Investigation of the role of nitric oxide/soluble guanylyl cyclase pathway in ascorbic acid-mediated protection against acute kidney injury in rats

Koul, Vaishali; Kaur, Anudeep; Singh, Amrit Pal

doi:10.1007/s11010-015-2392-4

Cited by 17 publications

(10 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A study by Koul et al that employed a rat model concluded that ascorbic acid protects against IRinduced acute kidney injury (38). Similar studies to ours have shown the protective role of vitamins C and E in attenuating oxidative stress following renal ischemia in a rat model (39), probably by radical scavenging and expressing antioxidant properties (40).…”

Section: Discussionsupporting

confidence: 82%

The Effects of Ascorbic Acid and U-74389G on Renal Ischemia-Reperfusion Injury in a Rat Model

Zografos

Chrysikos

Pittaras

et al. 2020

In Vivo

View full text Add to dashboard Cite

Background/Aim: U-74389G and ascorbic acid protect the cells from oxidation. This study aimed to depict their role in ischemia-reperfusion injury in a renal rat model. Materials and Methods: Sixty Wistars rats were randomized into six groups of 10 animals each. Group A Ischemia 30 min, reperfusion 60 min; Group B Ischemia 30 min, reperfusion 120 min; Group C Ischemia 30 min, ascorbic acid administration, reperfusion 60 min; Group D Ischemia 30 min, ascorbic acid administration, reperfusion 120 min; Group E Ischemia 30 min, U-74389G administration, reperfusion 60 min; Group F Ischemia 30 min, U-74389G administration, reperfusion 120 min. We then collected tissue and blood samples. Results: Histology and the significantly decreased malondialdehyde and tumor necrosis factor-α levels indicated that ascorbic acid was superior to U-74389G, at pre-defined time intervals. Conclusion: Ascorbic acid and U-74389G ameliorated renal damage induced by ischemia-reperfusion injury, suggesting a therapeutic effect.

show abstract

Section: Discussionsupporting

confidence: 82%

The Effects of Ascorbic Acid and U-74389G on Renal Ischemia-Reperfusion Injury in a Rat Model

Zografos

Chrysikos

Pittaras

et al. 2020

In Vivo

View full text Add to dashboard Cite

show abstract

“…Recently, research has mainly focused on miR-98 regulation of apoptosis and its target proteins including Bcl-2, Fas, caspase-3, and c-Myc ( 50 – 53 ). Expression of miR-98 was downregulated in osteoarthritis (OA) cartilage tissues.…”

Section: Discussionmentioning

confidence: 99%

Bta-miR-98 Suppresses Replication of Caprine Parainfluenza Virus Type 3 Through Inhibiting Apoptosis by Targeting Caspase-3

Zhong

Liao

et al. 2020

Front. Immunol.

View full text Add to dashboard Cite

Caprine parainfluenza virus type 3 (CPIV3) is an emerging respiratory pathogen that affects the sheep and goat industry in China and possibly other countries around the world. Accumulating evidence suggests that microRNAs play important roles in regulating virus-host interactions and can suppress or facilitate viral replication. In this study, we showed that CPIV3 infection induced apoptosis in Madin-Darby bovine kidney (MDBK) cells, as determined by morphological changes and flow cytometry. Caspase activity and the expression of pro-apoptotic genes further indicated that CPIV3 induced apoptosis by activating both the intrinsic and extrinsic pathways. We also demonstrated the involvement of bta-microRNA-98 (bta-miR-98) in regulating CPIV3-induced apoptosis. Bta-miR-98 was downregulated in MDBK cells infected with CPIV3. Overexpression of bta-miR-98 significantly decreased the activities of caspase-3, −8, and −9. Conversely, inhibition of bta-miR-98 had completely opposite effects. Furthermore, our data showed that bta-miR-98 markedly affected CPIV3 replication by regulating apoptosis. Importantly, we found that bta-miR-98 modulated CPIV3-induced apoptosis by targeting caspase-3, an effector of apoptosis. Collectively, our results may suggest that CPIV3 infection induced apoptosis and downregulated the levels of bta-miR-98, and this miRNA regulated viral replication through effected apoptosis. This study contributes to our understanding of the molecular mechanisms underlying CPIV3 pathogenesis.

show abstract

“…Some animal AKI studies have compared the effect of l -arginine (NO donor) and vitamin C supplementation on biomarkers of lipid, DNA and protein oxidation, and kidney function, and have demonstrated superior protection afforded by vitamin C [ 86 , 138 ]. These improvements in renal function and oxidative stress markers in I/R-induced AKI in rats, may involve NO/soluble guanylyl cyclase (cGC), as inhibitors of this pathway ( L -NAME and methylene blue) reduced the reno-protective effects of vitamin C [ 82 ]. Further, ascorbate increased tissue GSH and nitrate/nitrite levels, suggesting a preservation of NO • levels.…”

Section: Vitamin C and Renal Protectionmentioning

confidence: 99%

Protective Role for Antioxidants in Acute Kidney Disease

2017

View full text Add to dashboard Cite

Acute kidney injury causes significant morbidity and mortality in the community and clinic. Various pathologies, including renal and cardiovascular disease, traumatic injury/rhabdomyolysis, sepsis, and nephrotoxicity, that cause acute kidney injury (AKI), induce general or regional decreases in renal blood flow. The ensuing renal hypoxia and ischemia promotes the formation of reactive oxygen species (ROS) such as superoxide radical anions, peroxides, and hydroxyl radicals, that can oxidatively damage biomolecules and membranes, and affect organelle function and induce renal tubule cell injury, inflammation, and vascular dysfunction. Acute kidney injury is associated with increased oxidative damage, and various endogenous and synthetic antioxidants that mitigate source and derived oxidants are beneficial in cell-based and animal studies. However, the benefit of synthetic antioxidant supplementation in human acute kidney injury and renal disease remains to be realized. The endogenous low-molecular weight, non-proteinaceous antioxidant, ascorbate (vitamin C), is a promising therapeutic in human renal injury in critical illness and nephrotoxicity. Ascorbate may exert significant protection by reducing reactive oxygen species and renal oxidative damage via its antioxidant activity, and/or by its non-antioxidant functions in maintaining hydroxylase and monooxygenase enzymes, and endothelium and vascular function. Ascorbate supplementation may be particularly important in renal injury patients with low vitamin C status.

show abstract

Investigation of the role of nitric oxide/soluble guanylyl cyclase pathway in ascorbic acid-mediated protection against acute kidney injury in rats

Cited by 17 publications

References 34 publications

The Effects of Ascorbic Acid and U-74389G on Renal Ischemia-Reperfusion Injury in a Rat Model

The Effects of Ascorbic Acid and U-74389G on Renal Ischemia-Reperfusion Injury in a Rat Model

Bta-miR-98 Suppresses Replication of Caprine Parainfluenza Virus Type 3 Through Inhibiting Apoptosis by Targeting Caspase-3

Protective Role for Antioxidants in Acute Kidney Disease

Contact Info

Product

Resources

About