The present study investigated the possible involvement of
nitric oxide/
soluble guanylyl cyclase (NO/sGC) pathway in
ascorbic acid (AA)-mediated protection against
acute kidney injury (AKI) in rats. The rats were subjected to bilateral renal
ischemia by occluding renal pedicles for 40 min followed by reperfusion for 24 h. The AKI was assessed in terms of measuring
creatinine clearance (CrCl), blood
urea nitrogen (BUN), plasma
uric acid,
potassium level, fractional excretion of
sodium (FeNa), and microproteinuria. The NO level and oxidative stress in renal tissues were assessed by measuring
myeloperoxidase activity,
thiobarbituric acid reactive substances,
superoxide anion generation, and
reduced glutathione level. AA (50 and 100 mg/kg, p.o.) was administered for 3 days before subjecting rats to AKI. In separate groups, the
nitric oxide synthase inhibitor,
L-NAME (20 mg/kg, i.p.) and sGC inhibitor,
methylene blue (50 mg/kg, i.p.) was administered prior to AA treatment in rats. The significant decrease in CrCl and increase in BUN, plasma
uric acid,
potassium, FeNa, microproteinuria, and oxidative stress in renal tissues demonstrated
ischemia-reperfusion-induced AKI in rats. The AA treatment ameliorated
ischemia-reperfusion-induced AKI along with the increase in renal NO level. The pretreatment with
L-NAME and
methylene blue abolished protective effect of AA. It is concluded that AA protects against
ischemia-reperfusion-induced AKI. Moreover, the NO/sGC pathway finds its definite involvement in AA-mediated reno-protective effect.