Effects of peroxisome proliferator-activated receptor gamma agonist pioglitazone on neurocyte apoptosis and expression of ICAM-1 after traumatic brain injury / 中华创伤杂志

ABSTRACT

Objective To investigate the effects of peroxisome proliferator-activated receptor gamma (PPARγ) agonist pioglitazone on delayed neuronal death,apoptosis of neurocytes,and expression of intercellular adhesion molecule-1 ( ICAM-1 ) following traumatic brain injury (TBI) in rats.MethodsThirty-six Sprague-Dawley rats were randomized into sham injury group,control group and pioglitazone treatment group,with 12 rats in each group.TBI model was established by modified Feeney method.Treatment grouP received intragastric administration of pioglitazone at a dosage of 10 mg/kg,and the sham injury group and the control group were lavaged with isometric 0.2％ dimethyl sulphoxide.Paraffin sections of brain tissues collected at 48 hours after TBI were employed to observe delayed neuronal death,apoptosis of neurocytes and expression of ICAM-1 by Nissl staining,TUNEL staining and immunochemistry respectively.Results( 1 ) Cell loss rate of Nissl body in the treatment group [ ( 38.59 ± 1.97 ) ％ ]was significantly lower than that of the control group [ (51.25 ± 4.01 ) ％ ] ( P ＜ 0.05 ),but was higher than that of the sham injury group [ (8.65 ± 1.23 ) ％ ] ( P ＜ 0.01 ).(2) The number of apoptotic neurocytes of the treatment group (31.67 ± 4.76) was significantly lower than that of the control group (45.33 ± 4.68 ) ( P ＜ 0.05),but was higher than that of the sham injury group ( 16.83 ± 2.04 ) ( P ＜ 0.01 ).(3) The mean optical degree of ICAM-1 positive expression of the treatment group (0.26 ± 0.04) was significantly lower than that of the control group (0.31 ± 0.04) ( P ＜ 0.05 ),but was higher than that of the sham injury group (0.10 ± 0.02 ) ( P ＜ 0.01 ).ConclusionsThe PPARγagonist pioglitazone can reduce the apoptosis of neurocytes and protect neurons after TBI.Meanwhile,its suppression of ICAM-1 expression is probably a mechanism of the suppression of inflammatory reaction and neural protection.