was established by the modified Feeney method, while the control group 0.9% sodium chloride injection 2 ml / kg was given intraperitoneally into the abdominal cavity, and each group was given intraperitoneal injection of the same amount of PGZ or 0.9% sodium chloride injection every 24 hours until the animals were sacrificed. According to the time of injury, There were 7 subgroups at 1h, 3h, 6h, 12h, 24h, 3d and 7d, 6 subgroups each. The tissues around the lesion were detected by immunohistochemistry and the expression of NF-B and TNF-a in the brain tissue around contusive contusion were detected. TUNEL method was used to observe and compare the apoptosis of brain around contusion lesion. Results The levels of NF-B and TNF-α in PGZ group were significantly lower than those in control group (all <0.05). The regression equation Y (PGZ group) = - 0.432 + 0.271X, 2 = 0.947 (<0.01); Y (control group) = - 4.168 + 0.748 with the level of NF-B as the independent variable and the level of TNF- X, 2 = 0.961 (<0.01). Conclusion PGZ may play a protective role on nerve cells after traumatic brain injury by decreasing the activity of NF-B, controlling the inflammatory reaction and decreasing the apoptosis of the cells after craniocerebral injury.