ArticleInternational urology and nephrology2020
Myricitrin protects against cisplatin-induced kidney injury by eliminating excessive reactive oxygen species.
Article in International urology and nephrology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 20 citations in OpenAlex.
- Isothiocyanates inhibit the cisplatin-induced apoptosis and inflammation in human kidney HEK-293 cells.Nutrition research and practice · 2026Article
- Myricitrin inhibited ferritinophagy-mediated ferroptosis in cisplatin-induced human renal tubular epithelial cell injury.Frontiers in pharmacology · 2024Article
- Polyphenols and Their Metabolites in Renal Diseases: An Overview.Foods (Basel, Switzerland) · 2022Review
- Isoliquiritin Ameliorates Cisplatin-Induced Renal Proximal Tubular Cell Injury by Antagonizing Apoptosis, Oxidative Stress and Inflammation.Frontiers in medicine · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCisplatin could result in a wide range of kidney injuries. During the pathogenetic process, the excessive generation of reactive oxygen species (ROS) induced by cisplatin has been regarded as the initial and critical role, by which DNA damage and cell death could subsequently come up. Therefore the elimination of ROS has long been considered as effective mean to prevent cisplatin-induced kidney injury. Myricitrin is a newfound natural polyphenol hydroxy flavonoid glycoside compound, whose forceful anti-oxidative properties had been confirmed. Thus, we aim to investigate if myricitrin could protect against cisplatin-induced kidney injury.
methodsA cisplatin-induced kidney injury model was established in mice by intraperitoneal injection of cisplatin. The protective effect of myricitrin on kidney injury was evaluated by serum BUN and Cre level. The Kidney pathology was observed with H&E and TUNEL staining. Then cell viability and apoptosis rate were measured using MMT assay and flow cytometry to assess if myricitrin could protect KH-2 cells against cisplatin-induced injury. The intracellular ROS was detected by ROS fluorogenic probe and quantitatively analyzed by flow cytometry. Finally, the expression of Bcl-2 and Bax was investigated by western blotting to indicate the influence in apoptosis pathway.
resultsMyricitrin could significantly remit kidney injury induced by cisplatin and inhibit apoptosis of KH-2 cells. In mechanism, myricitrin could eliminate ROS and subsequently block activation of apoptosis pathway.
conclusionMyricitrin protects against cisplatin-induced kidney injury by eliminating excessive ROS.
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