| Objective:The aim of the present study was to observe changes in the temporomandibular joint (TMJ) of rats that had been subjected to chronic sleep restriction and to investigate whether Akt, Bad and Caspase3 play a role in the mechanism underlying the changes.Methods:One hundred and eighty male Wistar rats were randomly divided into three groups (n= 60 in each):cage control group, large-platform control group, and sleep restriction group. Each group was divided into three subgroups (n= 20 in each) of three different time points (7,14 and 21 days), respectively. The modified multiple platform method was used to induce chronic sleep restriction. Open field test (OFT) was performed, and the serum levels of corticosterone (CORT) andadrenocorticotropic hormone (ACTH) were tested to assess the mental status of rats. The TMJ tissue histology was studied by staining with haematoxylin and eosin. The expression of Akt, p-Aktser473, Bad, p-Badserl36 and Caspase3 proteins was detected by immunohistochernistry and western blotting. The expression of Akt, Bad and Caspase3 mRNAs was measured by real-time quantitative polymerase chain reaction (RT-qPCR).Results:Compared with the CON group, the crossing scores and rearing scores of CSR group rats in the open field were larger (p<0.05). The serum CORT and ACTH levels of the CSR group were significantly elevated (P<0.05).Compared with the large-platform and cage control groups, condylar cartilage pathological alterations were found in the sleep restriction group. There were significantly decreased expression levels of Akt, p-Aktser473 and p-Badser136 and significantly increased expression levels of Bad and Caspase3 after sleep restriction.Conclusion:These data suggest that sleep restriction may induce pathological alterations in the condylar cartilage of rats. Alterations in Akt, Bad and Caspase3 may be associated with the potential mechanism by which chronic sleep restriction influences the condylar cartilage. |
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