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Effect of Betulinic acid on diabetic atherosclerosis in apolipoprotein‐E gene knockout mice
Author(s) -
Yoon Jung Joo,
Lee Yun Jung,
Han Byung Hyuk,
Choi Eun Sik,
Namgung Seung,
Tan Rui,
Kho Min Chol,
Park Ji Hun,
Kang Dae Gill,
Lee Ho Sub
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.945.14
Subject(s) - medicine , endocrinology , endothelial dysfunction , enos , apolipoprotein e , triglyceride , diabetes mellitus , cholesterol , insulin resistance , chemistry , nitric oxide , nitric oxide synthase , disease
Atherosclerosis, a chronic and progressive disease, is a leading cause of endothelial dysfunction, diabetes mellitus, hypertension, and hypercholesterolemia. Betulinic acid (BA), a pentacyclic triterpene, has been reported to have a variety of biological effects, such as anti‐inflammatory and immunomodulatory properties. Diabetic apolipoprotein‐E gene knockout (ApoE KO) mice were treated with BA for 12 weeks to examine the beneficial effects on atherosclerosis. As a results that BA‐treated ApoE KO mice significantly lowered systolic blood pressure. Metabolic parameter showed that BA markedly decreased BUN, triglyceride and total‐cholesterol levels. Blood glucose, insulin, glucose tolerance test, and HOMA‐IR index were significantly better in BA treated ApopE KO mice. In addition, consistent with the change in lipid profile, Oil Red O and H&E staining revealed that treatment with BA significantly reduced atherosclerotic lesion such as roughened endothelial layers and fibrous cap formation. Furthermore, BA restored the reduction of endothelial nitric oxide synthase (eNOS) expression, leading to the inhibition of intracellular adhesion molecule‐1 (ICAM‐1) and endothelin‐1 (ET‐1) expression. These results suggest that BA may be useful in the treatment and prevention of early atherosclerosis via attenuation of the endothelial dysfunction in ApoE KO mice.