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Beta-carotene ameliorates diabetic nephropathy in rats: involvement of AMPK/SIRT1/autophagy pathway
Salma A El-Marasy1, Hadir Farouk1, Marwa S Khattab2
1Department of Pharmacology, Medical Research and Clinical Studies Institute, National Research Centre, Giza, Egypt.
Objective:
This study aimed to demonstrate the protective effect of beta-carotene against STZ-induced DN in rats and explore the possible underlying mechanisms that may have mediated such condition.
Material And Methods:
Wistar rats were allocated into four groups. Normal group received distilled water for 3 weeks. The other three groups were rendered diabetic by an intraperitoneal dose of STZ (50 mg/kg), 48 h later, group 2: received the vehicle and served as control, groups (3 &4) received orally beta-carotene in doses of 10 and 20 mg/kg, respectively for 3 weeks. Then serum and renal tissue were collected for biochemical, molecular, immunohistopathological, and histopathological examination.
Results:
Beta-carotene ameliorated the reduction in body weight, reduced blood glucose, elevated serum insulin, reduced blood urea nitrogen, and serum creatinine levels. Beta-carotene elevated phosphorylated 5' adenosine monophosphate-activated protein kinase (p-AMPK)/AMPK, alleviated phosphorylated mammalian target of rapamycin (p-mTOR)/mTOR, reduced interleukin 1 beta (IL-1β), increased Beclin 1, LC3II/LC3I, and reduced p62 renal contents. Moreover, it elevated renal SIRT1 gene expression and reduced renal tumor necrosis factor-alpha (TNF-α) and caspase-3 protein expressions.
Conclusion:
Beta-carotene exerted renoprotective effect against STZ-induced DN and histopathological alterations through alleviating hyperglycemia, attenuating inflammation, activating AMPK/SIRT1/autophagy pathway, and combating apoptosis.
Insights
Beta-carotene protects against diabetic nephropathy (DN) by reducing blood glucose and inflammation. It activates key cellular pathways, including AMPK/SIRT1 and autophagy, while reducing apoptosis, demonstrating a significant renoprotective effect.
Area of Science:
- Biochemistry
- Pharmacology
- Nephrology
Background:
- Diabetic nephropathy (DN) is a major complication of diabetes, leading to kidney damage.
- Strengthening understanding of protective mechanisms against DN is crucial for therapeutic development.
Purpose of the Study:
- To investigate the renoprotective effects of beta-carotene in a rat model of STZ-induced diabetic nephropathy.
- To elucidate the molecular mechanisms underlying beta-carotene's protective action against DN.
Main Methods:
- Wistar rats were induced with diabetes using streptozotocin (STZ) and treated with varying doses of beta-carotene.
- Collected serum and renal tissues were analyzed using biochemical, molecular, and histopathological techniques.
Main Results:
- Beta-carotene treatment improved body weight, reduced blood glucose, and normalized kidney function markers (BUN, creatinine).
- It modulated key signaling pathways, including activating AMPK/SIRT1 and autophagy (Beclin 1, LC3II/LC3I), while inhibiting mTOR, inflammation (IL-1β, TNF-α), and apoptosis (caspase-3).
Conclusions:
- Beta-carotene demonstrates significant renoprotective effects against STZ-induced DN in rats.
- These benefits are attributed to its ability to alleviate hyperglycemia, reduce inflammation, activate the AMPK/SIRT1/autophagy pathway, and inhibit apoptosis.
