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Nephroprotective potential of syringic acid in experimental diabetic nephropathy: Focus on oxidative stress and
Bhoomika Sherkhane1, Veera Ganesh Yerra2, Anjana Sharma3
1Department of Pharmacology and Toxicology, NIPER, Hyderabad, Balanagar, Telangana, India; Department of Medical Biochemistry and Cell Biology, University of Gothenburg, Sweden.
Background:
Diabetic nephropathy (DN) is a chronic hyperglycemic manifestation of microvascular damage in the kidneys. Widespread research in this area suggests the involvement of perturbed redox homeostasis and autophagy in renal cells phrase- promote the progression of DN.
Materials And Methods:
Reframed sentences-The present study investigates the pharmacological effect of Syringic acid (SYA), in streptozotocin (STZ, 55 mg/kg, i.p) induced diabetic nephropathy model and in high glucose (30 mM) challenged rat renal epithelial cells (NRK 52E) cells with a focus on oxidative stress and autophagy mechanisms.
Results:
Both in vivo and in vitro experimental data revealed elevated oxidative stress markers along with compromised levels of nuclear factor erythroid 2-related factor 2 (Nrf2), a pivotal cellular redox-regulated transcription factor in renal cells upon glycemic stress. Elevated blood glucose also reduced the autophagy process as indicated by low expression of light chain (LC) 3-IIB in diabetic kidney and in NRK 52E cells subjected to excess glucose. SYA (25 and 50 mg/kg, p.o.) administration for 4 weeks to diabetic rats, Reframed sentence-preserved the renal function as evidenced by reduced serum creatinine levels as well as improved urine creatinine and urea levles as compared to non treated diabetic animals. At the molecular level, SYA improved renal expression of Nrf2 and autophagy-related proteins (Atg5, Atg3, and Atg7) in diabetic rats. Similarly, SYA (10 and 20 μM) co-treatment in high glucose-treated NRK 52E cells displayed increased levels of Nrf2 and autophagy induction.
Conclusion:
Results from this study signify the renoprotective effect of SYA and highlight the modulation of oxidative stress and autophagy mechanisms to mitigate diabetic kidney disease.
Insights
Syringic acid (SYA) protects against diabetic kidney disease by reducing oxidative stress and enhancing autophagy. This study shows SYA improves kidney function and key molecular markers in diabetic models.
Area of Science:
- Nephrology
- Pharmacology
- Biochemistry
Background:
- Diabetic nephropathy (DN) is a kidney complication of diabetes, characterized by microvascular damage.
- Perturbed redox homeostasis and impaired autophagy are implicated in DN progression.
Purpose of the Study:
- To investigate the renoprotective effects of Syringic acid (SYA) in a diabetic nephropathy model.
- To explore SYA's impact on oxidative stress and autophagy mechanisms in diabetic kidney disease.
Main Methods:
- Induced diabetic nephropathy in rats using streptozotocin (STZ) and challenged rat renal epithelial cells (NRK 52E) with high glucose.
- Administered SYA to diabetic rats and co-treated high glucose-challenged cells with SYA.
- Assessed renal function markers, oxidative stress, and autophagy-related protein expression.
Main Results:
- Diabetic conditions elevated oxidative stress markers and reduced Nrf2 and autophagy protein levels (LC3-IIB).
- SYA treatment preserved renal function, indicated by improved serum and urine creatinine/urea levels.
- SYA increased Nrf2 expression and promoted autophagy (Atg5, Atg3, Atg7) in both in vivo and in vitro models.
Conclusions:
- Syringic acid (SYA) demonstrates significant renoprotective effects in diabetic kidney disease.
- SYA mitigates DN by modulating oxidative stress and enhancing autophagy pathways.
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