Luseogliflozin inhibits high glucose-induced TGF-


Journal

The Journal of international medical research
ISSN: 1473-2300
Titre abrégé: J Int Med Res
Pays: England
ID NLM: 0346411

Informations de publication

Date de publication:
May 2022
Historique:
entrez: 5 5 2022
pubmed: 6 5 2022
medline: 7 5 2022
Statut: ppublish

Résumé

Sodium-glucose cotransporter-2 (SGLT2) inhibitors exhibit cardioprotective properties in patients with diabetes. However, SGLT2 is not expressed in the heart, and the underlying molecular mechanisms are not fully understood. We investigated whether the SGLT2 inhibitor luseogliflozin exerts beneficial effects on high glucose-exposed cardiomyocytes via the suppression of sodium-hydrogen exchanger-1 (NHE-1) activity. Mouse cardiomyocytes were incubated under normal or high glucose conditions with vehicle, luseogliflozin, or the NHE-1 inhibitor cariporide. NHE-1 activity and gene expression were evaluated by the SNARF assay and real-time reverse transcription-polymerase chain reaction (RT-PCR) analysis, respectively. Six-week-old male db/db mice were treated with vehicle or luseogliflozin for 6 weeks, and the hearts were collected for histological, RT-PCR, and western blot analyses. High glucose increased NHE-1 activity and transforming growth factor Luseogliflozin may suppress cardiac hypertrophy in diabetes by reducing

Identifiants

pubmed: 35510669
doi: 10.1177/03000605221097490
pmc: PMC9082751
doi:

Substances chimiques

RNA, Messenger 0
Slc9a1 protein, mouse 0
Sodium-Glucose Transporter 2 0
Sodium-Hydrogen Exchanger 1 0
Transforming Growth Factor beta2 0
Sorbitol 506T60A25R
1,5-anhydro-1-(5-(4-ethoxybenzyl)-2-methoxy-4-methylphenyl)-1-thioglucitol C596HWF74Z
Glucose IY9XDZ35W2

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

3000605221097490

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Auteurs

Naoya Osaka (N)

Department of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan.

Yusaku Mori (Y)

Department of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Anti-glycation Research Section, Showa University School of Medicine, Shinagawa, Tokyo, Japan.

Michishige Terasaki (M)

Department of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan.

Munenori Hiromura (M)

Department of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan.

Tomomi Saito (T)

Department of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan.

Hironori Yashima (H)

Department of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan.

Yoshie Shiraga (Y)

Department of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan.

Raichi Kawakami (R)

Department of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan.

Makoto Ohara (M)

Department of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan.

Tomoyasu Fukui (T)

Department of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan.

Sho-Ichi Yamagishi (SI)

Department of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan.

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