Catechins: Therapeutic Perspectives in COVID-19-Associated Acute Kidney Injury
Abstract
:1. Introduction
2. Materials and Methods
3. Catechins: General Pharmacological Properties
4. Anti-SARS-CoV-2 Activity of Catechins
5. Reno-Protective Effect of Catechins in the Acute Kidney Injury
6. COVID-19 and Acute Kidney Injury (AKI)
7. Conclusions
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Acknowledgments
Conflicts of Interest
References
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Acute Kidney Injury Induced by Nephrotoxic Drugs | |||
---|---|---|---|
Experimental Model | Reno-Protective Effect | Mechanism | Reference |
Rhabdomyolysis-induced AKI (50% glycerol-8 mL/kg, i.m.) | Catechin (40 mg/kg) inhibited the increase of BUN and SCr | Reduced the lipid peroxidation and increased glutathione levels. Restored the activity of renal antioxidant enzymes (SOD, CAT and GR). | [90] |
Fe-NTA-induced AKI (8 mg iron/kg, i.p.) | Catechin (40 mg/kg) inhibited the increase of BUN and SCr | Reduced the lipid peroxidation and increased glutathione levels. Restored the activities of renal antioxidant enzymes (SOD, CAT and GR). | [83] |
Gentamicin-induced AKI (100 mg/kg/day, i.p, for 14 days) | Catechin hydrate (50 mg/kg) inhibited the increase of BUN and SCr | Restored levels of renal glutathione. | [91] |
Cisplatin-induced AKI (7, 8 and 20 mg/kg, i.p.) | EGCG (50 mg/kg) inhibited the increase of BUN and SCr | Restored the Se, Zn and Cu ion concentration in renal tissue. Restored the activities of renal SOD, GPX and CAT. Reduced lipid peroxidation. | [84] |
EGCG (100 mg/kg) improved cisplatin-induced tubular dilatation, cast formation, granulovaculoar degeneration and tubular cell necrosis | Restored the activities of renal antioxidant enzymes (MnSOD and GPX). Reduced production of TNF-α and IL-1β. Decreased accumulation of NF-κB in nucleus, and reduced p53 activation and apoptotic cell death. | [92] | |
ECG (5 mg/kg) inhibited the increase of BUN and SCr | Reduced the lipid peroxidation. Restored the activities of renal antioxidant enzymes (SOD and CAT). Increased GSH. Reduced TNF-α and IL-6. Attenuated the activation of MAPK pathway by decrease phosphorylation of ERK1/2, JNK and p38 in renal tissues. | [87] | |
Contrast-induced nephropathy (CIN) | EGCG (10 mg/kg) normalized SCr and BUN levels, and improved renal histopathological scoring | Reduced the lipid peroxidation. Restored the activities of renal antioxidant enzyme (SOD) and reduced IL-1β via up-regulation of HO-1. | [93] |
Ammonium metavanadate-induced AKI (5 mg/kg, i.p.) | EGCG (5 mg/kg) inhibited oxidative stress | Restored the activities of renal antioxidant enzymes (CAT, SOD and GPx). Reduced lipid peroxidation | [88] |
Acute kidney injury induced by obstructive nephropathy | |||
Unilateral ureteral obstruction (UUO) | Catechin (2.5, 5 and 10 mg/kg) inhibited oxidative stress | Increased GSH and ROS. Increased mRNA and protein expression of Nrf2 and γ-GCS. | [99] |
EGCG (5 mg/kg) alleviated glomerular and tubular injury and attenuated renal interstitial fibrosis in UUO mice | Decreased macrophage infiltration and reduced production of inflammatory cytokines. Decreased expression of kidney damage markers (KIM-1 and NGAL) via NF-κB and Nrf2 nuclear translocation. Promoted HO-1 production | [96,97] | |
Renal ischemia-reperfusion injury | Catechin (40 mg/kg) inhibited the increase of BUN and SCr | Reduced lipid peroxidation, increased glutathione levels and restored activities of renal antioxidant enzymes (SOD, CAT and GR). | [89] |
EGCG (50 mg/kg) inhibited the increase of BUN and SCr | Reduced expression of TNF-α, IL-1β, IL-6, Bax and levels of cleaved caspase 3. | [90] | |
Acute kidney injury accompanying other morbidities | |||
Streptozotocin-induced diabetic nepropathy | Catechins (35 mg/day) prevented functional and morphological deterioration of kidneys, reduced albuminuria and increased creatinine clearance | Catechins reduced lipid peroxidation. | [32,33] |
Salt-induced hypertension and renal injury in Dahl salt-sensitive rats (8%) | EGCG (50 mg/kg) reduced of urinary volume, urine protein and renal fibrosis, and increased CCr | Reduced the lipid peroxidation. Decreased the numbers of infiltrating macrophages and T cells. Induced the apoptosis of NRK-49F cells. | [99] |
Cardiopulmonary by-pass-induced AKI | EGCG (1 mmol/L) inhibited the increase of SCr | Reduced oxidative stress and kidney damage as demonstrated by lower expression of KIM-1 and less production of 8-hydroxy-20 -deoxyguanosine | [85] |
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Diniz, L.R.L.; Elshabrawy, H.A.; Souza, M.T.d.S.; Duarte, A.B.S.; Datta, S.; de Sousa, D.P. Catechins: Therapeutic Perspectives in COVID-19-Associated Acute Kidney Injury. Molecules 2021, 26, 5951. https://doi.org/10.3390/molecules26195951
Diniz LRL, Elshabrawy HA, Souza MTdS, Duarte ABS, Datta S, de Sousa DP. Catechins: Therapeutic Perspectives in COVID-19-Associated Acute Kidney Injury. Molecules. 2021; 26(19):5951. https://doi.org/10.3390/molecules26195951
Chicago/Turabian StyleDiniz, Lúcio Ricardo Leite, Hatem A. Elshabrawy, Marilia Trindade de Santana Souza, Allana Brunna Sucupira Duarte, Sabarno Datta, and Damião Pergentino de Sousa. 2021. "Catechins: Therapeutic Perspectives in COVID-19-Associated Acute Kidney Injury" Molecules 26, no. 19: 5951. https://doi.org/10.3390/molecules26195951