Tokushima University / Educator and Researcher Directory --- Horikawa, Io

Search:

Tokushima University ⟩ University Hospital ⟩ Division of Pharmacy ⟩

(Files for researchmap) [PDF manual] [Auto-propagate to researchmap]

Research

Personal Web Page

https://researchmap.jp/io_hrkw (researchmap)

https://orcid.org/0009-0003-3634-9028 (ORCID)

Field of Study

○	Pharmacology

Subject of Study

○	リアルワールドデータを活用した化学療法誘発性うつ病予防薬の開発

Book / Paper

(See https://researchmap.jp/io_hrkw (researchmap) for Published Book / Papers / Presentations.)

Academic Paper (Judged Full Paper):

1.	Takahashi Shimon, Mitsuhiro Goda, Kanda Masaya, Yoshioka Toshihiko, Itobayashi Sayuri, Sakamoto Yoshika, Kuniki Yurika, Sugimoto Yugo, Ishida Tomoaki, Hashita Tadahiro, Io Horikawa, Takahiro Niimura, Fuka Aizawa, Yuki Izawa-Ishizawa, Kei Kawada and Keisuke Ishizawa : Protective effects of Eucommia ulmoides Oliv. leaf extract on cisplatin-induced kidney injury in mice, Fundamental Toxicological Sciences, 13, 2, 85-92, 2026.
2.	Mizusa Hyodo, Kei Kawada, Tomoaki Ishida, Yuki Izawa-Ishizawa, Ryoko Matoba, Rina Okamoto, Kohei Jobu, Io Horikawa, Fuka Aizawa, Kenta Yagi, Takahiro Niimura, Yayoi Kawano, Shinji Abe, Yukihiro Hamada, Mitsuhiro Goda and Keisuke Ishizawa : Atractylodes lancea (Thunb.) DC. [Asteraceae] Rhizome-Derived Exosome-like Nanoparticles Suppress Lipopolysaccharide-Induced Inflammation by Reducing Toll-like Receptor 4 Expression in BV-2 Murine Microglial Cells, Pharmaceuticals, 18, 8, 1099, 2025. (Tokushima University Institutional Repository) ● Metadata: 2013580 (Link to Publication Site) ● Publication site (DOI): 10.3390/ph18081099 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.3390/ph18081099 (Tokushima University Institutional Repository: 2013580, DOI: 10.3390/ph18081099)
3.	Rui Yamada, Hirotaka Nagai, Io Horikawa, Wenran Qiu, Yunhui Zhu, Kohei Ota and Tomoyuki Furuyashiki : C57BL/6J and C57BL/6N mice show distinct aging-associated behavioral alterations., Journal of Pharmacological Sciences, 157, 2, 124-129, 2025. (Summary) Aging affects emotional, cognitive, and social functions, increasing susceptibility to neuropsychiatric conditions. C57BL/6 mice are commonly used to study aging mechanisms, yet differences between C57BL/6J and C57BL/6N substrains remain underexplored. This study compared aging-related behavioral changes in these substrains. Aging reduced exploratory activity and heightened anxiety in C57BL/6J, but not C57BL/6N, mice. Conversely, aging reduced social novelty preference in C57BL/6N, but not C57BL/6J, mice. Male mice of both substrains exhibited increased female urine sniffing with age. These findings highlight substrain-specific aging effects, underscoring the importance of substrain selection in behavioral studies of aged mice for drug development. (Keyword) Animals / Mice, Inbred C57BL / aging / Male / female / Behavior, Animal / Anxiety / Exploratory Behavior / knockout mice / Species Specificity / social behavior (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jphs.2025.01.002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39828392 ● Search Scopus @ Elsevier (PMID): 39828392 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jphs.2025.01.002 (DOI: 10.1016/j.jphs.2025.01.002, PubMed: 39828392)
4.	Io Horikawa, Hirotaka Nagai, Masayuki Taniguchi, Guowei Chen, Masakazu Shinohara, Tomohide Suzuki, Shinichi Ishii, Yoshio Katayama, Shiho Kitaoka and Tomoyuki Furuyashiki : Chronic stress alters lipid mediator profiles associated with immune-related gene expressions and cell compositions in mouse bone marrow and spleen., Journal of Pharmacological Sciences, 154, 4, 279-293, 2024. (Summary) Despite the importance of lipid mediators in stress and depression and their link to inflammation, the influence of stress on these mediators and their role in inflammation is not fully understood. This study used RNA-seq, LC-MS/MS, and flow cytometry analyses in a mouse model subjected to chronic social defeat stress to explore the effects of acute and chronic stress on lipid mediators, gene expression, and cell population in the bone marrow and spleen. In the bone marrow, chronic stress induced a sustained transition from lymphoid to myeloid cells, accompanied by corresponding changes in gene expression. This change was associated with decreased levels of 15-deoxy-d12,14-prostaglandin J2, a lipid mediator that inhibits inflammation. In the spleen, chronic stress also induced a lymphoid-to-myeloid transition, albeit transiently, alongside gene expression changes indicative of extramedullary hematopoiesis. These changes were linked to lower levels of 12-HEPE and resolvins, both critical for inhibiting and resolving inflammation. Our findings highlight the significant role of anti-inflammatory and pro-resolving lipid mediators in the immune responses induced by chronic stress in the bone marrow and spleen. This study paves the way for understanding how these lipid mediators contribute to the immune mechanisms of stress and depression. (Keyword) knockout mice / Animals / Spleen / Bone Marrow / Chromatography, Liquid / Tandem Mass Spectrometry / inflammation / Lipids / gene expression (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jphs.2024.02.010 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38485346 ● Search Scopus @ Elsevier (PMID): 38485346 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jphs.2024.02.010 (DOI: 10.1016/j.jphs.2024.02.010, PubMed: 38485346)
5.	Satoshi Akiyama, Hirotaka Nagai, Shota Oike, Io Horikawa, Masakazu Shinohara, Yabin Lu, Takashi Futamura, Ryota Shinohara, Shiho Kitaoka and Tomoyuki Furuyashiki : Chronic social defeat stress increases the amounts of 12-lipoxygenase lipid metabolites in the nucleus accumbens of stress-resilient mice., Scientific Reports, 12, 1, 2022. (Summary) Severe and prolonged social stress induces mood and cognitive dysfunctions and precipitates major depression. Neuroinflammation has been associated with chronic stress and depression. Rodent studies showed crucial roles of a few inflammation-related lipid mediators for chronic stress-induced depressive-like behaviors. Despite an increasing number of lipid mediators identified, systematic analyses of synthetic pathways of lipid mediators in chronic stress models have not been performed. Using LC-MS/MS, here we examined the effects of chronic social defeat stress on multiple synthetic pathways of lipid mediators in brain regions associated with stress susceptibility in mice. Chronic social defeat stress increased the amounts of 12-lipoxygenase (LOX) metabolites, 12-HETE and 12-HEPE, specifically in the nucleus accumbens 1 week, but not immediately, after the last stress exposure. The increase was larger in stress-resilient mice than stress-susceptible mice. The S isomer of 12-HETE was selectively increased in amount, indicating the role of 12S-LOX activity. Among the enzymes known to have 12S-LOX activity, only Alox12 mRNA was reliably detected in the brain and enriched in brain endothelial cells. These findings suggest that chronic social stress induces a late increase in the amounts of 12S-LOX metabolites derived from the brain vasculature in the nucleus accumbens in a manner associated with stress resilience. (Keyword) 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid / Animals / Arachidonate 12-Lipoxygenase / Chromatography, Liquid / Endothelial Cells / knockout mice / Mice, Inbred C57BL / Nucleus Accumbens / Social Defeat / Tandem Mass Spectrometry (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-022-15461-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35790870 ● Search Scopus @ Elsevier (PMID): 35790870 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-022-15461-7 (DOI: 10.1038/s41598-022-15461-7, PubMed: 35790870)
6.	Hirofumi Hohjoh, Io Horikawa, Kimie Nakagawa, Eri Segi-Nishida and Hiroshi Hasegawa : Induced mRNA expression of matrix metalloproteinases Mmp-3, Mmp-12, and Mmp-13 in the infarct cerebral cortex of photothrombosis model mice., Neuroscience Letters, 739, 2020. (Summary) A strong therapeutic target of ischemic stroke is controlling brain inflammation. Recent studies have implicated the critical role of C-C chemokine receptor 5 (CCR5) in neuroinflammation during ischemic stroke. It has been reported that the expression of the matrix metalloproteinases, MMP-3, MMP-12, and MMP-13, is controlled by CCR5; however, their expressional regulation in the infarct brain has not been clearly understood. This study investigated the mRNA expression of Mmp-3, -12, and -13 in the ischemic cerebral cortex of photothrombosis mouse model. The three Mmps were highly upregulated in the early stages of ischemic stroke and were expressed in different types of cells. Mmp-3 and Mmp-13 were expressed in blood vessel endothelial cells after ischemia-induction, whereas Mmp-12 was expressed in activated microglia. The expression of Mmp-13 in resting microglia and in neurons of uninjured cerebral cortex was lost in the infarct region. Therefore, the MMPs responding to CCR5 are differentially regulated during ischemic stroke. (Keyword) Animals / Cerebral Infarction / Disease Models, Animal / Matrix Metalloproteinase 12 / Matrix Metalloproteinase 13 / Matrix Metalloproteinase 3 / Mice, Inbred C57BL / RNA, Messenger / Stroke / Up-Regulation (Link to Publication Site) ● Publication site (DOI): 10.1016/j.neulet.2020.135406 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32987131 ● Search Scopus @ Elsevier (PMID): 32987131 ● Search Scopus @ Elsevier (DOI): 10.1016/j.neulet.2020.135406 (DOI: 10.1016/j.neulet.2020.135406, PubMed: 32987131)
7.	Nurhanani Razali, Io Horikawa, Hirofumi Hohjoh, Chihiro Yoshikawa and Hiroshi Hasegawa : Prostaglandin-Modulated Interaction of Thymic Progenitor Cells with Blood Vessels during Estradiol-Induced Thymic Involution, BPB Reports, 2, 4, 39-47, 2019. (Summary) Thymic involution-associated disfunction of thymus is implicated in aging, microbial infection, pregnancy, improper nutrition, and etc., therefore it is clinically important especially in aged societies. Excess administration of estradiol to male mice is known to induce thymic involution and used as a mouse model of thymic involution, whereas the mechanisms of which have not been well understood. Here we examined the role of prostanoids in the estradiol-induced thymic involution in mice. The administration of 17β-estradiol for 7 consecutive days induced thymic involution. In the involute thymus, the expression of mRNAs for some synthetic enzymes of prostanoids, including Ptgs1, Ptgs2, Ptgds, Hpgds, Ptges1, and Tbxas, are upregulated. In order to examine the roles of prostanoids in the thymic involution, we treated the mice with an NSAID, etodolac, following 17β-estradiol-administration. The etodolac-treatment partially inhibited the estradiol-induced reduction of thymic size and disorganization of the boundary between thymic cortex and medulla, as indicated by keratin 5 expression as well as by localization of innate immune cells. CD34-positive thymic progenitor cells localized near the blood vessels in the estradiol-administered thymus, although they were more dispersed by the etodolac-treatment. The association of CD34-positive cells with blood vessels is known to be mediated by E- and P-selectins, whose expressions were also regulated by estradiol-administration in an etodolac-sensitive manner. These results indicated the role of prostanoids in the histological change of thymus during estradiol-induced thymic involution. (Link to Publication Site) ● Publication site (DOI): 10.1248/bpbreports.2.4_39 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1391130851453580544 ● Search Scopus @ Elsevier (DOI): 10.1248/bpbreports.2.4_39 (DOI: 10.1248/bpbreports.2.4_39, CiNii: 1391130851453580544)

Proceeding of International Conference:

1.	Itokazu Shuto, Yuki Izawa-Ishizawa, Hyodo Mizusa, Miyata Tatsumi, Tsujinaka Kaito, Kondo Masateru, Io Horikawa, Takahiro Niimura, Fuka Aizawa, Kenta Yagi, Kei Kawada, Mitsuhiro Goda and Keisuke Ishizawa : Role of vascular endothelial ERK5 signaling in the development of aortic diseases., 20th World Congress of Basic and Clinical Pharmacology, Jul. 2026.
2.	Hyodo Mizusa, Yuki Izawa-Ishizawa, Miyata Koji, Itokazu Shuto, Miyata Tatsumi, Takahiro Niimura, Tsujinaka Kaito, Fuka Aizawa, Io Horikawa, Kenta Yagi, Kei Kawada, Mitsuhiro Goda and Keisuke Ishizawa : Identifying sex differences in immune-related cardiac events using VigiBase, the WHO global database., ASCPT 2026 Annual Meeting Denver, Mar. 2026.
3.	Kei Kawada, Ishida Tomoaki, Hyodo Mizusa, Io Horikawa, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa, Takahiro Niimura, Mitsuhiro Goda and Keisuke Ishizawa : Anti-neuroinflammatory effects and mechanism of exosome-like nanoparticles derived from Atractylodes lancea rhizome., FIP Congress 2025, Sep. 2025.

Proceeding of Domestic Conference:

1.	MIYATA Tatsumi, Yuki Izawa-Ishizawa, Fuka Aizawa, Takahiro Niimura, Io Horikawa, Kei Kawada, Mitsuhiro Goda and Keisuke Ishizawa : 大動脈解離易発症モデルマウスを用いた性差の影響の検討, 第9回フレッシャーズ・カンファレンス, Jul. 2026.
2.	Kei Kawada, SHINONAGA Hiroshi, 石田智晃, Mitsuhiro Goda, Io Horikawa, Takahiro Niimura, Fuka Aizawa, Kenta Yagi, Yuki Izawa-Ishizawa, 加地努 and Keisuke Ishizawa : 心不全患者における生活機能に基づくトルバプタン関連高ナトリウム血症の新規リスク層別化:医療ビッグデータと臨床レジストリの統合解析, 医療薬学フォーラム2026 / 第34回クリニカルファーマシーシンポジウム, Jun. 2026.
3.	Mitsuhiro Goda, Masaya Kanda, 渡部純也, KOYAMA Haruki, Shimon Takahashi, OKAMOTO Naoki, Takahisa Inoue, Atsushi Ogawa, Io Horikawa, Kei Kawada and Keisuke Ishizawa : SGLT2阻害薬はNHE3–MATE連関を介してシスプラチン腎内蓄積を抑制する:動物モデルと臨床データからの知見, 医療薬学フォーラム2026 / 第34回クリニカルファーマシーシンポジウム, Jun. 2026.
4.	Shuto Itokazu, Yuki Izawa-Ishizawa, HYOHDOH Mizusa, MIYATA Tatsumi, FUKUOKA Himeno, YAMAO Tamami, TSUJINAKA Kaito, Masateru Kondoh, Io Horikawa, Takahiro Niimura, Fuka Aizawa, Kenta Yagi, Kei Kawada, Mitsuhiro Goda and Keisuke Ishizawa : 大動脈疾患発症における血管内皮ERK5シグナルの役割検討, 日本薬学会第146年会, Mar. 2026.
5.	HYOHDOH Mizusa, Yuki Izawa-Ishizawa, Kohji Miyata, Shuto Itokazu, Takahiro Niimura, TSUJINAKA Kaito, Fuka Aizawa, Io Horikawa, Kenta Yagi, Kei Kawada, Mitsuhiro Goda and Keisuke Ishizawa : 個別症例安全性報告データベースを用いた免疫チェックポイント阻害薬関連心血管障害の性差分析, 第46回日本臨床薬理学会学術総会, Dec. 2025.
6.	MIYATA Tatsumi, Yuki Izawa-Ishizawa, HYOHDOH Mizusa, Shuto Itokazu, FUKUOKA Himeno, YAMAO Tamami, 藤澤凛, NAKAYAMA Riki, Kohji Miyata, Fuka Aizawa, Takahiro Niimura, Io Horikawa, Kei Kawada, Mitsuhiro Goda and 石澤啓介 : 大動脈疾患発症における性差の影響の検討, 第148回日本薬理学会近畿部会, Nov. 2025.
7.	Hiroshi Bandou, 北川航平, Mitsuhiro Goda, Atsushi Ogawa, Io Horikawa, Fuka Aizawa, Takahiro Niimura, Kei Kawada, Kei Kawada and Keisuke Ishizawa : クロザピン誘発心筋炎に対するHMG-CoA還元酵素阻害薬の予防効果, 第35回日本医療薬学会年会(神戸), Nov. 2025.
8.	Masaya Kanda, Mitsuhiro Goda, KAWAZOE Jin, NAKASHIMA Hitomi, Io Horikawa, Fuka Aizawa, Takahiro Niimura, Kenta Yagi, Kei Kawada, Yuki Izawa-Ishizawa, 神山直也, Masayuki Chuma, 松本成史, 田崎嘉一 and Keisuke Ishizawa : 糖尿病状態がシスプラチン腎障害に及ぼす性差の検討:KK-Ay/Taマウスを用いた前臨床研究, 第35回日本医療薬学会年会(神戸), Nov. 2025.
9.	前田和輝, Kei Kawada, 児山蒼太, 林稔展, Io Horikawa, Takahiro Niimura, Fuka Aizawa, Kenta Yagi, Mitsuhiro Goda, Fuka Aizawa, Yuki Izawa-Ishizawa and Keisuke Ishizawa : オキサリプラチン・イリノテカン併用療法における制吐薬ホスアプレピタント及びホスネツピタントの有効性の検討, 第35回日本医療薬学会年会(神戸), Nov. 2025.
10.	Sohta Koyama, Kei Kawada, 前田和輝, 林稔展, Toshihiko Yoshioka, Chiemi Sato, Takaaki Yamamoto, Io Horikawa, Takahiro Niimura, Fuka Aizawa, Kenta Yagi, Mitsuhiro Goda, Yuki Izawa-Ishizawa, Shinji Abe and Keisuke Ishizawa : オキザリプラチン・イリノテカン併用療法における制吐薬ホスアプレピタント及びホスネツピタントの癌種別有効性の検討, 第35回日本医療薬学会年会(神戸), Nov. 2025.
11.	Sohta Koyama, Kei Kawada, 前田和輝, 林稔展, 吉岡俊彦, Chiemi Sato, Takaaki Yamamoto, Io Horikawa, Takahiro Niimura, Fuka Aizawa, Kenta Yagi, Mitsuhiro Goda, Yuki Izawa-Ishizawa, Keisuke Ishizawa and Shinji Abe : オキザリプラチン・イリノテカン併用療法におけるホスアプレピタントとホスネツピタントの制吐効果に関する後方視的・癌種別検討, 第64回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会 (徳島), Nov. 2025.
12.	Masaya Kanda, Mitsuhiro Goda, KAWAZOE Jin, NAKASHIMA Hitomi, Io Horikawa, Fuka Aizawa, Takahiro Niimura, Kei Kawada, Yuki Izawa-Ishizawa, 神山直也, Masayuki Chuma, 松本成史, 田﨑嘉一 and Keisuke Ishizawa : SGLT2阻害薬は腎臓へのシスプラチン蓄積量を減少させることでシスプラチン誘発腎障害を軽減する:リアルワールドデータと動物モデルからの知見, 第19回次世代を担う若手のための医療薬科学シンポジウム, Sep. 2025.
13.	HYOHDOH Mizusa, Kei Kawada, 石田智滉, Io Horikawa, Fuka Aizawa, Kenta Yagi, Takahiro Niimura, Mitsuhiro Goda, Yuki Izawa-Ishizawa and Keisuke Ishizawa : 植物由来エクソソーム様ナノ粒子によるミクログリア細胞における炎症抑制効果の機序解明, 第34回霧島神経薬理フォーラム, Aug. 2025.
14.	Mizusa Hyohdoh, Yuki Izawa-Ishizawa, Shuto Itokazu, Tatsumi Miyata, Himeno Fukuoka, Tamami Yamao, Fuka Aizawa, Takahiro Niimura, Io Horikawa, Kenta Yagi, Kei Kawada, Mitsuhiro Goda and Keisuke Ishizawa : 大動脈疾患発症における血管内皮ERK5シグナルの役割検討, 第147回日本薬理学会近畿部会, Jun. 2025.

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

Search by Researcher Number (91024587)