Early effect of laser irradiation in signaling pathways of diabetic rat submandibular salivary glands

Cíntia Yuki Fukuoka; Hugo Passos Vicari; Carla Renata Sipert; Ujjal Kumar Bhawal; Yoshimitsu Abiko; Victor Elias Arana-Chavez; Alyne Simões

doi:10.1371/journal.pone.0236727

Early effect of laser irradiation in signaling pathways of diabetic rat submandibular salivary glands

PLoS One. 2020 Aug 4;15(8):e0236727. doi: 10.1371/journal.pone.0236727. eCollection 2020.

Authors

Cíntia Yuki Fukuoka¹, Hugo Passos Vicari¹, Carla Renata Sipert², Ujjal Kumar Bhawal³, Yoshimitsu Abiko³, Victor Elias Arana-Chavez¹, Alyne Simões¹

Affiliations

¹ Laboratory of Oral Biology, Department of Biomaterials and Oral Biology, School of Dentistry, University of São Paulo, São Paulo, Brazil.
² Division of Endodontics, Department of Restorative Dentistry, School of Dentistry, University of São Paulo, São Paulo, Brazil.
³ Department of Biochemistry and Molecular Biology, Nihon University School of Dentistry at Matsudo, Matsudo, Chiba, Japan.

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.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Animals
Apoptosis
Cyclic AMP / metabolism
Cyclic AMP Response Element-Binding Protein / metabolism
Diabetes Mellitus, Experimental / radiotherapy*
Female
HMGB1 Protein / genetics
HMGB1 Protein / metabolism
Low-Level Light Therapy*
Mitogen-Activated Protein Kinases / metabolism
NF-kappa B / metabolism
Phosphorylation
RNA, Messenger / metabolism
Rats
Rats, Wistar
Signal Transduction / radiation effects*
Submandibular Gland / radiation effects*
Tumor Necrosis Factor-alpha / metabolism

Substances

Creb1 protein, rat
Cyclic AMP Response Element-Binding Protein
HMGB1 Protein
Hbp1 protein, rat
NF-kappa B
RNA, Messenger
Tumor Necrosis Factor-alpha
Cyclic AMP
Mitogen-Activated Protein Kinases

Grants and funding

The authors wish to express their gratitude to the Brazilian Federal Agency for Support and Evaluation of Graduate Education - CAPES, scholarship process BEX 18807/12-7, PNPD 20131614-33002010141P2 and grants nº 2014/21214-1 and 2020/09547-6, Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP). This work was also supported by Grants-in-Aid from the Ministry of Education, Culture, Sports, Science and Technology of Japan.