PMID- 22898621
OWN - NLM
STAT- MEDLINE
DCOM- 20130617
LR  - 20211021
IS  - 1742-2094 (Electronic)
IS  - 1742-2094 (Linking)
VI  - 9
DP  - 2012 Aug 17
TI  - Hydrogen sulfide attenuates spatial memory impairment and hippocampal 
      neuroinflammation in beta-amyloid rat model of Alzheimer's disease.
PG  - 202
AB  - BACKGROUND: Endogenously produced hydrogen sulfide (H(2)S) may have multiple 
      functions in brain. An increasing number of studies have demonstrated its 
      anti-inflammatory effects. In the present study, we investigated the effect of 
      sodium hydrosulfide (NaHS, a H(2)S donor) on cognitive impairment and 
      neuroinflammatory changes induced by injections of Amyloid-beta(1-40) (Abeta(1-40)), 
      and explored possible mechanisms of action. METHODS: We injected Abeta(1-40) into 
      the hippocampus of rats to mimic rat model of Alzheimer's disease (AD). Morris 
      water maze was used to detect the cognitive function. Terminal deoxynucleotidyl 
      transferase-mediated dUTP nick end labeling (TUNEL) assay was performed to detect 
      neuronal apoptosis. Immunohistochemistry analyzed the response of glia. The 
      expression of interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha was measured 
      by enzyme-linked immunosorbent assay (ELISA) and quantitative real-time 
      polymerase chain reaction (qRT-PCR). The expression of Abeta(1-40), phospho-p38 
      mitogen-activated protein kinase (MAPK), phospho-p65 Nuclear factor (NF)-kappaB, and 
      phospho-c-Jun N-terminal Kinase (JNK) was analyzed by western blot. RESULTS: We 
      demonstrated that pretreatment with NaHS ameliorated learning and memory deficits 
      in an Abeta(1-40) rat model of AD. NaHS treatment suppressed Abeta(1-40)-induced 
      apoptosis in the CA1 subfield of the hippocampus. Moreover, the over-expression 
      in IL-1beta and TNF-alpha as well as the extensive astrogliosis and microgliosis in the 
      hippocampus induced by Abeta(1-40) were significantly reduced following 
      administration of NaHS. Concomitantly, treatment with NaHS alleviated the levels 
      of p38 MAPK and p65 NF-kappaB phosphorylation but not JNK phosphorylation that 
      occurred in the Abeta(1-40)-injected hippocampus. CONCLUSIONS: These results 
      indicate that NaHS could significantly ameliorate Abeta(1-40)-induced spatial 
      learning and memory impairment, apoptosis, and neuroinflammation at least in part 
      via the inhibition of p38 MAPK and p65 NF-kappaB activity, suggesting that 
      administration of NaHS could provide a therapeutic approach for AD.
FAU - Xuan, Aiguo
AU  - Xuan A
AD  - Department of Anatomy, Guangzhou Medical University, Guangzhou, China. 
      xag2005@sohu.com
FAU - Long, Dahong
AU  - Long D
FAU - Li, Jianhua
AU  - Li J
FAU - Ji, Weidong
AU  - Ji W
FAU - Zhang, Meng
AU  - Zhang M
FAU - Hong, Lepeng
AU  - Hong L
FAU - Liu, Jihong
AU  - Liu J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120817
PL  - England
TA  - J Neuroinflammation
JT  - Journal of neuroinflammation
JID - 101222974
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Peptide Fragments)
RN  - 0 (amyloid beta-protein (1-40))
RN  - YY9FVM7NSN (Hydrogen Sulfide)
SB  - IM
MH  - Alzheimer Disease/chemically induced/pathology/*prevention & control
MH  - Amyloid beta-Peptides/*toxicity
MH  - Animals
MH  - *Disease Models, Animal
MH  - Hippocampus/*drug effects/pathology
MH  - Hydrogen Sulfide/pharmacology/*therapeutic use
MH  - Inflammation/chemically induced/pathology/prevention & control
MH  - Male
MH  - Memory Disorders/chemically induced/pathology/*prevention & control
MH  - Peptide Fragments/*toxicity
MH  - Random Allocation
MH  - Rats
MH  - Rats, Wistar
MH  - Spatial Behavior/drug effects
PMC - PMC3458984
EDAT- 2012/08/18 06:00
MHDA- 2013/06/19 06:00
PMCR- 2012/08/17
CRDT- 2012/08/18 06:00
PHST- 2012/05/08 00:00 [received]
PHST- 2012/08/04 00:00 [accepted]
PHST- 2012/08/18 06:00 [entrez]
PHST- 2012/08/18 06:00 [pubmed]
PHST- 2013/06/19 06:00 [medline]
PHST- 2012/08/17 00:00 [pmc-release]
AID - 1742-2094-9-202 [pii]
AID - 10.1186/1742-2094-9-202 [doi]
PST - epublish
SO  - J Neuroinflammation. 2012 Aug 17;9:202. doi: 10.1186/1742-2094-9-202.