An aqueous extract of the herb Phyllanthus urinaria L (PU) reduced kidney injury, inflammation, apoptosis and oxidative stress in mice exposed to cisplatin, a widely used chemotherapy drug whose dose-limiting kidney toxicity affects nearly 30% of recipients, according to research published in Pediatric Discovery in 2025.
The findings matter because acute kidney injury is common among hospitalized patients and rises sharply in intensive care, yet treatment options remain largely supportive. Drug-induced kidney injury accounts for a substantial share of cases, and cisplatin is a leading culprit: it accumulates in renal tubular epithelial cells and triggers inflammation, apoptosis and oxidative stress. Current management relies heavily on renal replacement therapy because effective preventive medicines are lacking.
Researchers at the Children's Hospital of Chongqing Medical University and affiliated laboratories in Chongqing, China, tested a PU aqueous extract in 24 male C57BL/6 mice with cisplatin-induced acute kidney injury, combining biochemical assays, histology, quantitative polymerase chain reaction, Western blot and immunofluorescence. The full findings were reported under DOI 10.1002/pdi3.70000.
The experiment used three groups: control, cisplatin and cisplatin plus PU. All mice received a single intraperitoneal injection of cisplatin at 20 mg/kg; the treatment group also received PU at 250 mg/kg by oral gavage on days 0 through 2, with kidney and blood samples collected on day 4. All mice survived.
Cisplatin raised blood urea nitrogen and serum creatinine and disrupted tubular architecture, with inflammatory cell infiltration and increased neutrophil gelatinase-associated lipocalin. PU significantly attenuated these changes. Gene expression analysis showed cisplatin increased messenger RNA levels of Il1b, Il6 and Tnf, while PU suppressed these responses. PU also lowered Bax and cleaved caspase-3 and raised Bcl-2, indicating less apoptosis. It reduced malondialdehyde, increased superoxide dismutase activity and restored NRF2 and NQO1 expression, supporting stronger antioxidant defense. Histology showed more organized tubules in the PU group than in cisplatin-only mice.
The authors said the study provides a multi-pathway rationale for PU in cisplatin-induced kidney injury rather than a single-target effect, with the extract appearing to protect renal tubules by calming inflammatory signaling, limiting apoptotic cell death and reinforcing NRF2/NQO1-linked antioxidant defenses.
For patients receiving cisplatin, a nephroprotective adjunct could widen therapeutic options and reduce treatment interruptions. But the researchers cautioned that PU is not ready for clinical use on the basis of this mouse study, describing the findings as a foundation for translational work rather than a clinical recommendation. Next steps should define active compounds, optimize dosing and test safety and efficacy in clinically relevant models. Key questions include whether PU interferes with cisplatin's anticancer activity and whether kidney protection can be balanced with unchanged tumor killing.
