Melatonin (MLT) plays a role in preserving bone health, a function that may depend on homeostatic effects on both mature osteoblasts and mesenchymal stem cells (MSCs) of the bone tissue. In this study, these functions of MLT have been investigated in rat bone (femur) and in human adipose MSC (hMSC) during chronic exposure to low‐grade cadmium (Cd) toxicity, a serious public health concern. The in vivo findings demonstrate that MLT protects against Cd‐induced bone metabolism disruption and accumulation of bone marrow adipocytes, a cue of impaired osteogenic potential of skeletal MSC niches. This latter symptom was recapitulated in hMSCs in which Cd toxicity stimulated adipogenic differentiation. MLT was found to rescue, at least in part, the osteogenic differentiation properties of these cells. This study reports on a new bone cytoprotection function of MLT pertinent to Cd toxicity and its interfering effect on skeletal MSC differentiation properties that is worth investigating for its possible impact on human bone pathophysiology.
Several animal experimental and clinical studies have shown the effectiveness of melatonin in the treatment of some symptoms of Parkinson's disease (PD). However, the antinociceptive effect of melatonin against pain associated to PD has not been fully investigated. Thus, the present study investigated the possible antiallodynic and antinociceptive effects of acute and chronic melatonin treatments in Parkinsonian model of rats. This model was created by unilateral injection of 6-hydroxydopamine (6-OHDA) into the left medial forebrain bundle (MFB). The electronic von Frey test was used to analyze the antiallodynic effect of melatonin on this PD animal model. In addition, c-Fos immunostaining was also used as a marker of nociception to evaluate the neuronal activity related to the nociception processing. The results showed that unilateral injection of 6-OHDA induced a significant decrease in paw withdrawal threshold in both ipsilateral and contralateral paws, which indicate mechanical allodynia induction. This allodynia was transitorily reversed by apomorphine as a dopamine agonist. Melatonin treatment significantly increased threshold of allodynia. Melatonin administration of both acutely or chronically significantly downregulated the c-Fos expression of neurons in 6-OHDA treated animals. In conclusion, 6-OHDA treatment can induces a bilateral mechanical hypernociception in rats while melatonin treatment produces profound antinociceptive effect. This finding paves the way to use melatonin as an antinociceptive agent for PD clinically.
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