Protective and therapeutic effects of Trianthema portulacastrum against atherosclerosis in male albino rats via G-protein-coupled receptor 124

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Abstract

Atherosclerosis is a severe cardiovascular disease characterized by narrowing of the lumen, plaque formation, and blood flow turbulence as a result of cholesterol and lipid accumulation in the inner lining of arteries. Bishkhapra (Trianthema portulacastrum Linn.) is a well-known common weed belonging to the family Aizoaceae. Several bioactive compounds have been isolated from this weed and widely used against several diseases. The present study evaluated the protective and therapeutic efficacies of T. portulacastrum against atherosclerosis in a rat model. The animals were divided into the sham, control (diabetes- + atherosclerosis-inducing diet), 100 mg/kg T. portulacastrum treatment, 200 mg/kg T. portulacastrum treatment, and positive control groups. Blood glucose, cholesterol, triglyceride, and other lipid parameters, as well as the expression of G-protein-coupled receptor 124 (GPR124), were measured. Glucose, cholesterol, and triglycerides were significantly reduced to near normal levels. The serum levels of fibrinogen, sVCAM-1, and oxidized low density lipoproteins were substantially increased in control rats. Treatment with the T. portulacastrum extract reversed these levels to near normal levels. The mRNA expression of GPR124 was increased by 150% in the control group. However, treatment with T. portulacastrum extract decreased the mRNA expression up to 40% compared with the control group. Rats treated with 100 and 200 mg/kg T. portulacastrum extract showed a decrease in GPR124 protein expression by 9.5% and 33.3%, respectively. Taken together, the results suggest that an extract of T. portulacastrum is effective against atherosclerosis in streptozotocin-induced diabetic rats.

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Wu, H., Gao, T., Cao, Y., Diao, J., Chang, F., Qi, J., & Wang, C. (2019). Protective and therapeutic effects of Trianthema portulacastrum against atherosclerosis in male albino rats via G-protein-coupled receptor 124. AMB Express, 9(1). https://doi.org/10.1186/s13568-019-0901-7

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