Fig. 6

Luseogliflozin-mediated amelioration of oxidative stress and enhancement of Nrf2, the master regulator of anti-oxidative responses. (a and b) Histological findings and quantification of reactive oxygen species in the kidney with dihydroethidium (DHE) staining at 1 week post ischemia/reperfusion (I/R) injury. (c and d) Histological findings and quantification of immunostaining for nitrotyrosine in the kidney at 1 week post I/R injury in the following groups: vehicle-treated + sham-operated (n = 5), luseogliflozin-treated + sham-operated (n = 5), vehicle-treated + I/R-injured (nv8), and luseogliflozin-treated + I/R-injured (n = 8). (e and f) Western blot analysis and quantification of kidney expression of Nrf2 at 1 week post I/R injury in the following groups: vehicle-treated + sham-operated (n = 6), luseogliflozin-treated + sham-operated (n = 6), vehicle-treated + I/R-injured (n = 6), and luseogliflozin-treated + I/R-injured (n = 6). (g–i) Quantification of mRNA levels of GCLM (g), GSR (h), and TXNRD1 (i) in the kidney at 1 week post I/R injury; *P < 0.05, **P < 0.01, as determined by one-way analysis of variance. n.s., not significant.