LIPID PROFILE EVALUATION IN ANGIOTENSIN II ADMINISTRATION AND THE EFFECT OF HESPERIDIN INTAKE ON FEMALE WISTAR RATS

Student: Peace Eteng Ifere
Supervisor: Prof E E Nkanu
HOD: Dr Ujong G O
Department of Human Physiology
Basic Medical Sciences
University of Cross River State, Calabar

Abstract

Cardiovascular diseases (CVDs) are a major global health concern, with dyslipidaemia being a significant risk factor. Angiotensin II, a hormone involved in CVD pathogenesis, is known to modulate lipid metabolism. Therefore, this study seeks to evaluate lipid profile changes in female Wistar rats following angiotensin II administration and to investigate the potential protective effects of hesperidin intake on these changes. A total of 36 female Wistar rats weighing between 120 – 170 mg/kg were used for this experiment. The animals were allowed to acclimatize for 4 weeks and they were selected randomly into 6 different groups with 6 rats in each group described as follows; Group 1: Control, rats were given feed and water only; Group 2: Angiotensin II, rats were given angiotensin II only (0.001 ml/kg); Group 3: Angiotensin II + Telmisartan, rats were given Angiotensin II (0.001 ml/kg) + Telmisartan (0.002 ml/kg); Group 4: Angiotensin II + Hesperidin, rats were given Angiotensin II (0.001 ml/kg) + Hesperidin (0.001 ml/kg); Group 5: Telmisartan, rat were given Telmisartan only (0.002 ml/kg), and Group 6: Hesperidin, rats were given Hesperidin (0.001 ml/kg). At the end of the 4-week experimental period, the rats were subjected to an overnight fast and anaesthetized. The anaesthetized animals were bled by cardiac puncture and kidney tissue was harvested and homogenized. The whole blood was collected, allowed to be clotted and then centrifuged. The serum was carefully collected and thereafter stored at -20 oC for lipid profile assay. The result revealed that total cholesterol levels were significantly lower in the hesperidin-supplemented groups compared to the control and AT II-only groups. Similar trends were observed for triglycerides and LDL-c levels. More so, the histological examination revealed normal kidney histology characterized by well-defined glomeruli and tubules, as seen in the control group. However, AT II administration resulted in various forms of kidney damage, including severe glomerular atrophy, tubular pyknosis, and capsular hypercellularity. In contrast, the groups treated with hesperidin exhibited significantly less kidney damage. Plates depicting mild tubular hypertrophy and focal glomerular atrophy in the hesperidin-supplemented groups suggest that while some damage was present, it was substantially mitigated compared to the AT II-only groups. In conclusion, the study’s findings revealed improvements in lipid profiles and kidney histology highlighting hesperidin's potential as a therapeutic agent for mitigating toxic insults and preserving organ function.

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