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Updated: Mar 28, 2026
Acute Kidney Injury Model Induced by Cisplatin in Adult Zebrafish
Published on: May 15, 2021
[Intraperitoneal administration of Allium macrostemon-derived carbon quantum dots alleviates cisplatin-induced acute
Jianming Yang1, Long Yang2, Kaiwen Hong2
1Department of Blood Purification, Taida Hospital, Tianjin University, Tianjin 300457, China.
Objectives:
To investigate the protective effects of carbon quantum dots (CQDs) derived from Allium macrostemon (Xiebai) administered orally or via intraperitoneal injection in a mouse model of cisplatin-induced acute kidney injury (AKI) and explore the underlying mechanisms.
Methods:
Male C57BL/6 mice were randomly divided into control group, AKI model group, intraperitoneal injection group, and oral administration group (n=6). In all but the control group, the mice received a single intraperitoneal injection of cisplatin (20 mg/kg) on day 3 to induce AKI; intraperitoneal injections of Xiebai-derived CQDs (0.25 mL/day) were administered on a daily basis for 5 consecutive days, and oral CQD solution was given at the dose of 1 mL/day. On day 6, blood samples were collected to measure serum creatinine (CRE) and blood urea nitrogen (BUN). HE staining and transmission electron microscopy (TEM) were used to evaluate kidney tissue structure, mitochondrial morphology, and podocyte injury. Expression levels of renal injury markers (KIM-1 and NGAL) and inflammatory cytokines (IL-6, TNF‑α, and IL-1β) were determined with with RT-qPCR and Western blotting.
Results:
Compared with those in the control group, AKI mice exhibited significant weight loss, renal enlargement, increased kidney-to-body weight ratio, and elevated serum CRE and BUN levels. In both Xiebai CQDs treatment groups, kidney/body weight ratios and serum CRE and BUN levels were reduced and the expression levels of KIM-1, NGAL, and inflammatory cytokines were lowered significantly. Histological and ultrastructural analyses revealed more intact renal architecture, reduced inflammatory infiltration, restored mitochondrial morphology, and alleviated podocyte foot process fusion and basement membrane thickening in the two treatment groups, particularly in the intraperitoneal injection group.
Conclusions:
Intraperitoneal administration of Xiebai-derived CQDs effectively attenuates cisplatin-induced AKI in mice, improves renal function, suppresses inflammatory responses, and repairs mitochondrial damage, thus offering better renal targeting and protective effects for AKI prevention and treatment.
