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首页> 外文期刊>Acta pharmacologica Sinica >Adenovirus viral interleukin-10 inhibits adhesion molecule expressions induced by hypoxia/reoxygenation in cerebrovascular endothelial cells
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Adenovirus viral interleukin-10 inhibits adhesion molecule expressions induced by hypoxia/reoxygenation in cerebrovascular endothelial cells

机译：Adenovirus viral interleukin-10 inhibits adhesion molecule expressions induced by hypoxia/reoxygenation in cerebrovascular endothelial cells

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Aim:To investigate the effects of recombinant adenovirus encoding viral interleukin-10(vIL-10),a potent anti-inflammatory cytokine,on adhesion molecule expressions and the adhesion rates of leukocytes to endothelial cells in cerebrovascular endothelial cells injured by hypoxia/reoxygenation(H/R).Methods:Arecombinant adenovirus expressing vIL-10(Ad/vIL-10(or the green fluorescent protein(Ad/GFP)gene was constructed.A cerebrovascular endothelial cell line bEnd.3 was pretreated with a different multiplicity of infection(MOI)of Ad/vIL-10 or Ad/GFP and then exposed to hypoxia for 9 h followed by reoxygenation for 12 h.The culture supernatants were tested for the expression of vIL-10 and endogenous murine IL-10(mIL-10)by ELISA.The effects of Ad/vIL-10 on monocyte-endothelial cell adhesion were represented as the adhesion rate.Subsequently,the expressions of intercellular adhesion molecule l(ICAM-l)and vascular cell adhesion molecule 1( VCAM-1)in the endothelial cells after treatment with Ad/vIL-10 and H/R were analyzed by Western blotting and real-time PCR.Results:vIL-10 was expressed in cultured bEnd.3 after Ad/vIL-10 transfec-tion and was significantly increased by H/R.Ad/vIL-10 or Ad/GFP did not affect the mIL-10 level.H/R increased the mIL-10 expression,but insignificantly.Monocyte-endothelial cell adhesion induced by H/R was significantly inhibited by pretreatment with Ad/vIL-10(MOI:80).ICAM-1,and VCAM-1 in bEnd.3 and were significantly increased after H/R,while pretreatment with Ad/vIL-10(MOI:80)significantly inhibited their expressions.Ad/GFP did not markedly affect monocyte-endothelial adhesion and the expressions of ICAM-1 and VCAM-1 induced by H/R.Conclusion:Ad/vIL-10 significantly inhibits the upregulation of endothelial adhesion molecule expressions and the increase of adhesion of monocytes-endothelial cells induced by H/R,indicating that vIL-10 gene transfer is of far-reaching significance in the therapy of cerebrovascular inflammatory diseases,and anti-adhesion treatment may reduce H/R injury.

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