3.6 Leonurine protects against CI-AKI
Based on the effect of leonurine on ferroptosis in vitro, we further evaluated its potential effects on CI-AKI in vivo. Compared to those in the control group, the SCr and BUN levels in mice receiving the cisplatin injection were significantly increased; however, the levels were reversed by leonurine treatment (Fig. 6A-B). HE staining of renal tissue further indicated the protective effect of leonurine on kidney damage. The severe tubular dilatation, marked tubular epithelial cell edema, and obvious cast formation induced by cisplatin were inhibited by leonurine treatment (Fig. 6C-D). In addition, the levels of two other known tubule damage biomarkers, KIM-1 and NGAL were elevated by cisplatin injection and reduced by leonurine treatment (Fig. 6E-F). Macrophages have been shown to be the primary cause of inflammatory infiltration in AKI. F4/80 staining was used to further evaluate the macrophage infiltration in cisplatin-challenged kidneys. As shown in Fig. 6G, the number of F4/80-positive cells was dramatically increased in the cisplatin treatment group but significantly decreased in the leonurine treatment group.