摘要
目的:探讨白介素10(IL-10)对大鼠脑缺血梗死灶周围神经细胞凋亡的作用。方法:成年雄性Sprague-Darley大鼠36只,随机分为假手术组(Sham组)、局灶性脑缺血组(MCAO组)和脑缺血+IL-10干预组(IL-10组),术后24h断头取脑,TUNEL法(Terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling)测定梗死灶周围凋亡神经细胞的数目,免疫组化和RT-PCR法检测促凋亡基因Fas、FasL和caspase-3的表达。结果:脑缺血诱导神经细胞凋亡显著增多(P<0.05),Fas,FasL和caspase-3表达显著上调(P<0.05);IL-10干预可显著减少脑缺血神经细胞凋亡(P<0.05),并抑制FasL和caspase-3的表达(P<0.05),而对Fas的表达无明显作用(P>0.05)。结论:IL-10可抑制大鼠脑缺血梗死灶周围神经细胞凋亡,其机制可能与抑制促凋亡基因FasL和caspase-3的表达有关。
AIM： To investigate the effect of interleukin- 10 on neurocyte apoptosis in cerebral ischemia in rats. METHODS： 36 adult male Sprague-Dawley rats were randomly assigned into 3 groups： sham operation group, middle cerebral artery occlusion（MCAO） group and MCAO ＋ interleukin-10 treatment group. Terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling （TUNEL） staining was used to detect in situ cell apoptosis, immunohistochemical staining and RT-PCR were used to detect the expression of proapoptotic gene Fas, Fas ligand （FasL） and caspase-3 in peri-infarct, respectively. RESULTS： Cerebral ischemia significantly induced neurocyte apoptosis and upregulated the expression of Fas, FasL and caspase-3, repcetively （ P 〈 0. 05）. IL-10 treatment significantly inhibited neurocyte apoptosis, and suppressed the expression of proapoptotic gene FasL and caspase-3, repcetively （ P 〈 0. 05 ）, but had no obvious effect on Fas expression （P〉0.05）. CONCLUSION： IL-10 can suppress neurocyte apoptosis in cerebral ischemia, whose mechanisms seemed related to inhibiting the expression of proapoptotic gene FasL and caspase-3.
出处
《细胞与分子免疫学杂志》
CAS
CSCD
北大核心
2007年第6期498-500,共3页
Chinese Journal of Cellular and Molecular Immunology
基金
福建省教育厅资助课题(C0440009)
福建省科技厅资助课题(2005K046)
