Abstract
Low-power laser irradiation (LPLI) is clinically used to modulate inflammation, proliferation and apoptosis. However, its molecular mechanisms are still not fully understood. This study aimed to describe the effects of LPLI upon inflammatory, apoptotic and proliferation markers in submandibular salivary glands (SMGs) in an experimental model of chronic disorder, 24h after one time irradiation. Diabetes was induced in rats by the injection of streptozotocin. After 29 days, these animals were treated with LPLI in the SMG area, and euthanized 24h after this irradiation. Treatment with LPLI significantly decreased diabetes-induced high mobility group box 1 (HMGB1) and tumor necrosis factor alpha (TNF-α) expression, while enhancing the activation of the transcriptional factor cAMP response element binding (CREB) protein. LPLI also reduced the expression of bax, a mitochondrial apoptotic marker, favoring the cell survival. These findings suggest that LPLI can hamper the state of chronic inflammation and favor homeostasis in diabetic rats SMGs.
Highlights
Photobiomodulation therapy (PBMT) using low-power laser irradiation (LPLI) is a promising treatment for inflammatory disorders and biomodulation processes
Since LPLI-induced effects can be mediated by cyclic adenosine monophosphate [31], we investigated its pathway in diabetic submandibular salivary glands (SMGs)
To further elucidate the potential mechanism of LPLI in biomodulation, we investigated its early effects on the cyclic adenosine monophosphate (cAMP)/cAMP response element binding (CREB) signaling pathway, as well as, upon inflammatory and apoptotic markers in submandibular salivary glands
Summary
Photobiomodulation therapy (PBMT) using low-power laser irradiation (LPLI) is a promising treatment for inflammatory disorders and biomodulation processes. It shows great results in Sjogren syndrome, oral mucositis and rheumatoid arthritis treatment by its effects upon the biomodulation of the inflammation and tissue repair processes [1,2,3]. Diabetes is a disease characterized by chronic hyperglycemia that results in damage in many organs [8]. It increases the formation of advanced glycation end-products (AGEs) [9, 10], activating the receptor for advanced glycation end-products (RAGE) and self-sustaining
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