Rats with a fibromyalgia-like disease showed improvements in spontaneous motor activity and other physical changes associated with the disease after treatment with melatonin, the naturally occurring substance that regulates sleep.
The study titled, “Oral Supplementation of Melatonin Protects against Fibromyalgia-Related Skeletal Muscle Alterations in Reserpine-Induced Myalgia Rats,” was published in the International Journal of Molecular Sciences.
Melatonin is a well-known anti-inflammatory, antioxidant, and analgesic agent. Researchers hypothesized that it also could offer clinical benefits in fibromyalgia.
In the study, 90 rats received reserpine, a drug that induces a fibromyalgia-like disease, and then were treated with different doses of melatonin. The frequency with which rats initiated activity on an exercise wheel was then compared among the groups.
Results showed that treatment with melatonin improved the animals’ motor activity, with an increase in both the number of times rats ran on the exercise wheel and the distance they covered. This indicates that movement-induced pain was lower in these animals.
“Probably, melatonin treatment causes an improvement in rat’s spontaneous running activity because of its antioxidants and anti-inflammatory mechanisms of action,” the researchers wrote. “Although these beneficial effects are potentially related also to analgesic melatonin properties, experimental studies as well as clinical trials in humans have demonstrated that melatonin has an analgesic properties in chronic, acute, inflammatory and neuropathic pain conditions, including fibromyalgia.”
The rats’ gastrocnemius muscles, which are powerful muscles in the back part of the leg, were removed and studied extensively for muscle atrophy. The results showed that melatonin treatment caused a significant increase in muscle weight and in the muscle fibers’ diameter compared to control animals, which were treated with melatonin after receiving reserpine or only with tap water.
Electron microscope analysis of the health of mitochondria, energy-producing organelles in cells, showed that the mitochondria appeared intact in the melatonin-treated group, whereas they were damaged in rats treated only with reserpine.
Researchers also found that the levels of a protein called Nod-like receptor protein 3 (NLRP3) were increased in rats treated with reserpine but not in control animals. The authors suggest that because NLRP3 is known to promote inflammation, oxidative stress (an imbalance in oxygen metabolism), and cell death, it might be an important factor in the progression of fibromyalgic disease. NLRP3 levels were lower in rats treated with melatonin.
“In summary, we suggest that melatonin through its important inhibiting effect against NLRP3 activation together with its known antioxidant, anti-inflammatory and analgesic properties may block the fibromyalgic pathological processes,” the team concluded.
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