Minocycline attenuated rapid eye movement (REM) sleep deprivation-induced liver dysfunction in mice
Context: Sleep deprivation (SD) is a stressor that has been shown to increase the generation of free radicals therefore inducing mild organ injury through oxidative stress. Minocycline is a known antibiotic with anti-inflammatory and anti-apoptotic effects.
Aim: This study evaluated the effect of minocycline on lipid profile parameters and oxidative stress markers caused by rapid eye movement (REM) sleep deprivation in mice.
Settings and Design: A total of 30 Albino mice weighing 22+2g were allotted into five groups of six animals each. Group 1 served as control, Group 2 was sleep deprived, mice in groups 3-5 in addition to being sleep deprived for 72 hrs, received minocycline (25mg/kg), minocycline (50mg/kg), astaxanthin (50mg/kg) respectively. Glucose levels, organ weights, liver enzymes, lipid profile, oxidative stress parameters were assessed thereafter.
Methods and Material: REM sleep deprivation was induced using the multiple platforms over water model.
Statistical analysis used: All data were analysed using one-way ANOVA followed by post-hoc tests. The Graph Pad InStat® Biostatistics software was used to determine the criterion for significance in all tests.
Results: The results showed that sleep deprivation increased levels of pro-oxidants, decreased levels of antioxidants but increased glucose and triglyceride levels. It also decreased high-density lipoproteins, liver enzyme activity and bilirubin. Conversely, these effects were significantly attenuated by minocycline as well as astaxanthin.
Conclusions: In summary, REM sleep deprivation produced hepatotoxic alterations in sleep deprived mice and these alterations were reversed by minocycline.
Key-words: Sleep deprivation, Minocycline, Oxidative stress, Hepatic function