Abstract
Vascular complications induced by diabetes constitute the principal cause of morbidity and mortality in diabetic patients. It’s reported that carvacrol (CAR) possess a wide range of biological activities. The effect of CAR on diabetes-induced vasculopathy remains unknown. In this study, diabetic mice were created by intraperitoneal injection of streptozotocin to investigate whether CAR provided a protective effect against diabetes-induced vasculopathy and the underlying mechanisms. We found that CAR decreased blood glucose level of diabetic mice. Moreover, CAR ameliorated diabetes-induced aorta morphological alteration, evidenced by increased thickness of intima-media width and increased number of vascular smooth muscle cell (VSMC) layer. Further studies revealed that CAR inhibited the hypercontractility in the aorta of diabetic mice and VSMC in response to hyperglycemia, evidenced by decreased expression of smooth muscle (SM)-α-actin, and increased expression of Ki67 and PCNA. Furthermore, PI3K/Akt signal pathway was inhibited in the aorta of diabetic mice and VSMC in response to hyperglycemia, while CAR treatment activated PI3K/Akt signaling pathway. In conclusion, our results strongly suggested that CAR played a protective role in diabetes-induced aorta hypercontractility, possibly by activating PI3K/Akt signaling pathway. CAR is a potential drug for the treatment of diabetic vasculopathy.
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