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Chronic administration of troxerutin protects mouse kidney against D-galactose-induced oxidative DNA damage
Chan-Min Liu1, Jie-Qiong Ma, Yao Lou
1School of Life Science, Xuzhou Normal University, No 101, Shanghai Road, Tangshan New Area, Xuzhou City 221116, Xuzhou City, PR China. lcm9009@126.com
Abstract:
Troxerutin, a natural bioflavonoid, has been reported to have many benefits and medicinal properties. In this study, we evaluated the protective effect of troxerutin against D-gal-induced oxidative DNA damage in mouse kidney, and explored the potential mechanism of its action. Our data showed that troxerutin significantly decreased levels of urea, uric acid and creatinine in serum and the renal histological injury in D-gal-treated mice. Troxerutin markedly restored Cu/Zn-SOD, CAT and GPx activities in the kidney of D-gal-treated mouse. Furthermore, the increase of 8-hydroxydeoxyguanosine (a marker of oxidative DNA damage) induced by d-gal was effectively suppressed by troxerutin. Internucleosomal DNA ladder fragmentation and the number of terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP) nick-end-labeling (TUNEL)-positive cells in D-gal-treated mice were inhibited by troxerutin, which might be attributed to its antioxidant property by decreasing activities of nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase) and levels of reactive oxygen species (ROS). In conclusion, these results suggested that troxerutin could protect the mouse kidney against D-gal-induced injury by improving renal function, attenuating histopathologic changes, reducing ROS production, renewing the activities of antioxidant enzymes and decreasing DNA oxidative damage. This study provided novel insights into the protective mechanisms of troxerutin in D-gal-induced kidney injury.
Insights
Troxerutin protects mouse kidneys from D-galactose-induced injury by reducing oxidative stress and DNA damage. This bioflavonoid enhances antioxidant enzyme activity and improves overall kidney function.
Area of Science:
- Biochemistry
- Pharmacology
- Nephrology
Background:
- Troxerutin, a natural bioflavonoid, possesses known medicinal properties.
- D-galactose (D-gal) administration induces oxidative DNA damage in mouse kidneys.
- Understanding troxerutin's protective mechanisms against D-gal-induced kidney injury is crucial.
Purpose of the Study:
- To evaluate the protective effects of troxerutin against D-galactose-induced oxidative DNA damage in mouse kidneys.
- To elucidate the underlying mechanisms of troxerutin's renoprotective action.
Main Methods:
- Mice were treated with D-galactose to induce kidney injury.
- Troxerutin administration was assessed for its effects on renal function markers (urea, uric acid, creatinine).
- Kidney tissues were analyzed for antioxidant enzyme activities (Cu/Zn-SOD, CAT, GPx), oxidative DNA damage marker (8-hydroxydeoxyguanosine), DNA fragmentation, and cell apoptosis (TUNEL assay). NADPH oxidase activity and ROS levels were also measured.
Main Results:
- Troxerutin significantly reduced serum urea, uric acid, and creatinine levels, and ameliorated renal histological damage in D-gal-treated mice.
- Troxerutin restored the activities of antioxidant enzymes (Cu/Zn-SOD, CAT, GPx) in the kidney.
- Troxerutin suppressed D-gal-induced 8-hydroxydeoxyguanosine levels, internucleosomal DNA ladder fragmentation, and TUNEL-positive cells, likely by decreasing NADPH oxidase activity and ROS production.
Conclusions:
- Troxerutin demonstrates significant renoprotective effects against D-galactose-induced kidney injury.
- The protective mechanisms involve improving renal function, reducing oxidative stress (ROS production), enhancing antioxidant enzyme activity, and mitigating DNA damage.
- These findings provide novel insights into troxerutin's therapeutic potential for kidney protection.
