ArticleImmunity, inflammation and disease2023
Epimedium sagittatum Maxim ameliorates adriamycin-induced nephropathy by restraining inflammation and apoptosis via the PI3K/AKT signaling pathway.
Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 8 citations in OpenAlex.
- An Overview of the Phytochemistry, Biological Activities and Therapeutic Potential ofPlants (Basel, Switzerland) · 2026Review
- Anthracycline-induced cardiorenal toxicity: from molecular mechanisms to clinical management.Frontiers in cardiovascular medicine · 2026Review
- Epimedium sagittatum Maxim ameliorates adriamycin-induced nephropathy by restraining inflammation and apoptosis via the PI3K/AKT signaling pathway.Immunity, inflammation and disease · 2023Article
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Authors and funding
12 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundModern pharmacological studies show that Epimedium sagittatum Maxim (EPI) has antioxidant, antiapoptotic, anti-inflammatory effects. However, the effects of EPI on adriamycin-induced nephropathy are unclear.
aimThe main purpose of this study is to investigate the effects of EPI on adriamycin-induced nephropathy in rats.
methodsThe chemical composition of EPI was detected by high performance liquid chromatography. Network pharmacology was used to collect the effects of EPI on adriamycin nephropathy; renal histological changes, podocyte injury, inflammatory factors, oxidative stress levels, apoptosis levels, and the PI3K/AKT signaling pathway were examined. Moreover, analyze the effects of icariin (the representative component of EPI) on adriamycin-induced apoptosis and PI3K/AKT signaling pathway of NRK-52e cells.
resultsNetwork pharmacological results suggested that EPI may ameliorate adriamycin-induced nephropathy by inhibiting inflammatory response and regulating the PI3K/AKT signaling pathway. The experimental results showed that EPI could improve pathological injury, renal function, podocyte injury, and inhibit inflammation, oxidative stress, apoptosis in adriamycin-induced nephropathy rats through the PI3K/AKT signaling pathway. Furthermore, icariin inhibited adriamycin-induced mitochondrial apoptosis in NRK-52e cells.
conclusionThis study suggested that EPI ameliorates adriamycin-induced nephropathy by reducing inflammation and apoptosis through the PI3K/AKT signaling pathway, icariin may be the pharmacodynamic substance basis for this effect.
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