caa a22 4500 606236244 CHVBK 20210128101246.0 cr unu---uuuuu 210128e20150801xx s 000 0 eng 10.1007/s11010-015-2392-4 doi (NATIONALLICENCE)springer-10.1007/s11010-015-2392-4 Investigation of the role of nitric oxide/soluble guanylyl cyclase pathway in ascorbic acid-mediated protection against acute kidney injury in rats [Elektronische Daten] [Vaishali Koul, Anudeep Kaur, Amrit Singh] 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 40min followed by reperfusion for 24h. 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 100mg/kg, p.o.) was administered for 3days before subjecting rats to AKI. In separate groups, the nitric oxide synthase inhibitor, L-NAME (20mg/kg, i.p.) and sGC inhibitor, methylene blue (50mg/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. Springer Science+Business Media New York, 2015 Ischemia nationallicence Acute kidney injury nationallicence Nitric oxide nationallicence Ascorbic acid nationallicence Koul Vaishali Department of Pharmaceutical Sciences, Guru Nanak Dev University, 143005, Amritsar, India aut Kaur Anudeep Department of Pharmaceutical Sciences, Guru Nanak Dev University, 143005, Amritsar, India aut Singh Amrit Department of Pharmaceutical Sciences, Guru Nanak Dev University, 143005, Amritsar, India aut Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 406/1-2(2015-08-01), 1-7 0300-8177 406:1-2<1 2015 406 11010 https://doi.org/10.1007/s11010-015-2392-4 text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 research-article jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s11010-015-2392-4 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Koul Vaishali Department of Pharmaceutical Sciences, Guru Nanak Dev University, 143005, Amritsar, India aut NATIONALLICENCE 700 1- Kaur Anudeep Department of Pharmaceutical Sciences, Guru Nanak Dev University, 143005, Amritsar, India aut NATIONALLICENCE 700 1- Singh Amrit Department of Pharmaceutical Sciences, Guru Nanak Dev University, 143005, Amritsar, India aut NATIONALLICENCE 773 0- Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 406/1-2(2015-08-01), 1-7 0300-8177 406:1-2<1 2015 406 11010