4‑Methoxybenzylalcohol protects brain microvascular endothelial cells against oxygen‑glucose deprivation/reperfusion‑induced injury via activation of the PI3K/AKT signaling pathway
- Qing Lin
- Weili Wang
- Liping Yang
- Xiaohua Duan
Affiliations: Department of Pharmacology, Yunnan University of Chinese Medicine, Kunming, Yunnan 650500, P.R. China, Yunnan Key Laboratory of Dai and Yi Medicine, University of Chinese Medicine, Kunming, Yunnan 650500, P.R. China
- Published online on: January 24, 2021 https://doi.org/10.3892/etm.2021.9684
Copyright: © Lin
et al. This is an open access article distributed under the
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Damage to the blood‑brain barrier (BBB) during the process of cerebral ischemic injury is a key factor that affects the treatment of this condition. The present study aimed to assess the potential effects of 4‑methoxybenzyl alcohol (4‑MA) on brain microvascular endothelial cells (bEnd.3) against oxygen‑glucose deprivation/reperfusion (OGD/Rep) using an in vitro model that mimics in vivo ischemia/reperfusion injury. In addition, the present study aimed to explore whether this underlying mechanism was associated with the inhibition of pro‑inflammatory factors and the activation status of the PI3K/Akt signaling pathway. bEnd.3 cells were subjected to OGD/Rep‑induced injury before being treated with 4‑MA, following which cell viability, lactate dehydrogenase (LDH) release and levels of nitric oxidase (NO) were detected by colorimetry, pro‑inflammatory factors including tumor necrosis factor‑α (TNF‑α), interleukin (IL)‑1β and IL‑6, were detected by ELISA. The expression levels of occluding and claudin‑5were evaluated by immunofluorescence staining. The expression levels of AKT, phosphorylated (p)‑Akt, endothelial nitric oxide synthase (eNOS) and p‑eNOS were also measured by western blot analysis. After bEnd.3 cells were subjected to OGD/Rep‑induced injury, cell viability and NO levels were significantly decreased, whilst LDH leakage and inflammatory factor (TNF‑α, IL‑1β and IL‑6) levels were significantly increased. Treatment with 4‑MA significantly ameliorated cell viability, LDH release and the levels of NO and pro‑inflammatory factors TNF‑α, IL‑1β and IL‑6 as a result of OGD/Rep. Furthermore, treatment with 4‑MA upregulated the expression of occludin, claudin‑5, Akt and eNOS, in addition to increasing eNOS and AKT phosphorylation in bEnd.3 cells. These results suggest that 4‑MA can alleviate OGD/Rep‑induced injury in bEnd.3 cells by inhibiting inflammation and by activating the PI3K/AKT signaling pathway as a possible mechanism. Therefore, 4‑MA can serve as a potential candidate for treating OGD/Rep‑induced injury.