title: The Effects of Low-Power Laser Irradiation on Inflammation and Apoptosis in Submandibular Glands of Diabetes-Induced Rats.
abstract: Diabetes can lead to dysfunction of the secretory capacity in salivary glands. Activation of the receptor for advanced glycation end products (RAGE) and its ligands has been suggested to participate in chronic disorders such as diabetes and its complications. In this study, the expression of RAGE, high mobility group box 1 (HMGB1) and advanced glycation end products (AGE), as well as the effects of low-power laser irradiation (LPLI) in salivary glands of diabetic rats were evaluated, and the mechanisms involved were characterized. The expression of RAGE and HMGB1 at the protein and mRNA levels was observed in submandibular glands (SMGs) of streptozotocin-induced diabetic rats. A diode laser was applied at 660 nm, 70 mW, 20 J/cm2, 0.56 J/point, with a spot area of 0.028 cm2 and its in vivo effects and the pathways involved were evaluated. Immunohistochemistry and western blotting analysis were performed for inflammatory and apoptosis markers. Diabetes up-regulates HMGB1/AGE/RAGE axis gene expression in SMGs that is associated with activation of the nuclear factor kappa B (NF-κB) pathway. Interestingly, LPLI suppresses NF-κB activation induced by inflammation. LPLI also reduces diabetes-induced apoptosis. That effect was accompanied by decreased levels of Bax, and cleaved caspase 3, which were up-regulated in diabetes. Taken together, our data suggest that LPLI reduces diabetes-induced inflammation by reducing the induction of HMGB1, ultimately leading to inhibition of apoptosis in submandibular glands of diabetic rats.
authors.affiliation: Department of Biomaterials and Oral Biology, São Paulo University, School of Dentistry, São Paulo, Brazil.
authors.forename: Cíntia Yuki
authors.initials: CY
authors.lastname: Fukuoka
authors.affiliation: Department of Biomaterials and Oral Biology, São Paulo University, School of Dentistry, São Paulo, Brazil.
authors.forename: Alyne
authors.initials: A
authors.lastname: Simões
authors.affiliation: Department of Social Dentistry (Medical Informatics), Nihon University School of Dentistry at Matsudo, Matsudo, Chiba, Japan.
authors.forename: Toshikazu
authors.initials: T
authors.lastname: Uchiyama
authors.affiliation: Department of Biomaterials and Oral Biology, São Paulo University, School of Dentistry, São Paulo, Brazil.
authors.forename: Victor Elias
authors.initials: VE
authors.lastname: Arana-Chavez
authors.affiliation: Department of Biochemistry and Molecular Biology, Nihon University School of Dentistry at Matsudo, Matsudo, Chiba, Japan.
authors.forename: Yoshimitsu
authors.initials: Y
authors.lastname: Abiko
authors.affiliation: Research Institute of Oral Science, Nihon University School of Dentistry at Matsudo, Matsudo, Chiba, Japan.
authors.forename: Noboru
authors.initials: N
authors.lastname: Kuboyama
authors.affiliation: Department of Biochemistry and Molecular Biology, Nihon University School of Dentistry at Matsudo, Matsudo, Chiba, Japan.
authors.forename: Ujjal K
authors.initials: UK
authors.lastname: Bhawal
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000528:radiation effects; D003921:Diabetes Mellitus, Experimental / Q000150:complications* / Q000473:pathology; D005260:Female; D017127:Glycation End Products, Advanced / Q000378:metabolism; D024243:HMGB1 Protein / Q000378:metabolism; D028022:Low-Level Light Therapy; D051381:Rats; D017208:Rats, Wistar; D000067759:Receptor for Advanced Glycation End Products / Q000378:metabolism; D012793:Sialadenitis / Q000378:metabolism / Q000473:pathology / Q000532:radiotherapy*; D013363:Submandibular Gland / Q000473:pathology / Q000528:radiation effects*
chemical_list: C000593874:Ager protein, rat; D017127:Glycation End Products, Advanced; D024243:HMGB1 Protein; C104200:Hbp1 protein, rat; D000067759:Receptor for Advanced Glycation End Products