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首页> 外文期刊>Experimental and clinical endocrinology and diabetes: Official journal, German Society of Endocrinology [and] German Diabetes Association >Estrone, but not 17 beta-estradiol, attenuates kainate-induced seizures and toxicity in male mice.
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Estrone, but not 17 beta-estradiol, attenuates kainate-induced seizures and toxicity in male mice.

机译：雌酮，但不是17β-雌二醇，可以减轻海因酸盐诱导的癫痫发作和雄性小鼠的毒性。

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Estrogens change the susceptibility to seizures in humans and experimental animals. In this study, the effect of estrone and 17 beta-estradiol on kainate-induced seizures and neurotoxicity was investigated in male mice. Pre-treatment with estrone (250-1000 micrograms/kg) at 24 and 2 hours before kainate (40 mg/kg) administration significantly decreased both the percentage of animals with clonic seizures and their mortality (the latter at a dose of 1000 micrograms/kg only). On the other hand, 17 beta-estradiol (10-500 micrograms/kg) had no effect on seizures, and its dose of 10 micrograms/kg increased mortality. When given alone at a dose of 1 mg/kg, tamoxifen, an antagonist at estrogene receptors, did not affect the kainate-induced seizures, but prevented the anticonvulsant effect of estrone. A histological analysis showed that 73% of mice injected with vehiculum and kainate incurred hippocampal damage. Estrone (2000 micrograms/kg) decreased the percentage of animals with hippocampal neuronal loss down to 43%, and that effect was not antagonized by tamoxifen. Pretreatment of mice with 17 beta-estradiol had no effect on the kainate-induced neuronal loss. Additionally, we found that kainate injected i.p. had a profound effect on the immune system of mice, as reflected by a decrease in the thymus weight and an increased metabolic activity of splenocytes. The anticonvulsive dose of estrone (1000 micrograms/kg) did not change the immunoreactivity of either control or kainate-treated mice. In conclusion, the obtained data indicate that estrone, but not 17 beta-estradiol, attenuates the kainate-induced seizures, mortality and excitotoxicity in male mice. Moreover, it is suggested that the suppressive effect of estrone on clonic seizures involves intracellular receptors, whereas its antineurotoxic activity seems to depend on a non-genomic mechanism.
机译：雌激素改变了人类和实验动物癫痫的易感性。在这项研究中，雄性小鼠研究了雌酮和17β-雌二醇对海藻酸盐诱导的癫痫发作和神经毒性的作用。在施用海藻酸盐（40 mg / kg）之前的24和2小时内，用雌酮（250-1000微克/千克）进行预处理可显着降低患有阵挛性癫痫的动物的百分比及其死亡率（后者以1000微克/千克的剂量）公斤）。另一方面，17β-雌二醇（10-500微克/千克）对癫痫发作没有影响，而其10微克/千克的剂量增加了死亡率。当单独服用1 mg / kg的剂量时，他莫昔芬（雌激素受体的拮抗剂）不会影响海因酸盐诱导的癫痫发作，但会阻止雌酮的抗惊厥作用。组织学分析表明，注射有载体和海藻酸盐的小鼠中有73％遭受了海马损伤。雌酮（2000微克/千克）使海马神经元丢失的动物百分比降低至43％，而他莫昔芬并未拮抗这种作用。用17β-雌二醇预处理小鼠对海藻酸盐诱导的神经元丢失没有影响。另外，我们发现海藻酸盐注射了ip。胸腺重量的减少和脾细胞新陈代谢的增强反映了对小鼠免疫系统的深远影响。雌酮的抗惊厥剂量（1000微克/千克）不会改变对照组或海因酸盐治疗小鼠的免疫反应性。总之，获得的数据表明，雌酮可减轻海藻酸盐诱导的癫痫发作，死亡率和兴奋性毒性，但不能抑制17β-雌二醇。此外，建议雌酮对阵挛性癫痫的抑制作用涉及细胞内受体，而其抗神经毒活性似乎取决于非基因组机制。

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