Metformin attenuate PTZ-induced apoptotic neurodegeneration in human cortical neuronal cells | Bibi | Pakistan Journal of Medical Sciences Old Website
 

Metformin attenuate PTZ-induced apoptotic neurodegeneration in human cortical neuronal cells

Fehmida Bibi, Ikram Ullah, Myeong Ok Kim, Muhammad Imran Naseer

Abstract


Objective: Seizures are one of the neurodegenerative disorders of human being. Metformin has antioxidant properties and commonly used as an oral antidiabetic drug. The current study was aimed to observe the neuroprotective effect of metformin against PTZ-induced apoptotic neurodegeneration in human cortical neuronal cell culture.

Methods: To observe that exposure of pentylenetetrazol (PTZ) at the dose of (30mM) for 30 minutes induced neuronal cell death by activation of caspase-3 in human cortical neuronal 2 (HCN-2) cell line. While the metformin at the dose of (20mM) along with PTZ for 30 minutes showed neuroprotection against PTZ-induced neuronal cell loss by MTT assay and Western blot analysis.

Results: The results of this study showed that PTZ-induced neuronal cell death by activation of pro apoptotic proteins caspase-3 and 9 whereas the exposure of metformin showed its protective effect against neuronal loss in HCN-2 cell line. Finally, our results showed that exposure of metformin can prevent the harmful effect induced by PTZ in neuronal cells cultures.

Conclusions: Our finding suggest that metformin exposure attenuates PTZ-induced neuronal cell death may act as a safe therapeutics and neuroprotective agent for the treatment of neuronal loss as result of seizure.

doi: https://doi.org/10.12669/pjms.333.11996

How to cite this:Bibi F, Ullah I, Kim MO, Naseer MI. Metformin attenuate PTZ-induced apoptotic neurodegeneration in human cortical neuronal cells. Pak J Med Sci. 2017;33(3):581-585.   doi: https://doi.org/10.12669/pjms.333.11996

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Full Text: PDF

Refbacks

  • There are currently no refbacks.


kalsob-01_1303_01