徳島大学 / 教育研究者総覧 --- 蔵本瞳

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徳島大学 ⟩ 大学院医歯薬学研究部 ⟩ 歯学域 ⟩ 先端歯学教育研究プロジェクト ⟩
徳島大学 ⟩ 大学院医歯薬学研究部 ⟩ 歯学域 ⟩ 口腔科学部門 ⟩ 臨床歯学系 ⟩ 小児歯科学 ⟩
徳島大学 ⟩ 病院 ⟩ 診療科 ⟩ 小児歯科 ⟩
徳島大学 ⟩ 歯学部 ⟩ 歯学科 ⟩ 発達育成系臨床歯学講座 ⟩ 小児歯科学 ⟩

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研究活動

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専門分野

○	歯科保存学

研究テーマ

○	歯髄炎の病態解析と新規歯髄保護療法の開発

著書・論文

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学術論文(審査論文):

1.	Ikuko Hosokawa, Hitomi Kuramoto, Yoshitaka Hosokawa and Keiichi Hosaka : Tooth Bleaching to Bring out the Patients Smile -Initiatives in Department of Cariology at Tokushima University Hospital-, Journal of Oral Health and Biosciences, 37, 2, 32-37, 2025. (要約) In recent years, in our super-aged society, where people are striving for health and longevity, aesthetic awareness and interest in the oral cavity are increasing among men and women of all ages and both sexes. In particular, the number of patients requesting tooth bleaching procedures for discolored teeth has been increasing. Tooth bleaching is a minimally invasive esthetic dentistry that can make patients smile. To meet the needs of these patients, Department of Cariology at the University of Tokushima Hospital has reestablished a system for patients to receive tooth bleaching treatment for discolored teeth. Therefore, we would like to report on the bleaching procedures we are performing at our department. (キーワード) tooth bleaching / patient's smile / tooth sensitivity / tooth coloration (徳島大学機関リポジトリ) ● Metadata: 2012983 (出版サイトへのリンク) ● Publication site (DOI): 10.20738/johb.37.2_32 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390866570018334592 ● Search Scopus @ Elsevier (DOI): 10.20738/johb.37.2_32 (徳島大学機関リポジトリ: 2012983, DOI: 10.20738/johb.37.2_32, CiNii: 1390866570018334592)
2.	Katsuhiro Mieda, Tadashi Nakanishi, Hitomi Kuramoto, Yoshitaka Hosokawa, Ikuko Hosokawa, Daisuke Takegawa and Keiichi Hosaka : Sudachitin reduces inflammatory mediator expression in toll-like receptor 2 ligand-stimulated human dental pulp cells, Cell Biochemistry and Biophysics, 2025. (要約) Sudachitin, which is a polymethoxy flavonoid derived from the peer of Citrus sudachi, has several biological properties. However, the effect of sudachitin on human dental pulp cells (HDPCs) remains unclear. The aim of this study was to investigate whether sudachitin could decrease the expression of inflammatory mediators such as cytokines and prostaglandin in HDPCs stimulated with Pam3CSK4, a ligand for toll-like receptor (TLR) 2. HDPCs were pre-incubated with different concentrations of sudachitin (6.25, 12.5, 25, or 50 μM) and stimulated with Pam3CSK4 (100 ng/mL). The quantification of inflammatory cytokines (interleukin (IL)-6, IL-8, and C-X-C motif chemokine ligand (CXCL) 10) and prostaglandin E (PGE) were performed by enzyme-linked immunosorbent assay (ELISA). The expression of cyclooxygenase (COX)-2, a key enzyme for PGE formation, was analyzed by western blot. Moreover, the activations of cell signal pathways were examined by western blot analysis. Sudachitin suppressed IL-6, IL-8, CXCL10, and PGE production and COX-2 protein expression in Pam3CSK4-stimulated HDPCs. In addition, we revealed that nuclear factor-kappa B (NF-κB) and protein kinase B (Akt) pathways in the Pam3CSK4-stimulated HDPCs were inhibited by sudachitin treatment. These findings suggest that sudachitin can reduce inflammatory mediator production in HDPCs stimulated with TLR2 ligand by inhibiting NF-κB and Akt activations. (キーワード) Dental pulp cells / 歯髄炎 (pulpitis) / Sudachitin / Anti-inflammatory / サイトカイン (cytokine) / Prostaglandin E2 (徳島大学機関リポジトリ) ● Metadata: 2013271 (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s12013-024-01652-8 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39739289 ● Search Scopus @ Elsevier (PMID): 39739289 ● Search Scopus @ Elsevier (DOI): 10.1007/s12013-024-01652-8 (徳島大学機関リポジトリ: 2013271, DOI: 10.1007/s12013-024-01652-8, PubMed: 39739289)
3.	Hitomi Kuramoto, Tadashi Nakanishi, Hiromichi Yumoto, Daisuke Takegawa, Katsuhiro Mieda and Keiichi Hosaka : Caffeic Acid Phenethyl Ester Enhances Bone Repair-related Factors in MC3T3-E1 Cells., Cell Biochemistry and Biophysics, 2025. (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s12013-024-01644-8 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39708213 ● Search Scopus @ Elsevier (PMID): 39708213 ● Search Scopus @ Elsevier (DOI): 10.1007/s12013-024-01644-8 (DOI: 10.1007/s12013-024-01644-8, PubMed: 39708213)
4.	Tadashi Nakanishi, Katsuhiro Mieda, Hitomi Kuramoto and Daisuke Takegawa : Effect of interleukin-17A on inflammatory mediator production in interleukin-1β-stimulated human dental pulp fibroblasts, European Journal of Oral Sciences, 132, 5, e13019, 2024. (要約) In response to pro-inflammatory cytokines such as interleukin (IL)-1β, dental pulp fibroblasts produce various inflammatory mediators, including IL-6, IL-8, CC chemokine ligand 20 (CCL20), and CXC chemokine ligand 10 (CXCL10), leading to the progression of pulpitis. IL-17/IL-17A (IL-17A) is a pro-inflammatory cytokine secreted by T helper (Th) 17 cells following their recruitment to inflamed sites; however, the roles of IL-17A during pulpitis remain unclear. The purpose of this study was to investigate the effect of IL-17A on IL-6, IL-8, CCL20 and CXCL10 production by human dental pulp fibroblasts (HDPFs) in vitro. IL-17A at a concentration of 100 ng/ml induced the production of 10 times more IL-8 and 4 times more CXCL10, but not IL-6 and CCL20, compared to controls. Co-stimulation of HDPFs with IL-17A and IL-1β synergistically enhanced the production of IL-6, CCL20, IL-8 and CXCL10. IL-1β increased expression of IL-17 receptor/IL-17RA (IL-17R) on HDPFs. Moreover, the cell signal pathways of p38 mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) were more potently activated by simultaneous stimulation with IL-17A and IL-1β. These findings suggest that IL-17A participates in the progression of dental pulp inflammation through the enhanced production of inflammatory mediators in HDPFs. (キーワード) chemokines / cytokines / endodontics / 歯髄炎 (pulpitis) (徳島大学機関リポジトリ) ● Metadata: 2012489 (出版サイトへのリンク) ● Publication site (DOI): 10.1111/eos.13019 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39302740 ● Search Scopus @ Elsevier (PMID): 39302740 ● Search Scopus @ Elsevier (DOI): 10.1111/eos.13019 (徳島大学機関リポジトリ: 2012489, DOI: 10.1111/eos.13019, PubMed: 39302740)
5.	Hitomi Kuramoto, Tadashi Nakanishi, Daisuke Takegawa, MIEDA Katsuhiro and Keiichi Hosaka : Caffeic Acid Phenethyl Ester Induces Vascular Endothelial Growth Factor Production and Inhibits CXCL10 Production in Human Dental Pulp Cells, Current Issues in Molecular Biology, 44, 11, 5691-5699, 2022. (要約) The survival rate of root non-vital teeth is lower than that of vital teeth. Therefore, to preserve the dental pulp is very important. The vascular endothelial growth factor (VEGF) is the most potent angiogenic factor involved in the vitality of dental pulp including reparative dentin formation. Caffeic acid phenethyl ester (CAPE) is a physiologically active substance of propolis and has some bioactivities such as anti-inflammatory effects. However, there are no reports on the effects of CAPE on dental pulp inflammation. In this study, we investigated the effects of CAPE on VEGF and inflammatory cytokine production in human dental pulp cells (HDPCs) to apply CAPE to an ideal dental pulp protective agent. We found that CAPE induced VEGF production from HDPCs. Moreover, CAPE induced the phosphorylation of p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinases (ERK), and stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) in HDPCs. Furthermore, CAPE inhibited C-X-C motif chemokine ligand 10 (CXCL10) production in Pam3CSK4- and tumor necrosis factor-alpha (TNF-α)-stimulated HDPCs. In conclusion, these results suggest that CAPE might be useful as a novel biological material for vital pulp therapy by exerting the effects of VEGF production and anti-inflammatory activities. (キーワード) anti-inflammatory effect / caffeic acid phenethyl ester / dental pulp cells / 歯髄炎 (pulpitis) / 血管内皮増殖因子 (vascular endothelial growth factor) / vital pulp therapy (徳島大学機関リポジトリ) ● Metadata: 2010572 (出版サイトへのリンク) ● Publication site (DOI): 10.3390/cimb44110385 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36421669 ● Search Scopus @ Elsevier (PMID): 36421669 ● Search Scopus @ Elsevier (DOI): 10.3390/cimb44110385 (徳島大学機関リポジトリ: 2010572, DOI: 10.3390/cimb44110385, PubMed: 36421669)
6.	Hitomi Kuramoto, Kouji Hirao, Hiromichi Yumoto, Yuki Hosokawa, Tadashi Nakanishi, Daisuke Takegawa, Ayako Washio, Chiaki Kitamura and Takashi Matsuo : Caffeic acid phenethyl ester (CAPE) induces VEGF expression and production in rat odontoblastic cells, BioMed Research International, Article ID 5390720, 2019. (要約) Caffeic acid phenethyl ester (CAPE), the main component of propolis, has various biological activities including anti-inflammatory effect and wound healing promotion. Odontoblasts located in the outermost layer of dental pulp play crucial roles such as production of growth factors and formation of hard tissue termed reparative dentin in host defense against dental caries. In this study, we investigated the effects of CAPE on the upregulation of vascular endothelial growth factor (VEGF) and calcification activities of odontoblasts, leading to development of novel therapy for dental pulp inflammation caused by dental caries. CAPE significantly induced mRNA expression and production of VEGF in rat clonal odontoblast-like KN-3 cells cultured in normal medium or osteogenic induction medium. CAPE treatment enhanced nuclear factor-kappa B (NF-B) transcription factor activation, and furthermore, the specific inhibitor of NF-B significantly reduced VEGF production. The expression of VEGF receptor- (VEGFR-) 2, not VEGFR-1, was up regulated in KN-3 cells treated with CAPE. In addition, VEGF significantly increased mineralization activity in KN-3 cells. These findings suggest that CAPE might be useful as a novel biological material for the dental pulp conservative therapy. (徳島大学機関リポジトリ) ● Metadata: 2007500 (出版サイトへのリンク) ● Publication site (DOI): 10.1155/2019/5390720 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31930126 ● Summary page in Scopus @ Elsevier: 2-s2.0-85077441042 (徳島大学機関リポジトリ: 2007500, DOI: 10.1155/2019/5390720, PubMed: 31930126, Elsevier: Scopus)
7.	平尾功治, 湯本浩通, 細川由樹, 蔵本瞳, 鷲尾絢子, 中西正, 武川大輔, 北村知昭, 松尾敬志 : ラット象牙芽細胞様細胞 (KN-3) におけるカテキンの抗炎症作用, 日本歯科保存学雑誌, 60, 5, 235-244, 2017年. (出版サイトへのリンク) ● Publication site (DOI): 10.11471/shikahozon.60.235 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390282680498132224 ● Search Scopus @ Elsevier (DOI): 10.11471/shikahozon.60.235 (DOI: 10.11471/shikahozon.60.235, CiNii: 1390282680498132224)

総説・解説:

1.	武川大輔, 米倉和秀, 蔵本瞳, 伊田百美香, 細川由樹, 細川育子, 細川義隆, 菅俊行, 中西正, 保坂啓一 : 2級コンポジットレジン修復のキーポイント, Journal of Oral Health and Biosciences, 36, 1, 8-12, 2023年9月. (キーワード) 歯科医療 (dental care) (徳島大学機関リポジトリ) ● Metadata: 2011365 (出版サイトへのリンク) ● Publication site (DOI): 10.20738/johb.36.1_8 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390016062665364224 ● Search Scopus @ Elsevier (DOI): 10.20738/johb.36.1_8 (徳島大学機関リポジトリ: 2011365, DOI: 10.20738/johb.36.1_8, CiNii: 1390016062665364224)
2.	蔵本瞳, 中西正 : 歯髄炎治療におけるカフェイン酸フェネチルエステル応用の可能性, メディカル・サイエンス・ダイジェスト, 48, 11, 48-49, 2022年10月. (キーワード) 歯髄炎 (pulpitis) / caffeic acid phenethyl ester / 血管内皮増殖因子 (vascular endothelial growth factor) / anti-inflammatory effect / vital pulp therapy
3.	Hiromichi Yumoto, Kouji Hirao, Yuki Hosokawa, Hitomi Kuramoto, Daisuke Takegawa, Tadashi Nakanishi and Takashi Matsuo : The Roles of Odontoblasts in Dental Pulp Innate Immunity, Japanese Dental Science Review, 54, 3, 105-117, Aug. 2018. (要約) Odontoblasts located in the outermost layer of dental pulp form a natural barrier between mineralized tissues, dentin, and soft tissues, dental pulp, of the vital tooth, and they first recognize caries-related pathogens and sense external irritations. Therefore, odontoblasts possess a specialized innate immune system to fight oral pathogens invading into dentin. Generally, the rapid initial sensing of microbial pathogens, especially pathogen-associated molecular patterns (PAMPs) shared by microorganisms, are mediated by pattern recognition receptors (PRRs), such as Toll-like receptor and the nucleotide-binding oligomerization domain (NOD). The innate immune responses in odontoblasts initiated by sensing oral pathogens provide host protective events, such as inflammatory reactions, to produce a variety of pro-inflammatory mediators, including chemokines and cytokines. These attract various inflammatory cells and cause antibacterial reactions, such as the production of defensins, to kill microorganisms in the proximal region of the odontoblast layer. This review focuses on innate immunity, especially cellular and molecular mechanisms regarding the sensing of PAMPs from oral pathogens by PRRs, in odontoblasts and provides information for future studies for the development of novel therapeutic strategies, including diagnosis and treatment, to prevent exceeding dental pulp inflammation and preserve the dental pulp tissues. (徳島大学機関リポジトリ) ● Metadata: 2006103 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.jdsr.2018.03.001 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30128058 ● Summary page in Scopus @ Elsevier: 2-s2.0-85044379499 (徳島大学機関リポジトリ: 2006103, DOI: 10.1016/j.jdsr.2018.03.001, PubMed: 30128058, Elsevier: Scopus)

国際会議:

1.	Hiromichi Yumoto, Kouji Hirao, Yuki Hosokawa, Hitomi Kuramoto, Katsuhiko Hirota, Yoichiro Miyake and Takashi Matsuo : Streptococcal histone-like DNA binding protein induces MINCLE expression on monocytes, 95th General Session & Exhibition of the International Association for Dental Research, San Francisco, Mar. 2017.
2.	Yuki Hosokawa, Hiromichi Yumoto, Kouji Hirao, Hitomi Kuramoto, Tadashi Nakanishi, Daisuke Takegawa and Takashi Matsuo : Anti-inflammatory effects of polyphenols on rat odontoblastic cells, 95th General Session & Exhibition of the International Association for Dental Research (San Francisco), Mar. 2017.

国内講演発表:

1.	水村江里, 上田(山口) 公子, 北村尚正, 前尾慶, 鈴木結加里, 蔵本瞳, 石井瞳, 嘉ノ海龍三, 岩﨑智憲 : 骨格性反対咬合児と機能性反対咬合児の咬筋の筋組成に関する研究, 第43回日本小児歯科学会中四国地方会大会及び総会, 2024年10月.
2.	三枝克啓, 中西正, 蔵本瞳, 細川義隆, 細川育子, 武川大輔, 保坂啓一 : Sudachitinがヒト歯髄細胞の炎症メディエーター発現に与える影響, 日本歯科保存学会 2023年度春季学術大会(第158回), 2023年6月.
3.	蔵本瞳, 中西正, 武川大輔, 三枝克啓, 保坂啓一 : Caffeic acid phenethyl ester (CAPE) がマウス骨芽細胞様細胞の組織修復関連因子発現に与える影響, 日本歯科保存学会 2023年度春季学術大会(第158回), 2023年6月.
4.	三枝克啓, 中西正, 蔵本瞳, 武川大輔, 保坂啓一 : Interleukin-22 がヒト歯髄細胞の炎症性メディエーター発現に及ぼす影響, 第4回象牙質歯髄治療学会学術大会, 2023年5月.
5.	蔵本瞳, 中西正, 武川大輔, 細川由樹, 三枝克啓, 保坂啓一 : Caffeic acid phenethyl ester (CAPE)が歯髄細胞のVEGF産生に与える影響, 日本歯科保存学会2021年度秋季学術大会(第155回), 2021年10月.
6.	蔵本瞳, 平尾功治, 細川由樹, 武川大輔, 湯本浩通, 中西正 : ラット象牙芽細胞(KN-3)におけるVEGFの石灰化誘導作用, 日本歯科保存学会 2019年度秋季学術大会(第151回) (福岡), 2019年11月.
7.	武川大輔, 中西正, 平尾功治, 湯本浩通, 細川由樹, 蔵本瞳, 松尾敬志 : NODリガンド刺激したヒト象牙芽細胞様細胞におけるインターフェロンγの影響, 第150回日本歯科保存学会 2019年度春季学術大会, 2019年6月.
8.	蔵本瞳, 湯本浩通, 平尾功治, 細川由樹, 松尾敬志 : Caffeic Acid Phenetyl Ester (CAPE)のラット象牙芽細胞(KN-3)におけるVEGF産生誘導機序の解析, 第40回日本歯内療法学会学術大会 (東京), 2019年6月.
9.	蔵本瞳 : ARONJの患者さんに対する歯科治療, 第18回西日本歯内療法学会, 2018年9月.
10.	蔵本瞳, 湯本浩通, 平尾功治, 細川由樹, 中西正, 武川大輔, 松尾敬志 : Caffeic Acid Phenetyl Ester (CAPE)の象牙芽細胞と骨芽細胞におけるVEGF産生誘導機序の解析, 第148回日本歯科保存学会春季学術大会, 2018年6月.
11.	Hitomi Kuramoto : The potential application of CAPE to conservative pulp therapy, Tokushima Bioscience Retreat 2017, Sep. 2017.
12.	平尾功治, 蔵本瞳, 湯本浩通, 細川由樹, 松尾敬志 : プロポリス生理活性物質(CAPE; Caffeic Acid Phenetyl Ester)を用いた新規覆髄材の開発, 第17回西日本歯内療法学会研修会, 2017年9月.
13.	蔵本瞳 : 外傷後の上顎切歯に対する歯内療法の長期経過, 第17回西日本歯内療法学会, 2017年9月.
14.	平尾功治, 湯本浩通, 細川由樹, 蔵本瞳, 松尾敬志 : ヒト歯髄組織ならびにラット象牙芽細胞(KN-3)におけるMincle発現と象牙芽細胞での機能解析, 第38回日本歯内療法学会学術大会 & 第14回日韓合同歯内療法学会学術大会, 2017年7月.
15.	蔵本瞳, 湯本浩通, 平尾功治, 細川由樹, 中西正, 武川大輔, 松尾敬志 : Caffeic Acid Phenethyl Ester (CAPE)のラット象牙芽細胞(KN-3)におけるVEGF産生に与える影響, 日本歯科保存学会2017年度春季学術大会(第146回), 2017年6月.
16.	湯本浩通, 平尾功治, 細川由樹, 蔵本瞳, 松尾敬志 : 40年以上前に外傷を受けた根未完成歯の根尖部に硬組織形成の誘導を試みた症例, 第16回西日本歯内療法学会研修会, 2016年9月.
17.	蔵本瞳 : 外傷後の上顎切歯に対する歯内療法, 第16回西日本歯内療法学会, 2016年9月.

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

抗炎症・抗酸化作用と骨芽細胞分化を期待したラリシレシノールの根尖性歯周炎治療戦略 (研究課題/領域番号: 25K20269 )
VEGF産生と抗炎症効果を期待した根尖性歯周炎治療に対するCAPEの発展的研究 (研究課題/領域番号: 22K17041 )
歯髄炎病変におけるCAPEの炎症制御機構とVEGF産生機構の解明 (研究課題/領域番号: 20K23084 )
研究者番号（70876060）による検索