中华创伤杂志
中華創傷雜誌
중화창상잡지
Chinese Journal of Traumatology
2012年
10期
941-945
,共5页
邓永兵%刘科%唐文渊%蒋雪
鄧永兵%劉科%唐文淵%蔣雪
산영병%류과%당문연%장설
过氧化物酶体增殖物激活受体%脑损伤%细胞凋亡%细胞黏附分子
過氧化物酶體增殖物激活受體%腦損傷%細胞凋亡%細胞黏附分子
과양화물매체증식물격활수체%뇌손상%세포조망%세포점부분자
Peroxisome proliferator-activated receptor%Brain injuries%Apoptosis%Cell adhesion molecules
目的 观察过氧化物酶体增殖物激活受体γ( peroxisome proliferator-activated receptor -γ,PPARγ)激动剂吡格列酮对大鼠创伤性脑损伤(traumatic brain injury,TBI)后迟发性神经元死亡、细胞凋亡及细胞间黏附分子-1(intercellular adhesion molecule-1,ICAM-1)表达的影响. 方法 将36只SD大鼠按随机数字表法分为假致伤组、对照组和吡格列酮治疗组,每组12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体积分数0.2％二甲基亚砜灌胃.致伤后48 h取脑组织,石蜡切片,分别行Nissl、TUNEL染色和ICAM -1免疫组化测定,观察迟发性神经元死亡、神经细胞凋亡程度及ICAM-1表达. 结果 (1)治疗组尼氏体脱失细胞率为(38.59±1.97)％,明显低于对照组的(51.25±4.01)％ (P ＜0.05),高于假致伤组的(8.65±1.23)％(P＜0.01)；(2)治疗组神经细胞凋亡计数为31.67±4.76,明显低于对照组45.33 ±4.68(P＜0.05),高于假致伤组16.83±2.04(P ＜0.01)；(3)治疗组ICAM-1表达阳性细胞的平均吸光度值为0.26±0.04,明显低于对照组0.31±0.04(P ＜0.05),高于假致伤组0.10±0.02(P＜0.01). 结论 PPARγ激动剂吡格列酮能减少TBI后的神经细胞凋亡,保护神经元；其抑制ICAM-1的表达可能是其抑制炎症反应、发挥神经保护作用的机制之一.
目的 觀察過氧化物酶體增殖物激活受體γ( peroxisome proliferator-activated receptor -γ,PPARγ)激動劑吡格列酮對大鼠創傷性腦損傷(traumatic brain injury,TBI)後遲髮性神經元死亡、細胞凋亡及細胞間黏附分子-1(intercellular adhesion molecule-1,ICAM-1)錶達的影響. 方法 將36隻SD大鼠按隨機數字錶法分為假緻傷組、對照組和吡格列酮治療組,每組12隻.採用改良的Feeney法製作腦創傷模型,治療組採用吡格列酮(10 mg/kg)灌胃,假緻傷組和對照組用等量體積分數0.2％二甲基亞砜灌胃.緻傷後48 h取腦組織,石蠟切片,分彆行Nissl、TUNEL染色和ICAM -1免疫組化測定,觀察遲髮性神經元死亡、神經細胞凋亡程度及ICAM-1錶達. 結果 (1)治療組尼氏體脫失細胞率為(38.59±1.97)％,明顯低于對照組的(51.25±4.01)％ (P ＜0.05),高于假緻傷組的(8.65±1.23)％(P＜0.01)；(2)治療組神經細胞凋亡計數為31.67±4.76,明顯低于對照組45.33 ±4.68(P＜0.05),高于假緻傷組16.83±2.04(P ＜0.01)；(3)治療組ICAM-1錶達暘性細胞的平均吸光度值為0.26±0.04,明顯低于對照組0.31±0.04(P ＜0.05),高于假緻傷組0.10±0.02(P＜0.01). 結論 PPARγ激動劑吡格列酮能減少TBI後的神經細胞凋亡,保護神經元；其抑製ICAM-1的錶達可能是其抑製炎癥反應、髮揮神經保護作用的機製之一.
목적 관찰과양화물매체증식물격활수체γ( peroxisome proliferator-activated receptor -γ,PPARγ)격동제필격렬동대대서창상성뇌손상(traumatic brain injury,TBI)후지발성신경원사망、세포조망급세포간점부분자-1(intercellular adhesion molecule-1,ICAM-1)표체적영향. 방법 장36지SD대서안수궤수자표법분위가치상조、대조조화필격렬동치료조,매조12지.채용개량적Feeney법제작뇌창상모형,치료조채용필격렬동(10 mg/kg)관위,가치상조화대조조용등량체적분수0.2％이갑기아풍관위.치상후48 h취뇌조직,석사절편,분별행Nissl、TUNEL염색화ICAM -1면역조화측정,관찰지발성신경원사망、신경세포조망정도급ICAM-1표체. 결과 (1)치료조니씨체탈실세포솔위(38.59±1.97)％,명현저우대조조적(51.25±4.01)％ (P ＜0.05),고우가치상조적(8.65±1.23)％(P＜0.01)；(2)치료조신경세포조망계수위31.67±4.76,명현저우대조조45.33 ±4.68(P＜0.05),고우가치상조16.83±2.04(P ＜0.01)；(3)치료조ICAM-1표체양성세포적평균흡광도치위0.26±0.04,명현저우대조조0.31±0.04(P ＜0.05),고우가치상조0.10±0.02(P＜0.01). 결론 PPARγ격동제필격렬동능감소TBI후적신경세포조망,보호신경원；기억제ICAM-1적표체가능시기억제염증반응、발휘신경보호작용적궤제지일.
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.Methods Thirty-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 ).Conclusions The 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.
