Adiponectin Mediates the Protection of H2S Against Chronic Restraint Stress-Induced Cognitive Impairment via Attenuating Hippocampal Damage

Emerging evidence shows that chronic restraint stress (CRS) can induce cognitive dysfunction, which involves in hippocampal damage. Our recent research reveals that hydrogen sulfide (H 2 S), a novel gasotransmitter, protects against CRS-induced cognitive impairment, but the underlying mechanism rema...

Full description

Saved in:
Bibliographic Details
Published in:Frontiers in behavioral neuroscience 2021-05, Vol.15, p.623644-623644
Main Authors: Tang, Qiong-Yan, Li, Min, Chen, Lei, Jiang, Jia-Mei, Gao, Sheng-Lan, Xiao, Fan, Zou, Wei, Zhang, Ping, Chen, Yong-Jun
Format: Article
Language:English
Subjects:
Adipocytes
Adiponectin
Alzheimer's disease
Apoptosis
BAX protein
Bcl-2 protein
Caspase-12
CCAAT/enhancer-binding protein
chronic restraint stress
Cognitive ability
cognitive impairment
Endoplasmic reticulum
Enzymes
Experiments
Glutathione
hippocampal damage
Hippocampus
Hydrogen sulfide
Laboratory animals
Life sciences
Malondialdehyde
Memory
Neurogenesis
Neuroprotection
Neuroscience
Oxidative stress
Pattern recognition
Physiology
Stainless steel
Superoxide dismutase
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Emerging evidence shows that chronic restraint stress (CRS) can induce cognitive dysfunction, which involves in hippocampal damage. Our recent research reveals that hydrogen sulfide (H 2 S), a novel gasotransmitter, protects against CRS-induced cognitive impairment, but the underlying mechanism remains unclear. Adiponectin, the most abundant plasma adipokine, has been shown to elicit neuroprotective property and attenuate cognitive impairment. Hence, the present work was aimed to explore whether adiponectin mediates the protective effect of H 2 S on CRS-induced cognitive impairment by inhibiting hippocampal damage. Results found that administration of Anti-Acrp30, a neutralizing antibody of adiponectin, obviously reverses sodium hydrosulfide (NaHS, an exogenous H 2 S donor)-induced the inhibition on CRS-induced cognitive impairment according to Y-maze test, Novel object recognition (NOR) test, and Morris water maze (MWM) test. In addition, Anti-Acrp30 blocked the protective effect of NaHS on hippocampal apoptosis in rats-subjected with CRS as evidenced by the pathological changes in hippocampus tissues in hematoxylin and eosin (HE) staining and the increases in the amount of the condensed and stained to yellowish-brown or brownish yellow neuron nucleuses in terminal deoxynucleotidyl transferase transfer-mediated dUTP nick end-labeling (TUNEL) staining as well as the expression of hippocampal pro-apoptotic protein (Bax), and a decrease in the expression of hippocampal anti-apoptotic protein (Bcl-2). Furthermore, Anti-Acrp30 mitigated the inhibitory effect of NaHS on CRS-induced oxidative stress as illustrated by the up-regulation of malondialdehyde (MDA) content and the down-regulation of superoxide dismutase (SOD) activity and glutathione (GSH) level in the hippocampus. Moreover, Anti-Acrp30 eliminated NaHS-induced the reduction of endoplasmic reticulum (ER) stress-related proteins including binding immunoglobulin protein (BIP), C/EBP homologous protein (CHOP), and Cleaved Caspase-12 expressions in the hippocampus of rats-exposed to CRS. Taken together, these results indicated that adiponectin mediates the protection of H 2 S against CRS-induced cognitive impairment through ameliorating hippocampal damage.
ISSN:1662-5153
1662-5153
DOI:10.3389/fnbeh.2021.623644