1. The anti-inflammatory properties of green tea extract protect against gentamicin-induced kidney injury.
- Author
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Ayusso LL, Girol AP, Ribeiro Souza H, Yoshikawa AH, de Azevedo LR, Carlos CP, Volpini RA, Schor N, and Burdmann EA
- Subjects
- Animals, Male, Rats, Antioxidants pharmacology, Oxidative Stress drug effects, Kidney drug effects, Kidney pathology, Kidney metabolism, Cytokines metabolism, Acute Kidney Injury chemically induced, Acute Kidney Injury prevention & control, Acute Kidney Injury pathology, NF-kappa B metabolism, Kidney Diseases prevention & control, Kidney Diseases chemically induced, Kidney Diseases pathology, Cyclooxygenase 2 metabolism, Protective Agents pharmacology, Inflammation Mediators metabolism, Gentamicins toxicity, Rats, Wistar, Anti-Inflammatory Agents pharmacology, Plant Extracts pharmacology, Tea chemistry
- Abstract
We assessed in vivo the protective effects and underlying antioxidant and anti-inflammatory properties of dry green tee extract (GTE) on glomerular and tubular kidney function and structure in an experimental model of gentamicin (GEN)-induced nephrotoxicity. Wistar rats were divided into four groups and treated daily for 10 days. The control group received distilled water; the GTE group received 20 μg/g body weight (BW) GTE by gavage; the GEN group received 100 mg/g BW GEN intraperitoneally; and the GEN+GTE group received GTE and GEN simultaneously, as described above. At the beginning and end of treatment, the serum creatinine, fractional excretion of sodium and potassium, and plasma heme oxygenase (HO)-1 levels and oxidative stress (OS) were assessed. At the end of the experiment, kidney fragments were collected for histological evaluation and immunohistochemical studies of cyclooxygenase (COX)-2 and nuclear factor (NF)kB. The levels of interleukin (IL)-1b, IL-4, IL-6, IL-10 and monocyte chemotactic protein (MCP)-1 were measured in kidney tissue. The results showed that GTE attenuated significantly kidney structural injury and prevented GEN-induced kidney functional injury (glomerular and tubular function). GTE significantly attenuated the kidney tissue increase of the proinflammatory mediators NF-kB, COX2, IL-1b and MCP-1 and significantly increased the kidney expression of the anti-inflammatory cytokines IL-6 and IL-10. However, GTE did not prevent OS increase in GEN-treated animals. In conclusion, GTE protected against GEN nephrotoxicity, likely due to direct blockade of the inflammatory cascade, which might had occurred independently of its antioxidant effect., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)
- Published
- 2024
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