Journal
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR
Volume 96, Issue 1, Pages 52-58Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pbb.2010.04.006
Keywords
H2S; LPS; Alzheimer's disease; Cognitive impairment; TNF-alpha; NF-kappa B
Funding
- National Natural Science foundation of China [30888002]
- National Basic Research Program of China (973 Program) [2010CB912600]
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The present study investigated the effect of sodium hydrosulfide (NaHS), a H2S donor, on cognitive impairment and neuroinflammatory changes induced by bilateral intracerebroventricular injections of LPS at a dose of 10 mu g/rat. Rats received 5 mg/kg NaHS or volume-matched vehicle administration by intraperitoneal injection 3 days before LPS injection then for 9 days once daily. Morris water maze was used to detect the cognitive function. Compared to the sham-treated rats, LPS injection significantly prolonged the mean escape latency in the navigation test (P<0.05) and shortened the adjusted escape latency by approximately 30% (P<0.05). Meanwhile, LPS injection decreased H2S level but increased pro-inflammatory mediators (i.e., TNF-alpha, TNFR1, degradation of I kappa B-alpha and thereafter activation of NF-kappa B) in hippocampus. However, these effects of LPS were significantly ameliorated with NaHS treatment (P<0.05 vs vehicle-treated group). The present data suggest that H2S attenuates LPS-induced cognitive impairment through reducing the overproduction of pro-inflammatory mediators via inhibition of NF-kappa B pathways in rats. This study sets the stage for exploring a novel H2S releasing agent for preventing or retarding the development or progression of neurological disorders such as Alzheimer's disease. (C) 2010 Elsevier Inc. All rights reserved.
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