Insulin blocks glutamate-induced neurotoxicity in differentiated SH-SY5Y neuronal cells.
Madhavan NampoothiriNeetinkumar D ReddyJessy JohnNitesh KumarGopalan Kutty NampurathMallikarjuna Rao ChamallamudiPublished in: Behavioural neurology (2014)
Insulin is a cytokine which promotes cell growth. Recently, a few published reports on insulin in different cell lines support the antiapoptotic effect of insulin. But the reports fail to explain the role of insulin in modulating glutamate-mediated neuronal cell death through excitotoxicity. Thus, we examined the neuroprotective effect of insulin on glutamate-induced toxicity on differentiated SH-SY5Y neuronal cells. Changes in cell viability were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) based assay, while apoptotic damage was detected by acridine orange/ethidium bromide and Hoechst staining. Intracellular reactive oxygen species (ROS) accumulation and morphological alterations were also measured. Treatment with glutamate induced apoptosis, elevated ROS levels and caused damage to neurons. Insulin was able to attenuate the glutamate-induced excitotoxic damage to neuronal cells.
Keyphrases
- induced apoptosis
- type diabetes
- oxidative stress
- cell death
- cell cycle arrest
- endoplasmic reticulum stress
- reactive oxygen species
- signaling pathway
- diabetic rats
- glycemic control
- high glucose
- dna damage
- emergency department
- systematic review
- insulin resistance
- cell proliferation
- spinal cord
- high throughput
- stress induced