Hydrogen sulfide suppresses homocysteine-induced glial activation and inflammatory response
Nitric Oxide, ISSN: 1089-8603, Vol: 90, Page: 15-28
2019
- 44Citations
- 37Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations44
- Citation Indexes44
- 44
- CrossRef31
- Captures37
- Readers37
- 37
Article Description
Neuro-inflammation plays a critical role in hyperhomocysteinemia (HHcy)-associated neurodegenerative disorders. Hydrogen sulfide (H 2 S) has been suggested as an endogenous neuromodulator and potent anti-inflammatory molecule. In present study, we have investigated the effect of NaHS supplementation (a H 2 S source) on inflammatory response in animals subjected to HHcy. NaHS adminstration restored the decreased levels of H 2 S and polysulfides with a concomitant increase in the activity of cystathionase (CSE) and cystathionine β‐synthase (CBS) in the brain regions of HHcy animals. NaHS supplementation reduced the expression of glial fibrillary acidic protein (GFAP) and ionized calcium binding adaptor molecule 1 (Iba1) suggesting attenuation of astrocyte and microglia activation in HHcy animals. Tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1) were decreased in the cortex and hippocampus of HHcy animals following NaHS supplementation. Moreover, NaHS supplementation also decreased the TNF-α, IL-6 and MCP-1 in the serum of HHcy animals. NaHS supplementation reduced nitrite levels, 3-nitrotyrosine (3-NT) modified proteins and inducible nitric oxide synthase (iNOS) in the cortex and hippocampus of HHcy animals. However, NaHS administration increased endothelial nitric oxide synthase (eNOS) expression in brain regions of Hcy treated animals. Expression of platelet endothelial cell adhesion molecule (PECAM) was decreased in the microvessels from HHcy animals supplemented with NaHS. Furthermore, HHcy-induced memory deficits assessed by Morris water maze and novel object recognition test were reversed by NaHS administration. Taken together, the findings suggest that NaHS supplementation ameliorates Hcy-induced glia mediated inflammatory response and cognitive deficits. Therefore, H 2 S may be a novel therapeutic molecule to treat HHcy associated neurological disorders and neuro-inflammatory conditions.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S1089860318303690; http://dx.doi.org/10.1016/j.niox.2019.05.008; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85067025528&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/31146011; https://linkinghub.elsevier.com/retrieve/pii/S1089860318303690; https://dx.doi.org/10.1016/j.niox.2019.05.008
Elsevier BV
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