A preclinical study published in Pediatric Discovery in 2025 has found that an aqueous extract of Phyllanthus urinaria L (PU) protected mice against acute kidney injury (AKI) caused by cisplatin, a widely used chemotherapy drug whose dose-limiting toxicity affects nearly 30% of recipients. The research, conducted at the Children’s Hospital of Chongqing Medical University and affiliated laboratories in Chongqing, China, provides a multi-pathway rationale for PU as a potential nephroprotective agent, though the authors stress that the findings are early and not a clinical recommendation.
The study, reported under DOI 10.1002/pdi3.70000, used 24 male C57BL/6 mice divided into three groups: control, cisplatin, and cisplatin plus PU. Cisplatin was given as a single intraperitoneal injection at 20 mg/kg, while the treatment group received PU at 250 mg/kg by oral gavage on days 0–2. Kidney and blood samples were collected on day 4. All mice survived. Cisplatin raised blood urea nitrogen (BUN) and serum creatinine (Scr), disrupted tubular architecture, and increased neutrophil gelatinase-associated lipocalin (NGAL), a marker of kidney injury. PU significantly attenuated these changes.
At the molecular level, PU suppressed the expression of pro-inflammatory cytokine genes Il1b, Il6, and Tnf, which encode interleukin-1β, interleukin-6, and tumor necrosis factor-α, respectively. It also rebalanced apoptosis-related proteins, lowering Bax and cleaved caspase-3 while raising Bcl-2, indicating less programmed cell death. Furthermore, PU reduced malondialdehyde (MDA), increased superoxide dismutase (SOD) activity, and restored nuclear factor erythroid 2-related factor 2 (NRF2) and NAD(P)H:quinone oxidoreductase 1 (NQO1) expression, supporting stronger antioxidant defense. Histology showed more organized tubules in the PU group compared with cisplatin-only mice.
The findings matter because AKI is common in 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, accumulating in renal tubular epithelial cells and triggering inflammation, apoptosis, and oxidative stress. Current management relies heavily on renal replacement therapy because effective preventive medicines are lacking. A nephroprotective adjunct could widen therapeutic options for patients receiving cisplatin and reduce treatment interruptions, but PU is not ready for clinical use on the basis of this mouse study.
The authors emphasize that the data are encouraging but early, and that next steps should define active compounds, optimize dosing, and test safety and efficacy in clinically relevant models. Key research priorities include identifying the constituents responsible for the effects, confirming target engagement in human cells or organoids, determining whether PU interferes with cisplatin’s anticancer activity, and evaluating safety, dosing, and drug interactions. Such work would need to balance kidney protection with unchanged tumor killing. The study offers a preclinical lead, not a prescription.
Funding for the research came from the Chongqing Science and Health Joint Traditional Chinese Medicine Technology Innovation and Application Development Project (2020ZY023877) and the Program for Youth Innovation in Future Medicine, Chongqing Medical University (W0056). The work was supported by Chuanlink Innovations, whose website is http://chuanlink-innovations.com.
