Influence and Possible Mechanisms of Cryptotanshinone on the Survival of PC12 Cells Promoted by IGF-1

MENG Qian; ZHENG Wen-hua

doi:10.11653/syfj2013100195

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Influence and Possible Mechanisms of Cryptotanshinone on the Survival of PC12 Cells Promoted by IGF-1

更新时间：2024-01-04

- Influence and Possible Mechanisms of Cryptotanshinone on the Survival of PC12 Cells Promoted by IGF-1
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 19, Issue 10, Pages: 195-198(2013)
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- DOI：10.11653/syfj2013100195
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- Published：2013
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MENG Qian, ZHENG Wen-hua. Influence and Possible Mechanisms of Cryptotanshinone on the Survival of PC12 Cells Promoted by IGF-1[J]. Chinese journal of experimental traditional medical formulae, 2013, 19(10): 195-198.
DOI：

MENG Qian, ZHENG Wen-hua. Influence and Possible Mechanisms of Cryptotanshinone on the Survival of PC12 Cells Promoted by IGF-1[J]. Chinese journal of experimental traditional medical formulae, 2013, 19(10): 195-198. DOI： 10.11653/syfj2013100195.

摘要

目的: 研究隐丹参酮对类胰岛素样生长因子-1(IGF-1)促进PC12细胞存活的影响及可能机制。方法: 首先采用剥夺血清造成细胞损伤模型确定IGF-1发挥促存活作用的剂量

然后不同剂量的隐丹参酮预先作用PC12细胞

再加入IGF-1处理

MTT检测隐丹参酮对IGF-1促PC12细胞存活的影响;Western blot检测隐丹参酮对IGF-1诱导其受体(IGF-1R)磷酸化及下游信号通路磷酯酰肌醇-3-激酶(PI3K)/蛋白激酶B(Akt)及细胞外信号调节激酶(ERK)1/2的影响。结果: MTT显示隐丹参酮能剂量依赖性地阻断IGF-1的促存活作用

抑制PC12细胞的增殖;Western blot结果显示IGF-1能明显诱导其受体(IGF-1R)磷酸化

而隐丹参酮则起抑制作用

并使下游Akt及ERK1/2的磷酸化水平下调

呈明显的剂量依赖性。结论: 隐丹参酮可通过抑制IGF-1R及其下游信号分子Akt和ERK1/2的磷酸化

从而抑制IGF-1的促存活功能

发挥其自身抑制细胞存活

促使细胞凋亡的作用。

Abstract

Objective: Study the effect of cryptotanshinone(CTS) on the survival of in PC12 cells promoted by insulin-like growth factor-1(IGF-1) and possible mechanisms. Method: The serum deprivation model was constructed to determine the dose of IGF-1 to play the survival-promoting effect

then pretreat PC12 cells with different concentrations of CTS

then treated with IGF-1 processing 24 hours

MTT assay was used to detect the effect of CTS on protective function of IGF-1.The effect of CTS and IGF-1 on the phosphorylation level of IGF-1 receptar(IGF-1R) were analyzed by Western blot and downstream targets were also detected such as protein kinase B(Akt) and extracellular signal regulated kinase(ERK). Result: After treatment with IGF-1

cell viability of PC12 cells was increased in a dose-dependent manner as same as the phosphorylation level of IGF-1R

whereas CTS attenuated the survival promoting effect of IGF-1 in PC12 cells and decreased the phosphorylated IGF-1R. Moreover

CTS attenuated the phosphorylation of Akt and ERK1/2 induced by IGF-1in a dose-dependent manner. Conclusion: These data indicate that CTS has an inhibitory effect on PC12 cells viability via down-regulate the phosphorylation of IGF-1R and downstream Akt and ERK.

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