ArticleInternational journal of molecular medicine2018
D‑Pinitol alleviates cyclosporine A‑induced renal tubulointerstitial fibrosis via activating Sirt1 and Nrf2 antioxidant pathways.
Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Potential targets and molecular mechanisms of D-pinitol against acute kidney injury based on network pharmacology and experimental validation.Renal failure · 2026Article
- D-Pinitol Mitigates Renal Senescence via Targeting the SARM1-cGAS-STING Signaling Axis to Restore Mitochondrial Function and Dampen Inflammatory Responses.Biomedicines · 2026Article
- Cyclosporine A promotes renal fibrosis through activating endoplasmic reticulum stress by targeting miR-212-5p/ATF6 axis.Journal of translational medicine · 2026Article
- D-pinitol extends the lifespan of Caenorhabditis elegans through integrated antioxidant defense, proteostasis, and autophagy signaling.npj aging · 2026Article
- Chronic Kidney Disease and Cellular Senescence.International journal of molecular sciences · 2026Review
- α-Lipoic acid alleviate myocardial infarction by suppressing age-independent macrophage senescence.Scientific reports · 2025Article
- Glabridin ameliorates oxidative stress and inflammation in a bovine intestinal cell line and a colitis mouse model.Iranian journal of veterinary research · 2025Article
- The potential mediating role of the gut microbiome and metabolites in the association between PFAS and kidney function in young adults: A proof-of-concept study.The Science of the total environment · 2024Article
- The regulation of MFG-E8 on the mitophagy in diabetic sarcopenia via the HSPA1L-Parkin pathway and the effect of D-pinitol.Journal of cachexia, sarcopenia and muscle · 2024Article
- Moderate exercise mitigates cardiac dysfunction and injury induced by cyclosporine A through activation of the PGIResearch in pharmaceutical sciences · 2023Article
- Anti-Alzheimer Potential of a New (+)-Pinitol Glycoside Isolated fromMetabolites · 2023Article
- Review
- The interaction between cellular senescence and chronic kidney disease as a therapeutic opportunity.Frontiers in pharmacology · 2022Review
- Physiologically Active Molecules and Functional Properties of Soybeans in Human Health-A Current Perspective.International journal of molecular sciences · 2021Review
- Heme Oxygenase 1: A Defensive Mediator in Kidney Diseases.International journal of molecular sciences · 2021Review
- The Role of Sirtuins in Kidney Diseases.International journal of molecular sciences · 2020Review
- Nontoxic concentration of ochratoxin A decreases the dosage of cyclosporine A to induce chronic nephropathy model via autophagy mediated by toll-like receptor 4.Cell death & disease · 2020Article
- d-Pinitol protects against endoplasmic reticulum stress and apoptosis in hepatic ischemia-reperfusion injury via modulation of AFT4-CHOP/GRP78 and caspase-3 signaling pathways.International journal of immunopathology and pharmacologyArticle
- Renal Oxidative Stress and Inflammatory Response in Perinatal Cyclosporine-A Exposed Rat Progeny and its Relation to Gender.Journal of microscopy and ultrastructureArticle
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the mechanism of cyclosporine A (CsA)‑induced renal injury remains to be fully elucidated, accumulating evidence suggests that oxidative stress is critical in producing CsA‑induced structural and functional renal impairment. The present study investigated the effect of D‑pinitol, a cyclitol present in soybean, on chronic CsA nephropathy. Male ICR mice were treated with vehicle, CsA (30 mg/kg/day), D‑pinitol (50 mg/kg/day) or a combination of CsA and D‑pinitol for 28 days. To assess which pathway responding to oxidative stress is augmented by D‑pinitol, the expression levels of several antioxidant enzymes and their possible regulators were measured. Treatment with D‑pinitol significantly suppressed the increase of serum creatinine and decrease of urine osmolality, compared with the CsA control group. Histological examination of Masson's trichrome‑ and α‑smooth muscle actin‑stained renal tissue demonstrated that the CsA‑induced tubulointerstitial fibrosis and inflammation were attenuated by D‑pinitol. Following the administration of D‑pinitol, there were increased expression levels of heme oxygenase‑1, NAD(P)H:quinone oxidoreductase 1, superoxide dismutase 1 and catalase in CsA‑treated kidneys. In addition, D‑pinitol increased the level of sirtuin 1 (Sirt1), and the total and nuclear expression levels of nuclear erythroid factor 2‑related factor 2 (Nrf2), suggesting that activation of the Sirt1 and Nrf2 pathways may induce the cellular antioxidant system against CsA‑induced nephropathy. Collectively, these data suggested that D‑pinitol may protect the kidney from CsA‑induced fibrosis, and that this renoprotective effect of D‑pinitol was due to the inhibition of oxidative stress through the activation of Sirt1 and Nrf2, and the subsequent enhancement of antioxidant enzymes.
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