Abstract

ABSTRACTAim Parinari curatellifolia seed flavonoid extract (PFE) and crude methanol extract (PME) were investigated for their effects on Triton X‐100 (TRT; 200 mg/kg i.p.)‐induced dyslipidemia in rats.MethodsExperimentally induced hyperlipidemic and un‐induced, normal rats were treated with nicotinic acid (300 mg/kg), PFE (20, 25, 30 mg/kg) or PME (100, 150 mg/kg) once daily by gavage for 10 days, following which the biochemistry and histology of the heart, aorta and sera were analyzed.ResultsThe seed extracts produced slight decreases in serum activities of the cardiac markers creatine kinase and lactate dehydrogenase, and did not perturb the cardiac antioxidant status of normal rats. TRT promoted cardiac oxidative stress, decreased high‐density lipoprotein cholesterol (75%, P < 0.001) and increased total cholesterol (TC; 97%, P < 0.001), triglycerides (138%, P < 0.001), low‐density lipoprotein cholesterol (LDL‐c; 281%, P < 0.001), coronary risk index (CRI; sixfold) and atherogenic risk index (ARI; 13‐fold). PFE (20 mg/kg) and PME (150 mg/kg), respectively, restored cardiac antioxidant status and significantly ameliorated the astronomical changes produced by TRT as regards TC (56% and 31%), triglycerides (70% and 66%), LDL‐c (96% and 46%), CRI (92% and 78%) and ARI (99% and 83%), with relatively better efficacy than the reference compound, nicotinic acid (P < 0.01/0.001). In addition, improved heart and aortic histological architecture was observed in rats treated with both extracts. On high‐performance liquid chromatography screening, kaempferol, rutin, and quercitrin were identified as some of the active phytochemicals in PFE.Conclusion P. curatellifolia seed flavonoids have remarkable anti‐hyperlipidemic and anti‐atherogenic effects in acute dyslipidemia caused by TRT.

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