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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 role of mitochondria induced by apoptosis of resveratrol (Res) and the effect of Res on mitochondrial permeability. The effect of Res on mitochondrial permeability transition channels and Ca2+-induced mitochondrial Ca2+ release was studied. Impact of CICR). Methods Rat liver mitochondria were extracted. The mitochondrial swelling of the mitochondria was measured by UV spectrophotometer to determine the open state of the mitochondrial PTP. The dual wavelength dual-beam ultraviolet spectrophotometer was used to detect the D(λ) value caused by the change of the Ca2+ concentration in the test system under the action of Res. Changes to reflect mitochondrial Ca2+ transport (ie, CICR). Results Res promoted Ca2+-induced PTP opening in rat liver mitochondria; and Res could accelerate Ca2+-mediated mitochondrial Ca2+ transport (CICR); Ca2+ channel inhibitors trifluoperazine and perylene red (RR) partially or completely inhibited Res, respectively. Promote effect. Conclusion Res promotes Ca2+-induced CICR in rat liver mitochondria. The effect of Res on PTP depends on the effect of Res on mitochondrial CICR. Res promotes mitochondrial membrane permeability may be a way for Res to induce apoptosis.