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Peer-reviewedCC BYInternational journal of molecular sciences

SMTP-44D Attenuates Renal Inflammatory/Oxidative Dysfunction in a Mouse Model of Ischemia-Reperfusion-Induced Acute Kidney Injury.

  • Keita Shibata1,2
  • Keiji Hasumi3,4
  • Koji Nobe1,2
4 affiliations
  1. 1Department of Pharmacology, Graduate School of Pharmacy, Showa University, Tokyo 142-8555, Japan.
  2. 2Pharmacological Research Center, Showa Medical University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.
  3. 3Department of Applied Biological Science, Tokyo University of Agriculture and Technology, 3-5-8 Saiwaicho, Fuchu, Tokyo 183-8509, Japan.
  4. 4Division of Research and Development, TMS Co., Ltd., Fuchu, Tokyo 183-0055, Japan.
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Abstract

Acute kidney injury (AKI) is a critical clinical challenge for which effective pharmacological therapies remain limited. Inflammation and oxidative stress play central roles in its pathogenesis. Here, we investigated the effects of Stachybotrys microspora triprenyl phenol-44D (SMTP-44D), a soluble epoxide hydrolase inhibitor that, unlike its analog SMTP-7, lacks thrombolytic activity, in a mouse model of renal ischemia-reperfusion (I/R)-induced AKI. SMTP-44D was administered either during or prior to ischemia. SMTP-44D improved renal functional parameters, including blood urea nitrogen, serum creatinine, and fractional sodium excretion in both protocols, with a protocol-dependent difference in creatinine clearance. An attenuation of tubular morphological alterations was observed when SMTP-44D was administered during ischemia, whereas pre-ischemic administration failed to demonstrate apparent morphological improvement. Mechanistic analysis was conducted using the pre-ischemic administration protocol. Urinary neutrophil gelatinase-associated lipocalin and kidney injury molecule 1 were significantly reduced. SMTP-44D also suppressed renal tumor necrosis factor alpha, interleukin-1 beta, and NADPH oxidase-1 levels. Collectively, these functional and molecular findings suggest that SMTP-44D provides anti-inflammatory and antioxidant renoprotection, while evidence supporting structural protection is lacking in the pre-ischemic administration protocol. SMTP-44D warrants further investigation as a potential therapeutic strategy for I/R-induced AKI.

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Cite

BibTeXRIS
BibTeX
@article{shibata2026smtp44d,
  title = {{SMTP-44D Attenuates Renal Inflammatory/Oxidative Dysfunction in a Mouse Model of Ischemia-Reperfusion-Induced Acute Kidney Injury.}},
  author = {Keita Shibata and Keiji Hasumi and Koji Nobe},
  journal = {International journal of molecular sciences},
  year = {2026},
  month = sep,
  doi = {10.3390/ijms27198506},
  url = {https://europepmc.org/article/MED/42883755},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - SMTP-44D Attenuates Renal Inflammatory/Oxidative Dysfunction in a Mouse Model of Ischemia-Reperfusion-Induced Acute Kidney Injury.
AU  - Keita Shibata
AU  - Keiji Hasumi
AU  - Koji Nobe
PY  - 2026
DA  - 2026/09/24
JO  - International journal of molecular sciences
DO  - 10.3390/ijms27198506
UR  - https://europepmc.org/article/MED/42883755
AB  - Acute kidney injury (AKI) is a critical clinical challenge for which effective pharmacological therapies remain limited. Inflammation and oxidative stress play central roles in its pathogenesis. Here, we investigated the effects of Stachybotrys microspora triprenyl phenol-44D (SMTP-44D), a soluble epoxide hydrolase inhibitor that, unlike its analog SMTP-7, lacks thrombolytic activity, in a mouse model of renal ischemia-reperfusion (I/R)-induced AKI. SMTP-44D was administered either during or prior to ischemia. SMTP-44D improved renal functional parameters, including blood urea nitrogen, serum creatinine, and fractional sodium excretion in both protocols, with a protocol-dependent difference in creatinine clearance. An attenuation of tubular morphological alterations was observed when SMTP-44D was administered during ischemia, whereas pre-ischemic administration failed to demonstrate apparent morphological improvement. Mechanistic analysis was conducted using the pre-ischemic administration protocol. Urinary neutrophil gelatinase-associated lipocalin and kidney injury molecule 1 were significantly reduced. SMTP-44D also suppressed renal tumor necrosis factor alpha, interleukin-1 beta, and NADPH oxidase-1 levels. Collectively, these functional and molecular findings suggest that SMTP-44D provides anti-inflammatory and antioxidant renoprotection, while evidence supporting structural protection is lacking in the pre-ischemic administration protocol. SMTP-44D warrants further investigation as a potential therapeutic strategy for I/R-induced AKI.
SN  - 1422-0067
ER  -