The Effects of Low-Power Laser Irradiation on Inflammation and Apoptosis in Submandibular Glands of Diabetes-Induced Rats
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, h...
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| description | 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. |
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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.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0169443</identifier><identifier>PMID: 28099448</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Activation ; Advanced glycosylation end products ; Animals ; Apoptosis ; Apoptosis - radiation effects ; BAX protein ; Biochemistry ; Biology and Life Sciences ; Biomedical materials ; Care and treatment ; Caspase ; Caspase-3 ; Cell growth ; Complications ; Dentistry ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Experimental - complications ; Diabetes Mellitus, Experimental - pathology ; Engineering and Technology ; Exocrine glands ; Female ; Gene expression ; Glands ; Glycation End Products, Advanced - metabolism ; Glycosylation ; Health aspects ; HMGB1 protein ; HMGB1 Protein - metabolism ; Homeostasis ; Hyperglycemia ; Immunohistochemistry ; Inflammation ; Irradiation ; Lasers ; Ligands ; Low-Level Light Therapy ; Medical lasers ; Medicine and Health Sciences ; Molecular biology ; NF-κB protein ; Oxidative stress ; Rats ; Rats, Wistar ; Receptor for Advanced Glycation End Products - metabolism ; Research and Analysis Methods ; Rodents ; Salivary glands ; Sialadenitis - metabolism ; Sialadenitis - pathology ; Sialadenitis - radiotherapy ; Signal transduction ; Streptozocin ; Submandibular gland ; Submandibular Gland - pathology ; Submandibular Gland - radiation effects ; Transcription factors ; Western blotting</subject><ispartof>PloS one, 2017-01, Vol.12 (1), p.e0169443</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Fukuoka et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2017 Fukuoka et al 2017 Fukuoka et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c725t-52af8799e02ad440dd85466ef3cc8a871835fced2a59dbbfdb4b57c50ca50d4e3</citedby><cites>FETCH-LOGICAL-c725t-52af8799e02ad440dd85466ef3cc8a871835fced2a59dbbfdb4b57c50ca50d4e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5242424/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5242424/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28099448$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fukuoka, Cíntia Yuki</creatorcontrib><creatorcontrib>Simões, Alyne</creatorcontrib><creatorcontrib>Uchiyama, Toshikazu</creatorcontrib><creatorcontrib>Arana-Chavez, Victor Elias</creatorcontrib><creatorcontrib>Abiko, Yoshimitsu</creatorcontrib><creatorcontrib>Kuboyama, Noboru</creatorcontrib><creatorcontrib>Bhawal, Ujjal K</creatorcontrib><title>The Effects of Low-Power Laser Irradiation on Inflammation and Apoptosis in Submandibular Glands of Diabetes-Induced Rats</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>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.</description><subject>Activation</subject><subject>Advanced glycosylation end products</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - radiation effects</subject><subject>BAX protein</subject><subject>Biochemistry</subject><subject>Biology and Life Sciences</subject><subject>Biomedical materials</subject><subject>Care and treatment</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Cell growth</subject><subject>Complications</subject><subject>Dentistry</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Experimental - complications</subject><subject>Diabetes Mellitus, Experimental - pathology</subject><subject>Engineering and Technology</subject><subject>Exocrine glands</subject><subject>Female</subject><subject>Gene expression</subject><subject>Glands</subject><subject>Glycation End Products, Advanced - metabolism</subject><subject>Glycosylation</subject><subject>Health aspects</subject><subject>HMGB1 protein</subject><subject>HMGB1 Protein - metabolism</subject><subject>Homeostasis</subject><subject>Hyperglycemia</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Irradiation</subject><subject>Lasers</subject><subject>Ligands</subject><subject>Low-Level Light Therapy</subject><subject>Medical lasers</subject><subject>Medicine and Health Sciences</subject><subject>Molecular biology</subject><subject>NF-κB protein</subject><subject>Oxidative stress</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptor for Advanced Glycation End Products - metabolism</subject><subject>Research and Analysis Methods</subject><subject>Rodents</subject><subject>Salivary glands</subject><subject>Sialadenitis - metabolism</subject><subject>Sialadenitis - pathology</subject><subject>Sialadenitis - radiotherapy</subject><subject>Signal transduction</subject><subject>Streptozocin</subject><subject>Submandibular gland</subject><subject>Submandibular Gland - 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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.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28099448</pmid><doi>10.1371/journal.pone.0169443</doi><tpages>e0169443</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 1932-6203 1932-6203 |
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| recordid | cdi_plos_journals_1859788259 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; PMC (PubMed Central); DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; Free Full-Text Journals in Chemistry |
| subjects | Activation Advanced glycosylation end products Animals Apoptosis Apoptosis - radiation effects BAX protein Biochemistry Biology and Life Sciences Biomedical materials Care and treatment Caspase Caspase-3 Cell growth Complications Dentistry Diabetes Diabetes mellitus Diabetes Mellitus, Experimental - complications Diabetes Mellitus, Experimental - pathology Engineering and Technology Exocrine glands Female Gene expression Glands Glycation End Products, Advanced - metabolism Glycosylation Health aspects HMGB1 protein HMGB1 Protein - metabolism Homeostasis Hyperglycemia Immunohistochemistry Inflammation Irradiation Lasers Ligands Low-Level Light Therapy Medical lasers Medicine and Health Sciences Molecular biology NF-κB protein Oxidative stress Rats Rats, Wistar Receptor for Advanced Glycation End Products - metabolism Research and Analysis Methods Rodents Salivary glands Sialadenitis - metabolism Sialadenitis - pathology Sialadenitis - radiotherapy Signal transduction Streptozocin Submandibular gland Submandibular Gland - pathology Submandibular Gland - radiation effects Transcription factors Western blotting |
| title | The Effects of Low-Power Laser Irradiation on Inflammation and Apoptosis in Submandibular Glands of Diabetes-Induced Rats |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-01T13%3A04%3A10IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20Effects%20of%20Low-Power%20Laser%20Irradiation%20on%20Inflammation%20and%20Apoptosis%20in%20Submandibular%20Glands%20of%20Diabetes-Induced%20Rats&rft.jtitle=PloS%20one&rft.au=Fukuoka,%20C%C3%ADntia%20Yuki&rft.date=2017-01-18&rft.volume=12&rft.issue=1&rft.spage=e0169443&rft.pages=e0169443-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0169443&rft_dat=%3Cgale_plos_%3EA478133190%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1859788259&rft_id=info:pmid/28099448&rft_galeid=A478133190&rft_doaj_id=oai_doaj_org_article_9baf8708920d42b9ad4ca808bad33e0f&rfr_iscdi=true |