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Assessment of Kidney Function in Mouse Models of Glomerular Disease
Published on: June 30, 2018
Morphological and morphometric study of protective effect of green tea in gentamicin-induced nephrotoxicity in rats
Milica Veljković1, Dragana R Pavlović2, Nenad Stojiljković1
1Department of Physiology, University of Niš, Faculty of Medicine, Bulevar Dr Zoran Djindjić 81, Niš, Serbia.
Aims:
One of the most popular beverages worldwide, green tea, was investigated for its potential protective effect in a rat model of gentamicin-induced nephrotoxicity by monitoring functional and morphological changes in kidneys.
Main Methods:
The study was conducted on four groups of rats: control group (C), treated with only gentamicin (GM), treated with only green tea (GT) and treated with both gentamicin and green tea (GT+GM). Kidney function, oxidant and antioxidant parameters of renal tissue, as well as histopathological studies were assessed. Morphometric analysis was used to quantify these histopathological changes.
Key Findings:
Gentamicin caused significant elevations in serum creatinine and urea and oxidative stress parameter (AOPP), while antioxidative enzyme catalase was significantly decreased. Histological sections of kidneys in GM group revealed necrosis of proximal tubules, vacuolation of cytoplasm and massive mononuclear inflammatory infiltrates in interstitium. Coadministration of green tea with gentamicin histologically showed renoprotective effect. Histological results were confirmed and quantified by morphometric analysis. Also in this group we measured ameliorated parameters of renal functions and antioxidative defense.
Significance:
Regenerative potential of green tea after renal injury induced by gentamicin could be explained through the decrease of oxidative stress and lipid peroxidation. Green tea is a natural antioxidant, with many health promoting effects, widely available and in accordance to that affordable. Because of the established habits, people largely consume it as a beverage. It could be beneficial in the reduction of oxidative stress and changes caused by it primarily in renal tubules and interstitium.
Insights
Green tea demonstrated a protective effect against gentamicin-induced kidney injury in rats. It reduced oxidative stress and improved renal function and morphology, highlighting its potential as a natural antioxidant for kidney health.
Area of Science:
- Nephrology
- Pharmacology
- Nutraceuticals
Background:
- Gentamicin is a common antibiotic with known nephrotoxic side effects.
- Oxidative stress plays a significant role in gentamicin-induced kidney damage.
- Green tea is a widely consumed beverage rich in antioxidants.
Purpose of the Study:
- To investigate the renoprotective effects of green tea in a rat model of gentamicin-induced nephrotoxicity.
- To evaluate the impact of green tea on kidney function, oxidative stress markers, and kidney tissue morphology.
Main Methods:
- Four groups of rats were used: control, gentamicin (GM), green tea (GT), and gentamicin + green tea (GT+GM).
- Kidney function tests, oxidant/antioxidant parameters, and histopathological studies with morphometric analysis were performed.
- Serum creatinine, urea, advanced oxidation protein products (AOPP), and catalase levels were assessed.
Main Results:
- Gentamicin administration significantly increased serum creatinine, urea, and AOPP, while decreasing catalase levels.
- Histopathological examination showed proximal tubule necrosis and inflammation in the GM group.
- Green tea co-administration with gentamicin ameliorated renal function, reduced oxidative stress, and demonstrated a renoprotective effect histologically.
Conclusions:
- Green tea exhibits a regenerative potential against gentamicin-induced kidney injury, likely by decreasing oxidative stress and lipid peroxidation.
- Its antioxidant properties suggest green tea could be beneficial in mitigating kidney damage, particularly in renal tubules and interstitium.
- Green tea's availability, affordability, and widespread consumption make it a promising natural intervention for reducing drug-induced nephrotoxicity.
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