PMID- 30206943
OWN - NLM
STAT- MEDLINE
DCOM- 20200120
LR  - 20200120
IS  - 1097-4652 (Electronic)
IS  - 0021-9541 (Linking)
VI  - 234
IP  - 3
DP  - 2019 Mar
TI  - Cerebroprotective effects of hydrogen sulfide in homocysteine-induced 
      neurovascular permeability: Involvement of oxidative stress, arginase, and matrix 
      metalloproteinase-9.
PG  - 3007-3019
LID - 10.1002/jcp.27120 [doi]
AB  - An elevated level of homocysteine (Hcy) leads to hyperhomocysteinemia (HHcy), 
      which results in vascular dysfunction and pathological conditions identical to 
      stroke symptoms. Hcy increases oxidative stress and leads to increase in 
      blood-brain barrier permeability and leakage. Hydrogen sulfide (H(2) S) 
      production during the metabolism of Hcy has a cerebroprotective effect, although 
      its effectiveness in Hcy-induced neurodegeneration and neurovascular permeability 
      is less explored. Therefore, the current study was designed to perceive the 
      neuroprotective effect of exogenous H (2) S against HHcy, a cause of 
      neurodegeneration. To test this hypothesis, we used four groups of mice: control, 
      Hcy, control + sodium hydrosulfide hydrate (NaHS), and Hcy + NaHS, and an HHcy 
      mice model in Swiss albino mice by giving a dose of 1.8 g of dl-Hcy/L in drinking 
      for 8-10 weeks. Mice that have 30 micromol/L Hcy were taken for the study, and a H 
      (2) S supplementation of 20 mumol/L was given for 8 weeks to all groups of mice. 
      HHcy results in the rise of the levels of superoxide and nitrite, although a 
      concomitant decrease in the level of superoxide dismutase, catalase, glutathione 
      peroxidase, reduced glutathione, and arginase in oxidative stress and a 
      concomitant decrease in the endogenous level of H (2) S. Although H (2) S 
      supplementation ameliorated, the effect of HHcy and the levels of H (2) S 
      returned to the average level in HHcy animals supplemented with H (2) S. 
      Interestingly, H (2) S supplementation ameliorated neurovascular remodeling and 
      neurodegeneration. Thus, our study suggested that H (2) S could be a beneficial 
      therapeutic candidate for the treatment of Hcy-associated neurodegeneration, such 
      as stroke and neurovascular disorders.
CI  - (c) 2018 Wiley Periodicals, Inc.
FAU - Nath, Nibendu
AU  - Nath N
AUID- ORCID: 0000-0003-4169-0581
AD  - Department of LifeScience and Bioinformatics, Assam University, Silchar, India.
FAU - Prasad, Himanshu Kishore
AU  - Prasad HK
AUID- ORCID: 0000-0003-0215-1323
AD  - Department of LifeScience and Bioinformatics, Assam University, Silchar, India.
FAU - Kumar, Munish
AU  - Kumar M
AD  - Department of Biochemistry, University of Allahabad, Allahabad, India.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180912
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Neuroprotective Agents)
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - EC 3.4.24.35 (Matrix Metalloproteinase 9)
RN  - YY9FVM7NSN (Hydrogen Sulfide)
SB  - IM
MH  - Animals
MH  - Blood-Brain Barrier/drug effects
MH  - Cerebrovascular Disorders/chemically induced/*drug therapy/metabolism/pathology
MH  - Disease Models, Animal
MH  - Homocysteine/toxicity
MH  - Humans
MH  - Hydrogen Sulfide/*pharmacology
MH  - Hyperhomocysteinemia/*drug therapy/genetics/metabolism/pathology
MH  - Matrix Metalloproteinase 9/genetics
MH  - Mice
MH  - Nerve Degeneration/chemically induced/*drug therapy/metabolism/pathology
MH  - Neuroprotective Agents/pharmacology
MH  - Oxidative Stress/drug effects
MH  - Permeability/drug effects
MH  - Stroke/drug therapy/metabolism/pathology
OTO - NOTNLM
OT  - MMP-9
OT  - arginase
OT  - blood-brain barrier
OT  - homocysteine
OT  - hydrogen sulfide
OT  - oxidative stress
EDAT- 2018/09/13 06:00
MHDA- 2020/01/21 06:00
CRDT- 2018/09/13 06:00
PHST- 2018/05/16 00:00 [received]
PHST- 2018/07/05 00:00 [accepted]
PHST- 2018/09/13 06:00 [pubmed]
PHST- 2020/01/21 06:00 [medline]
PHST- 2018/09/13 06:00 [entrez]
AID - 10.1002/jcp.27120 [doi]
PST - ppublish
SO  - J Cell Physiol. 2019 Mar;234(3):3007-3019. doi: 10.1002/jcp.27120. Epub 2018 Sep 
      12.