Xue Xing, Lv Ying, Leng Yufang, Zhang Yan
Department of Anesthesiology, The First Hospital of Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Department of Resource and Environmental Engineering, Gansu Agricultural University, Lanzhou, Gansu 730070, P.R. China.
Exp Ther Med. 2018 Oct;16(4):3011-3019. doi: 10.3892/etm.2018.6540. Epub 2018 Jul 30.
The neurotoxicity of local anesthetics has received an increasing amount of attention and more effective therapeutic agents are required. Extracellular polymeric substances from (EPS-A) are high molecular weight polysaccharides. The present study aimed to elucidate the protective effects of EPS-A on neurotoxicity induced by local anesthetics in an intraperitoneal injection bupivacaine rat model. The results of immunohistochemical staining inicated that following intraperitoneal injection of EPS-A the levels of apoptosis and caspase-3 decreased, and the expression levels of microtubule-associated protein 1A light chain 3 (LC3) and beclin1 increased. In order to further clarify the mechanism of the EPS-A-mediated protection, the expression of key proteins associated with autophagy was investigated by western blotting. The results suggested that the ratio of LC3-II/LC3-I and the expression level of beclin1 increased. Taken together, the results indicated that EPS-A induced neuroprotective effects on bupivacaine-induced neurotoxicity. The underlying mechanism may be associated with the inhibition of apoptosis, upregulation of autophagy and improvement of cell survival. The results suggested that EPS-A may be a candidate neuroprotective agent against neurotoxicity caused by local anesthetics.
局部麻醉药的神经毒性已受到越来越多的关注，需要更有效的治疗药物。来自（EPS-A）的细胞外聚合物是高分子量多糖。本研究旨在阐明EPS-A对腹腔注射布比卡因大鼠模型中局部麻醉药诱导的神经毒性的保护作用。免疫组织化学染色结果表明，腹腔注射EPS-A后，细胞凋亡水平和半胱天冬酶-3水平降低，微管相关蛋白1A轻链3（LC3）和贝林1的表达水平升高。为了进一步阐明EPS-A介导的保护机制，通过蛋白质印迹法研究了与自噬相关的关键蛋白的表达。结果表明，LC3-II/LC3-I的比值和贝林1的表达水平升高。综上所述，结果表明EPS-A对布比卡因诱导的神经毒性具有神经保护作用。潜在机制可能与抑制细胞凋亡、上调自噬和改善细胞存活有关。结果表明，EPS-A可能是一种针对局部麻醉药引起的神经毒性的候选神经保护剂。
