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Updated: Mar 16, 2026
Preparation of Naringenin Solution for In Vivo Application
Published on: August 10, 2021
Naringin protects against HIV-1 protease inhibitors-induced pancreatic β-cell dysfunction and apoptosis
Sanelisiwe Nzuza1, Duduzile E Ndwandwe1, Peter M O Owira1
1Molecular and Clinical Pharmacology Research Laboratory, Department of Pharmacology, Discipline of Pharmaceutical Sciences, School of Health Sciences, University of KwaZulu-Natal, P.O. Box X5401, Durban, South Africa.
Introduction:
The protective effects of grapefruit-derived naringin against HIV-1 Protease Inhibitors (PIs)-associated oxidative damage to pancreatic β-cells and apoptosis were investigated in RIN-5F cells in culture.
Methods:
Cells in culture medium were challenged with 11-25 mM glucose with or without nelfinavir (1-10 μM), saquinavir (1-10 μM) and atazanavir (5-20 μM), respectively for 24 h to determine insulin secretion. The cells were further treated with nelfinavir (10 μM), saquinavir (10 μM), atazanavir (20 μM) with and without naringin or glibenclamide (10 μM) for 24 h to determine insulin secretion, lipid peroxidation, Superoxide Dismutase (SOD) activity, glutathione (GSH) levels, ATP production and caspase-3 and-9 activities, respectively.
Results:
Glucose-dependent insulin secretion was significantly reduced by PIs in a concentration-dependent manner. Treatment with either naringin or glibenclamide significantly reduced lipid peroxidation, Superoxide Dismutase (SOD) activities and also increased glutathione (GSH) and ATP levels in the cells that were treated with PIs. Furthermore, naringin or glibenclamide significantly reduced caspase-3 and caspase-9 activities in cells that were treated with PIs.
Conclusions:
PIs impair β-cell functions by increasing oxidative stress and apoptosis. Treatment with naringin protected RIN-5F cells from PI-induced oxidative damage and apoptosis. Our results therefore suggest that nutritional supplements with naringin could prevent pancreatic β-cell dysfunction and the attendant metabolic complications caused by PIs in patients on antiretroviral therapy.
Insights
Grapefruit-derived naringin protects pancreatic beta-cells from HIV-1 Protease Inhibitor (PI) damage. Naringin reduces oxidative stress and apoptosis, suggesting its potential as a nutritional supplement to prevent PI-related metabolic complications.
Area of Science:
- Cell biology
- Biochemistry
- Pharmacology
Background:
- HIV-1 Protease Inhibitors (PIs) can cause oxidative damage and apoptosis in pancreatic beta-cells.
- This damage may lead to impaired insulin secretion and metabolic complications.
Purpose of the Study:
- To investigate the protective effects of naringin, a grapefruit-derived compound, against PI-induced damage in pancreatic beta-cells.
- To evaluate naringin's impact on oxidative stress, apoptosis, and insulin secretion.
Main Methods:
- RIN-5F cells were treated with PIs (nelfinavir, saquinavir, atazanavir) and varying glucose concentrations.
- Insulin secretion, lipid peroxidation, Superoxide Dismutase (SOD) activity, glutathione (GSH) levels, ATP production, and caspase activities were measured.
- Cells were also treated with naringin or glibenclamide to assess their protective effects.
Main Results:
- PIs significantly reduced glucose-dependent insulin secretion in a concentration-dependent manner.
- Naringin and glibenclamide treatments reduced lipid peroxidation and SOD activity while increasing GSH and ATP levels.
- Both naringin and glibenclamide significantly reduced caspase-3 and caspase-9 activities.
Conclusions:
- PIs impair beta-cell function through oxidative stress and apoptosis.
- Naringin effectively protected RIN-5F cells from PI-induced oxidative damage and apoptosis.
- Nutritional supplementation with naringin may help prevent pancreatic beta-cell dysfunction in patients on antiretroviral therapy.
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