ABSTRACT
Background
Cardiovascular diseases and its associated chronic disorders are was and tend to be a global threat for centuries. 80% of cardiovascular diseases were reported in the lower and middle income countries. Chronic atherosclerosis, a chronic circulatory disorder occurs due to the platelet aggregation, thrombosis formation and eventually rupture of atherosclerotic plaque causes excessive mortalities and morbidities worldwide. Previously elderly people were at risk of cardiovascular diseases whereas at present due to life style changes rise in premature chronic atherosclerosis mortality was observed. Since atherosclerosis is mostly asymptomatic diagnosis and treating the disease is a challenging task for the physicians. Lipids lowering drugs, anticoagulants, antiplatelet drugs, diuretics etc were prescribed to treat cardiovascular disease. This medication on long term usage causes enormous side effects which affects the quality of life of the patients. Natural drug are potential alternative for the allopathic drugs to various chronic diseases.
Objectives
In our study we examined the potency of lichen metabolite usnic acid potency to treat atherosclerosis induction in rats. Atherosclerosis was induced in Wistar rats with high fat diet model.
Materials and Methods
Food intake and body weight gain in experimental animals were monitored regularly. To confirm the induction of atherosclerosis in rats the complete lipid profile was assessed with commercially available kits. Atherogenic index, TC/HDLc and LDLc/HDLc were also calculated to further confirm the high fat diet induced hyperlipidemic condition. Cardiac profile was quantified to evaluate the ameliorative potency of usnic acid against high fat diet induced atherosclerosis. Inflammation the prime initiator of atherosclerosis hence pro-inflammatory cytokines and C-reactive protein were measured in the experimental rats. To assess the impact of usnic acid on high fat diet induced endothelial dysfunction the levels of NO, ET, 6-keto-PGF1a and TXB2 in serum of experimental rats. Finally, to confirm the anti-atherosclerotic property of usnic acid histological analysis of aorta was performed.
Results
Usnic acid significantly prevented weight gain, dysregulation of lipid and cardiac profile in high fat diet induced rats. It also inhibited the inflammatory response via decreasing the levels of pro-inflammatory cytokines. Usnic acid potentially increased the NO, 6-keto-PGF1a and decreased ET, TXB2 thereby prevented high fat diet induced endothelial dysfunction in experimental rats. Histopathological analysis endorses the ameliorative potency of usnic acid against high fat diet induced atherosclerosis in rats.
Conclusion
Altogether our study reveals usnic acid can be a potent drug to treat high fat diet induced atherosclerosis and can be subjected to further research.