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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。
Objective: To investigate the effect of interleukin-10 (IL-10) on the apoptosis of peripheral nerve cells in cerebral infarction rats. Methods: Thirty-six adult male Sprague-Darley rats were randomly divided into four groups: Sham group, MCAO group and IL-10 group. , And the number of apoptotic nerve cells around the infarcted area was determined by TUNEL method at 24 hours after operation. The expressions of Fas, FasL and FasL were detected by immunohistochemistry and RT-PCR And caspase-3 expression. Results: The apoptosis of neurons induced by cerebral ischemia increased significantly (P <0.05), and the expressions of Fas, FasL and caspase-3 were significantly increased (P <0.05); IL-10 treatment significantly decreased the apoptosis of neurons <0.05), and inhibited the expression of FasL and caspase-3 (P <0.05), but had no significant effect on the expression of Fas (P> 0.05). CONCLUSION: IL-10 can inhibit the apoptosis of peripheral nerve cells in rats with focal cerebral ischemia and its mechanism may be related to the inhibition of the expression of pro-apoptotic genes FasL and caspase-3.