Melatonin attenuates diabetes-induced oxidative stress in spleen and suppression of splenocyte proliferation in laboratory mice

Abstract

Hyperglycaemic condition induced oxidative stress in diabetic individuals caused oxidative damages of internal organs, including immune organ spleen. We studied the effects of low doses of melatonin (25, 50, and 100 µg/100g. B.wt./day) on histoarchitecture, oxidative stress, and splenocyte proliferation in streptozotocin-induced diabetic mice. Melatonin significantly resisted the increase in blood glucose levels and showed a dose-dependent effect on circulatory melatonin, body weight, and relative spleen weight in diabetic mice. Exogenous melatonin suppressed the diabetes-induced lipid peroxidation and increased the activity of the antioxidant enzymes and antioxidant GSH in the spleen tissue of diabetic mice in a dose-dependent manner. Melatonin improved the reactivity of Nrf-2 and HO-1 in the spleen of diabetic mice. Melatonin treatment normalised the splenic cellularity and increased the splenocyte proliferation in a dose-dependent manner. The present study may suggest the dose-dependent effect of melatonin in attenuation of oxidative stress and suppression of splenocyte proliferation in diabetic mice.

Keywords:

• Melatonin
• oxidative stress
• antioxidant enzymes
• splenocyte proliferation
• diabetes

Disclosure statement

No potential conflict of interest was reported by the author(s).

Acknowledgements

The authors thank DST-FIST, New Delhi for providing the infrastructural facility to the Department and establishment of State Biotech Hub, and Tripura University for extending help.

Additional information

Funding

The work was supported by University Grants Commission New Delhi [39–652/2010 (SR)] and Council of Scientific and Industrial Research, New Delhi [37 (1514)/11/EMR-II].