Hydrogen sulfide protects SH-SY5Y neuronal cells against d-galactose induced cell injury by suppression of advanced glycation end products formation and oxidative stress.

Neurochemistry international

PubMedID: 23274001

Liu YY, Nagpure BV, Wong PT, Bian JS. Hydrogen sulfide protects SH-SY5Y neuronal cells against d-galactose induced cell injury by suppression of advanced glycation end products formation and oxidative stress. Neurochem Int. 2013;62(5):603-9.
d-Galactose is widely used as an agent to cause aging effects in experimental animals. The present study aims to investigate the effects of hydrogen sulfide (H2S) in human neuroblastoma SH-SY5Y cells exposed to d-galactose. Cells were pretreated with NaHS, an H2S donor, and then exposed to d-galactose (25-400mM for 48h). We found that NaHS pretreatment significantly reversed the d-galactose-induced cell death and cellular senescence. MTT assay shows that NaHS significantly increased cell viability from 62.31±1.29% to 72.34±0.46% compared with d-galactose (200mM) treatment group. The underlying mechanism appeared to involve a reduction by NaHS in the formation of advanced glycation end products (AGEs), which are known to contribute to the progression of age-related diseases. In addition, NaHS decreased the elevation of reactive oxygen species from 151.17±2.07% to 124.8±2.89% and malondialdehyde from 1.72±0.07 to 1.10±0.08 (nmol/mg protein) in SH-SY5Y cells after d-galactose exposure. NaHS also stimulated activities of superoxide dismutase from 0.42±0.05 to 0.73±0.04 (U/mg protein) and glutathione peroxidase from 3.98±0.73 to 14.73±0.77 (nmol/min/mg protein) and upregulated the gene expression levels of copper transport protein ATOX1, glutathione synthetase (GSS) and thioredoxin reductase 1 (TXNRD1) while down-regulated aldehyde oxidase 1 (AOX1). In summary, our data indicate that H2S may have potentially anti-aging effects through the inhibition of AGEs formation and reduction of oxidative stress.