Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2020 Sep-Oct;34(5):2475-2484.
doi: 10.21873/invivo.12063.

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

Constantinos G Zografos #  1   2 , Dimosthenis Chrysikos #  1   2 , Theodoros Pittaras  1   3 , Vasileios Karampelias  4 , Aikaterini Chairakakis  1 , Antonis Galanos  1 , Ioannis Sfiniadakis  5 , Evangelos Felekouras  6 , George C Zografos  2 , Michail Sideris  7 , Konstantina Papadopoulou  1 , Apostolos E Papalois  8   9
Affiliations

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

Constantinos G Zografos et al. In Vivo. 2020 Sep-Oct.

Abstract

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.

Keywords: Antioxidants; ascorbic acid; kidney; reperfusion injury.

PubMed Disclaimer

Conflict of interest statement

The Authors declare no conflicts of interest regarding this study.

Figures

Figure 1
Figure 1. Main variables among the groups expressed as MEAN+SD after 60 min and 120 min of reperfusion.
Figure 2
Figure 2. Main variables among the groups expressed as MEAN+SD after 60 min and 120 min of reperfusion.
Figure 3
Figure 3. No statistically significant difference in TNF-α between the compared groups at 60 min reperfusion. U-74389G group presents statistically significantly higher values of TNF-α compared to the ascorbic acid group (p=0.049) at 120 min reperfusion.
Figure 4
Figure 4. Vascular dilatation and congestion with areas of necrosis (250×). Group C (kindly ischemia (30 min), ascorbic acid administration, followed by reperfusion for 60 min).
Figure 5
Figure 5. Vascular dilatation and congestion with areas of necrosis (400×). Group C [kidney ischemia (30 min), ascorbic acid administration, followed by reperfusion for 60 min].
Figure 6
Figure 6. Normal tubular architecture of the kidney (400×). Group E (kidney ischemia (30 min), U-74389G intravenous injection, and reperfusion for 60 min).
Figure 7
Figure 7. Isolated degenerated renal tubules mainly peripherally. Group E [kidney ischemia (30 min), U-74389G intravenous injection, and reperfusion for 60 min].
Figure 8
Figure 8. Few degenerated renal tubules with central distribution (250×). Group F [kidney ischemia (30 min), U-74389G intravenous injection, and reperfusion for 120 min].
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

References

    1. Ponticelli C. Ischaemia-reperfusion injury: a major protagonist in kidney transplantation. Nephrol Dial Transplant. 2014;29(6):1134–1140. doi: 10.1093/ndt/gft488. - DOI - PubMed
    1. Pefanis A, Ierino FL, Murphy JM, Cowan PJ. Regulated necrosis in kidney ischemia-reperfusion injury. Kidney Int. 2019;96(2):291–301. doi: 10.1016/j.kint.2019.02.009. - DOI - PubMed
    1. Bonventre JV, Yang L. Cellular pathophysiology of ischemic acute kidney injury. J Clin Invest. 2011;121(11):4210–4221. doi: 10.1172/JCI45161. - DOI - PMC - PubMed
    1. Ishimaru K, Mitsuoka H, Unno N, Inuzuka K, Nakamura S, Schmid-Schönbein GW. Pancreatic proteases and inflammatory mediators in peritoneal fluid during splanchnic arterial occlusion and reperfusion. Shock. 2004;22(5):467–471. doi: 10.1097/01.shk.0000142253.31006.8c. - DOI - PubMed
    1. Leindler L, Morschl E, László F, Mándi Y, Takács T, Jármai K, Farkas G. Importance of cytokines, nitric oxide, and apoptosis in the pathological process of necrotizing pancreatitis in rats. Pancreas. 2004;29(2):157–161. doi: 10.1097/00006676-200408000-00011. - DOI - PubMed

LinkOut - more resources