Zhang Xuyan1,2,
Ye Jing Ping3,
Wang Zhongjing1,2,
Ding Sheng1,2,
Li Li1,2,
Yang Fan1,2,
Mao Hong1,2 
For correspondence:- Mao Hong Email: maohong8787@163.com Tel:+862782211468
Accepted: 24 November 2017 Published: 29 December 2017
Citation: Xuyan Z, Ping YJ, Zhongjing W, Sheng D, Li L, Fan Y, et al. Melatonin reverses type 2 diabetes-induced cognitive deficits via attenuation of oxidative/nitrosative stress and NF-κβ-mediated neuroinflammation in rat hippocampus. Trop J Pharm Res 2017; 16(12):2865-2875 doi: 10.4314/tjpr.v16i12.10
© 2017 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..
Purpose: To evaluate the protective effect of melatonin on diabetes-induced cognitive dysfunction.
Methods: Rats were fed a high-fat diet + streptozotocin (HFD + STZ) for 15 weeks to induce type 2 diabetes (HFD + STZ group). At the end of the 15-week induction of diabetes, cognitive function in the diabetic rats was estimated using a Morris water maze and an object recognition task. Next, the diabetic rats were treated with melatonin (10 mg/ kg, po) for 3 weeks. Thereafter, cognitive function was re-evaluated in the melatonin-treated diabetic rats (melatonin group).
Results: There was a significant (p < 0.01) decrease in the serum glucose and insulin in melatonin-treated diabetes type 2 rats compared with that of diabetes type 2 rats exposed to only HFD + STZ. Treatment with melatonin (10 mg/kg, po) for 3 weeks in diabetic type 2 rats also caused a significant increase (p < 0.01) in the time spent in the target quadrant and preference index in diabetic rats compared with the HFD + STZ group. There were significant decreases in reactive oxygen species (ROS), oxido-nitrosative stress markers, including thiobarbituric acid reactive substances (TBARS), nitrite, and depleted glutathione (GSH) level in the hippocampus of melatonin-treated group, compared with the HFD + STZ-treated group. Moreover, the melatonin-treated group showed significant inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and reduction in the levels of proinflammatory cytokines.
Conclusion: The results demonstrate that melatonin prevents cognitive dysfunction in type 2 diabetic rats by attenuating oxido-nitrosative stress and NF-κB-mediated neuroinflammation. This effect suggests that melatonin may be useful for the management of cognitive dysfunction in patients suffering from diabetes
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