Zhu Shujuan, Qian Yihua, Shi Lili, Yang Weina, Feng Xinzheng, Li Cuiqin, Liu Yong
Department of Human Anatomy and Histology Embryology, Institute of Neurobiology, Key Laboratory of Environment and Gene Related Diseases of Education Ministry, Xi'an Jiaotong University College of Medicine, Xi'an 710061, China.
Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2010 Aug;35(8):840-6. doi: 10.3969/j.issn.1672-7347.2010.08.011.
To explore the effect of tanshinone IIA (TanIIA) on calcium current induced by beta-amyloid protein 25-35 (Abeta25-35) in neurons of nucleus basalis of Meynert (nbM).
Cell acute dissociated technique and the whole-cell recording model of patch-clamp technique of single-cell were used. The voltage-dependent calcium current in neurons of nbM was recorded in SD rats first. Then the effect of TanIIA on the voltage-dependent calcium current in the neurons was assayed. The change of calcium current induced by Abeta25-35 as well as the effect of TanIIA on the change of calcium current induced by Abeta25-35 in neurons of nbM were analyzed.
Extracellular fluid containing different concentrations of TanIIA was irrigated, respectively. The peak current did not change obviously. There was no difference in current density between the TanIIA group and the control group at 0 mV (P>0.05). Extracellular fluid containing 200 nmol/L Abeta25-35 was irrigated after the normal calcium current recorded under whole patch clamp, and the peak current changed obviously. There was distinct difference in the current density between the Abeta group and the control group at 0 mV (P<0.05). Extracellular fluid containing Abeta25-35 and different concentrations of TanIIA were irrigated after the normal calcium current was recorded under whole patch clamp, respectively, and the peak current did not change. There was no difference in current density between the TanIIA +Abeta group and the control group at 0 mV (P>0.05).
In vitro, TanIIA could inhibit the calcium current amplification induced by Abeta25-35 in neurons of nbM. TanIIA may protect neurons against the toxicity of Abeta and decrease the inward flow of Ca(2+).
探讨丹参酮IIA（TanIIA）对梅纳特基底核（nbM）神经元中β-淀粉样蛋白25-35（Abeta25-35）诱导的钙电流的影响。
采用细胞急性解离技术和单细胞膜片钳技术的全细胞记录模式。首先在SD大鼠中记录nbM神经元的电压依赖性钙电流。然后测定TanIIA对神经元中电压依赖性钙电流的影响。分析Abeta25-35诱导的钙电流变化以及TanIIA对nbM神经元中Abeta25-35诱导的钙电流变化的影响。
分别灌流含有不同浓度TanIIA的细胞外液。峰值电流无明显变化。TanIIA组与对照组在0 mV时的电流密度无差异（P>0.05）。在全细胞膜片钳记录到正常钙电流后，灌流含有200 nmol/L Abeta25-35的细胞外液，峰值电流明显变化。Abeta组与对照组在0 mV时的电流密度有显著差异（P<0.05）。在全细胞膜片钳记录到正常钙电流后，分别灌流含有Abeta25-35和不同浓度TanIIA的细胞外液，峰值电流无变化。TanIIA+Abeta组与对照组在0 mV时的电流密度无差异（P>0.05）。
在体外，TanIIA可抑制nbM神经元中Abeta25-35诱导的钙电流放大。TanIIA可能保护神经元免受Abeta的毒性并减少Ca(2+)的内流。
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