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Updated: Mar 24, 2026
Preparation of Naringenin Solution for In Vivo Application
Published on: August 10, 2021
Naringin Reduces Hyperglycemia-Induced Cardiac Fibrosis by Relieving Oxidative Stress
Olubunmi A Adebiyi1, Oluwafeyisetan O Adebiyi1, 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:
Hyperglycemia promotes myocardial fibrotic lesions through upregulation of PKC and p38 in response to redox changes. The effects of naringin on hyperglycemia-induced myocardial fibrotic changes and its putative effects on PKC-β and p38 protein expression in type 1 rat model of diabetes are hereby investigated.
Methods:
Male Sprague-Dawley rats were divided into six groups I-VI. Groups I and II, were orally treated with distilled water {3.0 ml/kg body weight (BW)} and naringin (50 mg/kg BW), respectively. Groups III, IV, V and VI were rendered diabetic by a single intraperitoneal injection of streptozotocin (60 mg/kg, BW) and were similarly treated with subcutaneous insulin (8.0 I.U/kg BW, twice daily), naringin (50 mg/kg BW), distilled water (3.0 ml/Kg BW) and ramipril (3.0 mg/kg/BW), respectively. The animals were sacrificed after 56 days by halothane overdose; blood and heart samples removed for further analysis.
Results:
The untreated diabetic rats exhibited significantly increased oxidative stress, NADPH oxidase activity, increased cardiac fibrosis, PKC-β and p38 mitogen activated protein kinase expression compared to controls. Naringin treatment significantly ameliorated these changes in diabetic rats compared to the untreated diabetic controls.
Conclusions:
Naringin's amelioration of myocardial fibrosis by modulating p38 and PKC-β protein expression possibly through its known antioxidant actions and may therefore be useful in retarding the progression of fibrosis in a diabetic heart.
Insights
Naringin, a natural compound, was found to reduce heart fibrosis in diabetic rats. It works by lowering oxidative stress and modulating specific protein expressions, offering potential benefits for diabetic heart conditions.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Diabetology
Background:
- Hyperglycemia in diabetes mellitus accelerates myocardial fibrosis.
- Protein kinase C (PKC) and p38 mitogen-activated protein kinase (MAPK) pathways are implicated in hyperglycemia-induced cardiac damage.
- Redox changes play a crucial role in the development of diabetic cardiomyopathy.
Purpose of the Study:
- To investigate the protective effects of naringin against hyperglycemia-induced myocardial fibrosis in a type 1 diabetes rat model.
- To determine naringin's impact on PKC-β and p38 protein expression in diabetic rat hearts.
- To explore the potential of naringin as a therapeutic agent for diabetic heart disease.
Main Methods:
- A type 1 diabetes mellitus rat model was established using streptozotocin.
- Diabetic rats were treated with naringin, insulin, or ramipril.
- Cardiac fibrosis, oxidative stress markers, and PKC-β and p38 protein levels were assessed.
Main Results:
- Untreated diabetic rats showed increased oxidative stress, NADPH oxidase activity, and cardiac fibrosis.
- Elevated levels of PKC-β and p38 MAPK were observed in diabetic rat hearts.
- Naringin treatment significantly reduced oxidative stress and cardiac fibrosis in diabetic rats compared to controls.
Conclusions:
- Naringin ameliorates myocardial fibrosis in diabetic rats, likely via its antioxidant properties.
- The compound modulates p38 and PKC-β protein expression, contributing to its cardioprotective effects.
- Naringin shows promise in retarding the progression of fibrosis in diabetic hearts.
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