AIM:To investigate the protective mechanism of calycosin(CA)on renal structure and antioxi-dant capacity in acute kidney injury(AKI)mice.METHODS:Thirty male C57BL/6J mice were allocated into control group,model group,and treatment group.The treatment group was further subdivided into low-dose CA,middle-dose CA,and high-dose CA groups,receiving 5 mg/kg,10 mg/kg,and 20 mg/kg CA solution by gavage for 6 days.After the pre-treatment phase,both the model and treatment groups were administered an intraperitoneal injection of 20 mg/kg of cis-platin(CDDP)to induce AKI modeling.Specimens from the mice were collected 72 hours post-modeling for further analy-sis.The body weight and the mean mass of both kidneys were assessed.Serum creatinine(SCr)and blood urea nitrogen(BUN)levels were assessed to evaluate kidney function.Kidney pathology was assessed with periodic acid-Schiff(PAS)staining,while protein levels of superoxide dismutase 1(SOD1),SOD2,glutathione peroxidase 1(GPX1),and catalase were evaluated using Western blot and immunohistochemistry assay.RESULTS:Compared with the control group,the model group exhibited a substantial reduction in body mass,a significant increase in the mean mass of bilateral kidneys,and elevated levels of SCr and BUN,indicating impaired renal function(P<0.01).PAS staining revealed pronounced structural damage to the glomeruli and renal tubules,with widespread appearance of tubular casts in model group.The re-sults of Western blot and immunohistochemical staining demonstrated significantly reduced expression of antioxidant en-zymes SOD1,SOD2,GPX1,and catalase(P<0.05).The body weight of mice in the low-dose and middle-dose CA groups exhibited a significant increase than those in the model group,and the kidney weights of mice in Low-dose,middle-dose,and high-dose CA groups were significantly lower than those of mice in the model group(P<0.05).Additionally,SCr and BUN levels were significantly reduced(P<0.01).PAS staining indicated obvious recovery of glomeruli and renal tubules after CA treatment.SOD1 and GPX1 levels were elevated in the middle-dose and high-dose CA groups,and SOD2 and catalase levels were significantly higher in the middle-dose CA group(P<0.05),compared with model group.CON-CLUSION:CA can alleviate CDDP-induced kidney injury in AKI mice by enhancing the expression of antioxidant enzymes SOD1,SOD2,GPX1,and catalase.

AIM:To investigate the protective mechanism of calycosin(CA)on renal structure and antioxi-dant capacity in acute kidney injury(AKI)mice.METHODS:Thirty male C57BL/6J mice were allocated into control group,model group,and treatment group.The treatment group was further subdivided into low-dose CA,middle-dose CA,and high-dose CA groups,receiving 5 mg/kg,10 mg/kg,and 20 mg/kg CA solution by gavage for 6 days.After the pre-treatment phase,both the model and treatment groups were administered an intraperitoneal injection of 20 mg/kg of cis-platin(CDDP)to induce AKI modeling.Specimens from the mice were collected 72 hours post-modeling for further analy-sis.The body weight and the mean mass of both kidneys were assessed.Serum creatinine(SCr)and blood urea nitrogen(BUN)levels were assessed to evaluate kidney function.Kidney pathology was assessed with periodic acid-Schiff(PAS)staining,while protein levels of superoxide dismutase 1(SOD1),SOD2,glutathione peroxidase 1(GPX1),and catalase were evaluated using Western blot and immunohistochemistry assay.RESULTS:Compared with the control group,the model group exhibited a substantial reduction in body mass,a significant increase in the mean mass of bilateral kidneys,and elevated levels of SCr and BUN,indicating impaired renal function(P<0.01).PAS staining revealed pronounced structural damage to the glomeruli and renal tubules,with widespread appearance of tubular casts in model group.The re-sults of Western blot and immunohistochemical staining demonstrated significantly reduced expression of antioxidant en-zymes SOD1,SOD2,GPX1,and catalase(P<0.05).The body weight of mice in the low-dose and middle-dose CA groups exhibited a significant increase than those in the model group,and the kidney weights of mice in Low-dose,middle-dose,and high-dose CA groups were significantly lower than those of mice in the model group(P<0.05).Additionally,SCr and BUN levels were significantly reduced(P<0.01).PAS staining indicated obvious recovery of glomeruli and renal tubules after CA treatment.SOD1 and GPX1 levels were elevated in the middle-dose and high-dose CA groups,and SOD2 and catalase levels were significantly higher in the middle-dose CA group(P<0.05),compared with model group.CON-CLUSION:CA can alleviate CDDP-induced kidney injury in AKI mice by enhancing the expression of antioxidant enzymes SOD1,SOD2,GPX1,and catalase.