Propranolol regulates ERK1/2 signaling pathway and promotes chronic wound healing in diabetic rats

X. Chang, S. Li, X.-D. Xue, F. Chang

Department of Endocrinology, Wuwei People’s Hospital, Wuwei, P.R. China. 895420334@qq.com

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• Pharmacology

OBJECTIVE: This study aimed to investigate if propranolol could regulate ERK1/2 signaling pathway and promote chronic wound healing in diabetic rats.
MATERIALS AND METHODS: Twenty-two rats were used to establish a diabetic chronic wound animal model. They were randomly separated into two groups: the propranolol group and the control group. The propranolol group was treated with propranolol ointment and the control group was treated with propranolol matrix cream to cover the wound surface. The expression of the p-ERK1/2 protein was detected by the Western Blot. RT-qPCR was used to detect the expression of VEGF. The concentrations of IL-6 and TNF-α were detected by ELISA.
RESULTS: The body weight of rats was significantly reduced after type 2 diabetes mellitus modeling. The healing rate of rats in the control group was significantly lower than that in the propranolol group (p<0.05). There was a significant increase in the expression of the p-ERK1/2 protein in the wound tissue of the propranolol group compared with that in the control group, except for the 11th day (p<0.05). The relative expression of Vascular Endothelial Growth Factor (VEGF) in the propranolol group was significantly higher than that in the control group on the 2nd day (p<0.05), while the relative expression of VEGF in the propranolol group was significantly increased on the 11th day after modeling (p<0.05). On the 20th day, the expressions of IL-6 and TNF-α in the propranolol group were significantly higher than those in the control group, and there were significant differences (p<0.05). It was found that the IL-6 and TNF-α expressions in the propranolol group reached the peak on the 11th day and then gradually decreased (p<0.05).
CONCLUSIONS: The results indicated that propranolol can accelerate the healing of diabetic wounds by regulating the expression of VEGF by phosphorylation of ERK1/2 protein, thus promoting chronic wound healing in diabetes.

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