Canagliflozin‐induced renal glutathione distribution mapping in non‐diabetic male rat kidneys

Abstract Canagliflozin, a sodium glucose cotransporter 2 (SGLT2) inhibitor, has direct renoprotective effects beyond lowering blood glucose levels. The inhibition of sodium reabsorption via SGLT2 reduces the overload on proximal tubules, thereby suppressing the generation of reactive oxygen species...

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Main Authors: Guy Watanabe, Shoichiro Horita, Reika Flora Moriya, Yusuke Masuishi, Shingen Misaka, Shu Taira, Kenju Shimomura, Michio Shimabukuro, Junichiro James Kazama
Format: Article
Language:English
Published: Wiley 2025-04-01
Series:Physiological Reports
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Online Access:https://doi.org/10.14814/phy2.70320
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author Guy Watanabe
Shoichiro Horita
Reika Flora Moriya
Yusuke Masuishi
Shingen Misaka
Shu Taira
Kenju Shimomura
Michio Shimabukuro
Junichiro James Kazama
author_facet Guy Watanabe
Shoichiro Horita
Reika Flora Moriya
Yusuke Masuishi
Shingen Misaka
Shu Taira
Kenju Shimomura
Michio Shimabukuro
Junichiro James Kazama
author_sort Guy Watanabe
collection DOAJ
description Abstract Canagliflozin, a sodium glucose cotransporter 2 (SGLT2) inhibitor, has direct renoprotective effects beyond lowering blood glucose levels. The inhibition of sodium reabsorption via SGLT2 reduces the overload on proximal tubules, thereby suppressing the generation of reactive oxygen species (ROS) and preventing a decline in renal function. To clarify the pharmacological mechanism of SGLT2 inhibitor, we investigated the effects of canagliflozin on oxidative stress in the kidneys of normal, non‐diabetic Sprague–Dawley rats. Screening using mass spectrometry images revealed a significant elevation map of the reduced form of glutathione in the renal cortex of canagliflozin‐treated non‐diabetic rats. These results suggest that canagliflozin reduces oxidative stress through ROS scavenging mechanisms. Considering that ROS play major roles in renal dysfunction regardless of diabetes mellitus, these findings suggest that canagliflozin is applicable to a broader range of renal diseases beyond diabetes.
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issn 2051-817X
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publishDate 2025-04-01
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series Physiological Reports
spelling doaj-art-5a23dfa2e599437d8b5f5ce44100da7d2025-08-20T03:10:39ZengWileyPhysiological Reports2051-817X2025-04-01137n/an/a10.14814/phy2.70320Canagliflozin‐induced renal glutathione distribution mapping in non‐diabetic male rat kidneysGuy Watanabe0Shoichiro Horita1Reika Flora Moriya2Yusuke Masuishi3Shingen Misaka4Shu Taira5Kenju Shimomura6Michio Shimabukuro7Junichiro James Kazama8Department of Nephrology and Hypertension Fukushima Medical University School of Medicine Fukushima JapanDepartment of Diabetes, Endocrinology, and Metabolism Fukushima Medical University School of Medicine Fukushima JapanDepartment of Nephrology and Hypertension Fukushima Medical University School of Medicine Fukushima JapanDepartment of Hygiene and Preventive Medicine Fukushima Medical University School of Medicine Fukushima JapanDepartment of Bioregulation and Pharmacological Medicine Fukushima Medical University School of Medicine Fukushima JapanFaculty of Food and Agricultural Sciences Fukushima University Fukushima JapanDepartment of Bioregulation and Pharmacological Medicine Fukushima Medical University School of Medicine Fukushima JapanDepartment of Diabetes, Endocrinology, and Metabolism Fukushima Medical University School of Medicine Fukushima JapanDepartment of Nephrology and Hypertension Fukushima Medical University School of Medicine Fukushima JapanAbstract Canagliflozin, a sodium glucose cotransporter 2 (SGLT2) inhibitor, has direct renoprotective effects beyond lowering blood glucose levels. The inhibition of sodium reabsorption via SGLT2 reduces the overload on proximal tubules, thereby suppressing the generation of reactive oxygen species (ROS) and preventing a decline in renal function. To clarify the pharmacological mechanism of SGLT2 inhibitor, we investigated the effects of canagliflozin on oxidative stress in the kidneys of normal, non‐diabetic Sprague–Dawley rats. Screening using mass spectrometry images revealed a significant elevation map of the reduced form of glutathione in the renal cortex of canagliflozin‐treated non‐diabetic rats. These results suggest that canagliflozin reduces oxidative stress through ROS scavenging mechanisms. Considering that ROS play major roles in renal dysfunction regardless of diabetes mellitus, these findings suggest that canagliflozin is applicable to a broader range of renal diseases beyond diabetes.https://doi.org/10.14814/phy2.70320canagliflozinglutathionemass spectroscopy imagingoxidative stressSGLT2 inhibitor
spellingShingle Guy Watanabe
Shoichiro Horita
Reika Flora Moriya
Yusuke Masuishi
Shingen Misaka
Shu Taira
Kenju Shimomura
Michio Shimabukuro
Junichiro James Kazama
Canagliflozin‐induced renal glutathione distribution mapping in non‐diabetic male rat kidneys
Physiological Reports
canagliflozin
glutathione
mass spectroscopy imaging
oxidative stress
SGLT2 inhibitor
title Canagliflozin‐induced renal glutathione distribution mapping in non‐diabetic male rat kidneys
title_full Canagliflozin‐induced renal glutathione distribution mapping in non‐diabetic male rat kidneys
title_fullStr Canagliflozin‐induced renal glutathione distribution mapping in non‐diabetic male rat kidneys
title_full_unstemmed Canagliflozin‐induced renal glutathione distribution mapping in non‐diabetic male rat kidneys
title_short Canagliflozin‐induced renal glutathione distribution mapping in non‐diabetic male rat kidneys
title_sort canagliflozin induced renal glutathione distribution mapping in non diabetic male rat kidneys
topic canagliflozin
glutathione
mass spectroscopy imaging
oxidative stress
SGLT2 inhibitor
url https://doi.org/10.14814/phy2.70320
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