白藜芦醇促进Ca^(2+)介导的线粒体Ca^(2+)转运发生

Resveratrol promotes Ca^(2+)-induced Ca^(2+) release from rat liver cell mitochondria mediated by Ca^(2+)

目的为探讨白藜芦醇(Tesveratrol,Res)诱导细胞凋亡过程中线粒体的作用,Res对线粒体通透性的影响,研究了Res对线粒体通透性转变孔道及Ca2+诱导的线粒体内Ca2+释放(CICR)发生的影响。方法提取大鼠肝线粒体。通过紫外分光光度仪检测Res作用下线粒体的膨胀,借此测定线粒体PTP的开放状态;采用双波长双光束紫外分光光度仪检测Res作用下测试体系内Ca2+浓度的变化引起的D(λ)值的变化,以反映线粒体Ca2+的转运情况(即CICR)。结果Res能促进Ca2+诱导的鼠肝线粒体PTP开放;并且Res可以加速Ca2+介导的线粒体Ca2+的转运(CICR);而Ca2+通道抑制剂trifluoperazine和钌红(RR)能分别部分或完全抑制Res的这种促进作用。结论Res能促进Ca2+诱导的鼠肝线粒体CICR过程。并且Res对PTP的作用依赖于Res对线粒体CICR的影响,Res促进线粒体膜的通透性可能是Res诱导细胞凋亡的一种途径。

Objective To investigate the effects of resveratrol （Res） on mitochondrial opening and Ca^2＋-induced Ca^2＋ release （CICR） from rat liver cell mitochondria mediated by Ca^2＋, Methods Wistar rat liver cell mitochondria ,was extracted and Res-induced mitochondrial swelling was assessed spectrophotometrically at 540 nm to examine the permeability transition pore （PTP） opening. The membrane potential changes of Res-treated mitochondia were measured with fluorescence spectrophotometery. Ca^2＋ uptake and release by the mitochondria was determined by absorbance change of arsenazo Ⅲ at 685-675 nm monitored by dual wavelength spectrophotometry. Results Res promoted Ca^2＋-mediated PTP opening, and this effect was completely inhibited by CsA and lowered by trifluoperazine. CICR accelerated by Res treatment was completely blocked by ruthenium red and partly by trifluoperazine. Conclusion Res can promote PTP opening by inducing CICR, which may be one of the pathways that Res induces cell apoptosis.