PMID- 31146011
OWN - NLM
STAT- MEDLINE
DCOM- 20200504
LR  - 20200505
IS  - 1089-8611 (Electronic)
IS  - 1089-8603 (Linking)
VI  - 90
DP  - 2019 Sep 1
TI  - Hydrogen sulfide suppresses homocysteine-induced glial activation and 
      inflammatory response.
PG  - 15-28
LID - S1089-8603(18)30369-0 [pii]
LID - 10.1016/j.niox.2019.05.008 [doi]
AB  - 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 
      beta-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-alpha), 
      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-alpha, 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.
CI  - Copyright (c) 2019 Elsevier Inc. All rights reserved.
FAU - Kumar, Mohit
AU  - Kumar M
AD  - Department of Biochemistry, Basic Medical Science Block-II, Panjab University, 
      Chandigarh, 160014, India.
FAU - Sandhir, Rajat
AU  - Sandhir R
AD  - Department of Biochemistry, Basic Medical Science Block-II, Panjab University, 
      Chandigarh, 160014, India. Electronic address: sandhir@pu.ac.in.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190528
PL  - United States
TA  - Nitric Oxide
JT  - Nitric oxide : biology and chemistry
JID - 9709307
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - YY9FVM7NSN (Hydrogen Sulfide)
SB  - IM
MH  - Animals
MH  - Homocysteine/*antagonists & inhibitors/pharmacology
MH  - Hydrogen Sulfide/*pharmacology
MH  - Inflammation/*drug therapy/metabolism
MH  - Male
MH  - Neuroglia/*drug effects/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
OTO - NOTNLM
OT  - Astrocytes
OT  - Glia
OT  - Homocysteine
OT  - Hydrogen sulfide
OT  - Inflammation
OT  - Memory
EDAT- 2019/05/31 06:00
MHDA- 2020/05/06 06:00
CRDT- 2019/05/31 06:00
PHST- 2018/12/17 00:00 [received]
PHST- 2019/04/30 00:00 [revised]
PHST- 2019/05/26 00:00 [accepted]
PHST- 2019/05/31 06:00 [pubmed]
PHST- 2020/05/06 06:00 [medline]
PHST- 2019/05/31 06:00 [entrez]
AID - S1089-8603(18)30369-0 [pii]
AID - 10.1016/j.niox.2019.05.008 [doi]
PST - ppublish
SO  - Nitric Oxide. 2019 Sep 1;90:15-28. doi: 10.1016/j.niox.2019.05.008. Epub 2019 May 
      28.