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Hydrogen sulfide (H2S) has the potential to protect the brain from neuroinflammation although it has been previously reported to play a pro-inflammatory role in septic shock, acute pancreatitis, and haemorrhagic shock.
In the latest study published in the Journal of Neurochemistry (2007) titled Hydrogen sulfide attenuates lipopolysaccharide-induced inflammation by inhibition of p38 nitrogen-activated protein kinase in microglia, a research team in the National University of Singapore, Department of Pharmacology, led by Dr Bian Jin-Song, Assoc Prof Peter Wong and Prof Philip Moore, provided the first evidence that H2S inhibits the production of two major pro-inflammatory factors – nitric oxide (NO) and tumour-necrosis factor alpha (TNF-a).
MICROGLIAL CELLS: Cells showing hydrogen sulfide-induced calcium elevation. Right: Cells showing normal microglial cells.
Microglia are immune cells which engulf dead or damaged cells in the brain, removing them from the system. In the process however, they also produce NO which further aggravates the injured site. H2S is however, able to moderate the production of NO by decreasing inducible nitric oxide synthase (iNOS) expression. iNOS is an NO producing enzyme that is induced by inflammation. The mechanism may also involve calcium. In an earlier paper published in Glia (2006) titled Hydrogen sulfide regulates calcium homeostasis in microglial cells, the NUS team found that H2S may have a positive tonic influence on intracellular calcium level.
Said Dr Bian: "These findings strongly suggest that H2S may function as an important neuromodulator facilitating signalling between neurons and microglial cells, and may thus provide a potential therapeutic approach for treatment of neuroinflammation."
Source: National University of Singapore
