| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2013493 | Pharmacology Biochemistry and Behavior | 2010 | 7 Pages |
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 μg/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-α, TNFR1, degradation of IκB-α and thereafter activation of NF-κB) 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-κB 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.
