Antidepressant-like and anxiolytic-like effects of hydrogen sulfide in streptozotocin-induced diabetic rats through inhibition of hippocampal oxidative stress. Issue 5 (August 2015)

• Record Type: Journal Article
• Authors: Tang, Zhuo-Jun; Zou, Wei; Yuan, Juan; Zhang, Ping; Tian, Ying; Xiao, Zhi-Fang; Li, Mang-Hong; Wei, Hai-Jun; Tang, Xiao-Qing
• Is Part Of: Behavioural pharmacology. Volume 26:Issue 5(2015)
• Publication Date: 2015-08
• Subjects: anxiety -- depression -- diabetes -- hydrogen sulfide -- oxidative stress -- rat -- streptozotocin; Psychopharmacology -- Periodicals; Nervous System -- drug effects -- Periodicals; Behavior -- drug effects -- Periodicals; 615.78
• DOI: 10.1097/FBP.0000000000000143
• Languages: English
• ISSNs: 0955-8810

Abstract

Abstract : Depression is highly prevalent in individuals with diabetes, and depressive symptoms are less responsive to current antidepressant therapies. Oxidative stress plays a major role both in the pathogenesis of diabetes and in major depression and anxiety disorders. Hydrogen sulfide (H2 S), the third gaseous mediator, is a novel signaling molecule in the brain that has both antioxidative activity and antidepressant-like and anxiolytic-like effects. We hypothesized that H2 S could produce antidepressant-like and anxiolytic-like effects in diabetic patients through its antioxidative effect. To test this hypothesis, we generated streptozotocin (STZ)-induced diabetic rats. We found that H2 S alleviated depressive-like behaviors of STZ-induced diabetic rats in the forced swimming and tail suspension tests and reduced their anxiety-like behaviors in the elevated plus maze test. We also found that H2 S significantly reduced levels of malondialdehyde and 4-hydroxynonenal and elevated levels of superoxide dismutase and reduced glutathione in the hippocampus of STZ-induced diabetic rats. The results provide evidence for antidepressant-like and anxiolytic-like effects of H2 S in STZ-induced diabetic rats and suggest that the therapeutic effects may result from inhibition of hippocampal oxidative stress. These findings suggest that elevating H2 S signaling is a potential target for treatment of depressive and anxiety disorders related to diabetes.