Department of Anatomy and Histology & Embryology, School of Biology and Basic Medical Sciences, Soochow University, 1 Shizi Street, Suzhou, 215006, China.
J Physiol Sci. 2012 Sep;62(5):385-92. doi: 10.1007/s12576-012-0215-x. Epub 2012 Jun 14.
Our previous work has shown that interleukin-6 (IL-6) implements its neuroprotective effect by inhibiting the intracellular Ca(2+) overload in neurons. Here, we examined whether regulation of L-type calcium channels (LCCs) activities is involved in the neuroprotective action of IL-6. In cultured cerebellar granule neurons (CGNs), patch-clamp recording showed that the whole-cell Ca(2+) current and LCC current were significantly reduced by IL-6 pretreatment (120 ng/ml, for 24 h). Calcium imaging data indicated that IL-6 significantly suppressed high K(+)-induced intracellular Ca(2+) overload and LCC Ca(2+) influx. Moreover, expression of the LCC subunit, Ca(v)1.2, was remarkably downregulated by IL-6 in cultured CGNs. These findings suggest that IL-6 exerts a neurotrophic effect by preventing Ca(2+) overload, at least partly through inhibition of LCC activity in cultured CGNs.
我们之前的工作表明,白细胞介素-6(IL-6)通过抑制神经元内的细胞内 Ca(2+)过载来发挥其神经保护作用。在这里,我们研究了 L 型钙通道(LCCs)活性的调节是否参与了 IL-6 的神经保护作用。在培养的小脑颗粒神经元(CGNs)中,膜片钳记录显示,IL-6 预处理(120ng/ml,24 小时)显著降低了全细胞 Ca(2+)电流和 LCC 电流。钙成像数据表明,IL-6 显著抑制高 K(+)诱导的细胞内 Ca(2+)过载和 LCC Ca(2+)内流。此外,IL-6 显著下调了培养 CGNs 中的 LCC 亚基 Ca(v)1.2 的表达。这些发现表明,IL-6 通过防止 Ca(2+)过载发挥神经营养作用,至少部分是通过抑制培养 CGNs 中的 LCC 活性来实现的。