2014•Journal of Apoplexy and Nervous DiseasesRequires access

IGF-1 inhibited the MPP~+ induced apoptosis of PC12 cells via PI3K /Akt signaling pathway

Huang Lu-q

Open publisher page 0 citations

Abstract

Objective To investigate the protective mechanism of IGF-1 on MPP+induced neurotoxicity in PC12 cells. Methods PC12 cells impaired by MPP+( 250 μmol/L) were used as the cell model of Parkinson's disease. The cultured cells were divided into such groups:( 1) control group;( 2) MPP+group;( 3) IGF-1 group;( 4) IGF-1 + MPP+group;( 5) IGF-1 + MPP++ LY294002 group. After incubation for 24 h,methyl thiazolyltetrazolium( MTT) was used to assay the viability of the PC12 cells. After incubation for 4 h,Western blot was used to detect the expression level of Akt、phospho-Akt. Results( 1) 100 nmol /L IGF-1 protect PC12 cells from MPP+.( 2) The level of total-Akt had not changed after all the treatment,however,the level of phospho-Akt was higher in IGF-1 treated group than that treated with MPP+.Conclusion These findings indicate that IGF-1 protects against apoptosis in PC12 cells exposed to MPP+,the protective effect is associated with an up-regulation of phospho-Akt.

About this research paper

What this paper is about

Objective To investigate the protective mechanism of IGF-1 on MPP+induced neurotoxicity in PC12 cells. Methods PC12 cells impaired by MPP+( 250 μmol/L) were used as the cell model of Parkinson's disease. The cultured cells were divided into such groups:( 1) control group;( 2) MPP+group;( 3) IGF-1 group;( 4) IGF-1 + MPP+group;( 5) IGF-1 + MPP++ LY294002 group. After incubation for 24 h,methyl thiazolyltetrazolium( MTT) was used to assay the viability of the PC12 cells. After incubation for 4 h,Western blot was used to detect the expression level of Akt、phospho-Akt. Results( 1) 100 nmol /L IGF-1 protect PC12 cells from MPP+.( 2) The level of total-Akt had not changed after all the treatment,however,the level of phospho-Akt was higher in IGF-1 treated group than that treated with MPP+.Conclusion These findings indicate that IGF-1 protects against apoptosis in PC12 cells exposed to MPP+,the protective effect is associated with an up-regulation of phospho-Akt.

Why it matters

A significance statement is not available in the OpenAlex record.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

Objective To investigate the protective mechanism of IGF-1 on MPP+induced neurotoxicity in PC12 cells. Methods PC12 cells impaired by MPP+( 250 μmol/L) were used as the cell model of Parkinson's disease. The cultured cells were divided into such groups:( 1) control group;( 2) MPP+group;( 3) IGF-1 group;( 4) IGF-1 + MPP+group;( 5) IGF-1 + MPP++ LY294002 group. After incubation for 24 h,methyl thiazolyltetrazolium( MTT) was used to assay the viability of the PC12 cells. After incubation for 4 h,Western blot was used to detect the expression level of Akt、phospho-Akt. Results( 1) 100 nmol /L IGF-1 protect PC12 cells from MPP+.( 2) The level of total-Akt had not changed after all the treatment,however,the level of phospho-Akt was higher in IGF-1 treated group than that treated with MPP+.Conclusion These findings indicate that IGF-1 protects against apoptosis in PC12 cells exposed to MPP+,the protective effect is associated with an up-regulation of phospho-Akt.

Key concepts: Protein kinase B, PI3K/AKT/mTOR pathway, Apoptosis, LY294002, Viability assay, Western blot, Incubation, MTT assay

Related papers

Back to paper searchBrowse research topicsOriginal source
IGF-1 inhibited the MPP~+ induced apoptosis of PC12 cells via PI3K /Akt signaling pathway — Research Paper | ScholarLens