Kaempferol ameliorates Cisplatin induced nephrotoxicity by modulating oxidative stress, inflammation and apoptosis via ERK and NF-κB pathways

AMB Express

Table 1 Antioxidant status in renal tissues in Cisplatin and Kaempferol treated mice

Markers of oxidative stress	Vehicle treated control	Kaempferol (200 mg/kg)	Cisplatin (20 mg/kg)	Kaempferol (100 mg/kg) + Cisplatin	Kaempferol (200 mg/kg) + Cisplatin
GSH levels	0.15 ± 0.01	0.17 ± 0.01	0.089 ± 0.01^@	0.117 ± 0.01	0.159 ± 0.02**
SOD activity	98.87 ± 1.44	102.88 ± 1.87	72.13 ± 1.35^#	82.55 ± 1.77**	84.66 ± 1.02**
CAT activity	12.44 ± 0.55	12.13 ± 0.63	9.11 ± 0.44^#	9.82 ± 0.22	11.45 ± 0.55**
GR activity	2.011 ± 0.35	2.39 ± 0.12	0.651 ± 0.12^#	1.811 ± 0.35**	1.997 ± 0.25***
GST activity	18.154 ± 1.22	19.855 ± 1.21	11.144 ± 0.77^@	15.994 ± 0.74*	24.112 ± 1.74***
NQO1	56.224 ± 4.11	69.221 ± 1.98	23.11 ± 0.44^#	39.445 ± 3.14	47.11 ± 2.88*

All the data are presented as mean ± S.E.M (n = 6). GSH mg/g tissue (reduced glutathione), SOD % of control (superoxide dismutase), CAT (U/mg of protein) Catalase, GR activity (Glutathione reductase) (U/mg protein), GST (glutathione S-transferase) nmol/min/mg/protein) and NQO1 (NAD quinone oxidoreductase 1) nmol of DCIP reduced/min/mg/protein
^@p < 0.01 compared to control, ^#p < 0.001 compared to control, *p < 0.05, **p < 0.01, ***p < 0.001 compared to control