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观察赛庚啶(Cyp)对大鼠脑突触体Ca~(2+)水平和Ca~(2+)·Mg~(2+)-ATP酶活性的影响,以探讨其对脑缺血再灌注损伤的保护作用机理。用Quin2/AM法测定,突触体静息游离Ca~(2+)浓度为88±16μmol·g~(-1)蛋白,1.0,2.5和5.0μmol·L~(-1)的Cyp对其基本无影响。对高K~+所致突触体Ca~(2+)浓度升高有抑制作用但不显著,由185±45μmol·g~(-1)蛋白分别降至182±41、181±41、178±38μmol·g~(-1)蛋白;使突触体Ca~(2+)·Mg~(2+)-ATP酶活性由78±15mmol·h~(-1)·g~(-1)蛋白下降至74±12,70±11和65±8mmol·h~(-1)·g~(-1)蛋白。表明,Cyp是通过抑制Ca~(2+)内流和选择性抑制Ca~(2+)·Mg~(2+)-ATP酶活性,而稳定内质网和腺粒体内Ca~(2+)浓度,从而达到对脑缺血再灌注损伤的保护作用。
To observe the effects of cyprimethamine on Ca 2+ and Ca 2+ Mg 2 + -ATPase activity in brain synaptosomes of rats to investigate its effect on cerebral ischemia Protective mechanism of perfusion injury. Quin2 / AM assay showed that the resting free Ca2 + concentration of synaptosomes was 88 ± 16μmol · g -1 protein, Cyp at 1.0,2.5 and 5.0μmol·L -1 Basically no effect. The inhibitory effect of Ca ~ (2+) on synaptosomes induced by high K ~ + was not significant but decreased from 185 ± 45μmol · g ~ (-1) to 182 ± 41,181 ± 41,178 The activity of Ca2 +, Mg2 +, ATPase in the synaptosome ranged from 78 ± 15 mmol · h -1 g · (-1) Protein decreased to 74 ± 12,70 ± 11 and 65 ± 8 mmol · h -1 g -1 protein. It is indicated that Cyp inhibits the Ca 2+ influx and selectively inhibits Ca 2+ Mg 2+ -ATPase activity while stabilizes the endoplasmic reticulum and intracellular calcium Ca 2+ ) Concentration, so as to achieve the protection of cerebral ischemia-reperfusion injury.