Fig. 3.

Canagliflozin (CANA) suppresses cisplatin-induced p53 and MAPK activation. A: representative immunoblots of total p53 and phosphorylated (p-)p53 (Ser¹⁵) in mouse kidneys. C57BL/6 mice with or without CANA were treated with 30 mg/kg cisplatin or saline for 3 days. Kidney cortical tissue lysates were extracted for analysis. GAPDH was used as an internal loading control. B: densitometric analysis of p53 and p-p53 (Ser¹⁵) normalized to GAPDH. C: representative immunoblots of total p53, p-p53 (Ser¹⁵), and p53-upregulated modulator of apoptosis (PUMA) in rat kidney proximal tubular cells (RPTCs) with densitometric analysis. RPTCs were treated with 15 μM CANA and coincubated with or without 20 μM cisplatin for 16 h to collect cell lysates for immunoblot analysis normalized by β-actin, the internal control. Values are means ± SD; n = 3. D: representative immunoblots of p-p38, total p38, p-JNK, total JNK, p-ERK1/2, and total ERK1/2 in RPTCs. Cyclophilin B was used as an internal loading control. E: densitometry analysis of p-p38 normalized to p38, p-JNK normalized to JNK, and p-ERK normalized to ERK. Data are expressed as means ± SD; n = 3. *P < 0.05 vs. the control group; #P < 0.05 vs. the cisplatin-treated group without CANA.