Effects of dexmedetomidine post‑treatment on BDNF and VEGF expression following cerebral ischemia/reperfusion injury in rats

Abstract

Brain‑derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF) serves a significant role in neural protection by activating the phosphatidylinositol 3‑kinase (PI3K)/Akt signaling pathway, which also was associated with the neuroprotective the treatment with dexmedetomidine (DEX). The present study aimed to further explore whether treatment with DEX post‑IR increased the expression level of BDNF and VEGF in the rat brain. A total of 30 healthy, clean male Wistar rats were randomly divided into 3 experimental groups: Control group, ischemia/reperfusion (I/R) group and DEX treatment group. Subsequently, BDNF and VEGF mRNA and protein expression levels were analyzed. The results indicated that the mRNA expression levels of BDNF and VEGF were higher in the I/R and DEX groups compared with expression levels in the Control group at 6 h and 1 day post‑treatment; the levels of BNDF mRNA expression were higher in the DEX group compared with the I/R group. The levels of BDNF and VEGF protein expression in the I/R and DEX groups were also significantly higher compared with those in the Control group. I/R surgery significantly increased the expression of BDNF and VEGF protein DEX group at 6 h, day 1 and day 3 compared with expression levels in the I/R group. Results from the present study indicated that post‑surgical treatment with DEX may increase the expression of BDNF and VEGF following I/R, which may serve a role in nerve protection.

Retracted: A multicentre randomised controlled trial of the effect of intra‐operative dexmedetomidine on cognitive decline after surgery

“…Postoperative reductions in serum brain‐derived neurotrophic factors were associated with cognitive dysfunction, which suggests reductions in cerebral concentrations 15,32. Dexmedetomidine increases cerebral brain‐derived neurotrophic factor concentrations and associated neuroprotective effects 33,34. Dexmedetomidine can reverse anaesthesia‐induced reductions in plasma concentrations within 24 postoperative hours 35.…”

The outcomes of dexmedetomidine and calcitriol on flap viability

“…The results of a study in an IR injury in rats, found that post-surgical treatment with dexmedetomidine may increase the expression of VEGF 34 and also studies showing that calcitriol increases VEGF expression and release in vascular smooth muscle cells 35,36 , which may have the role in increasing flap viability and support our findings. However, in our study, we have evaluated the oxidative mechanisms and assessed the angiogenesis morphologically in flap viability other than focusing on neovascular angiogenesis, tissue regeneration, or hypoxia with specific biomarkers such as VEGF, transforming growth factor beta (TGF-beta), and hypoxia inducible factor 1 (HIF-1); we think that studying these biomarkers definitely warrants a further study to confirm our results.…”

AG490 protects cerebral ischemia/reperfusion injury via inhibiting the JAK2/3 signaling pathway

“…Brain‐derived neurotrophic factor (BDNF) plays a pivotal role in neural development and diseases (Binder & Scharfman, 2004). It was reported that BDNF mRNA expression was higher in the I/R model in vivo from 6 hr to 3 days post‐I/R surgery (Li et al., 2018). Here, we examined that AG490 treatment further enhanced the expression of BDNF not only in the serum but also in the brain.…”