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.