AIM: To explore whether human umbilical cord mesenchymal stem cell (hUCMSC)-derived exosomes (hUCMSC-Exos) protect rat retinal neurons in high-glucose (HG) conditions by activating the brain-derived neurotrophic factor (BDNF)-TrkB pathway. METHODS: hUCMSC-Exos were collected with differential ultracentrifugation methods and observed by transmission electron microscopy. Enzyme-linked immunosorbent assays (ELISAs) was used to quantify BDNF in hUCMSC-Exos, and Western blot was used to identify surface markers of hUCMSC-Exos. Rat retinal neurons were divided into 4 groups. Furthermore, cell viability, cell apoptosis, and TrkB protein expression were measured in retinal neurons. RESULTS: hUCMSCs and isolated hUCMSC-Exos were successfully cultured. All hUCMSC-Exos showed a diameter of 30 to 150 nm and had a phospholipid bimolecular membrane structure, as observed by transmission electron microscopy. ELISA showed the BDNF concentration of hUCMSCs-Exos was 2483.16±281.75. hUCMSCs-Exos effectively reduced the apoptosis of retinal neuron rate and improved neuron survival rate, meanwhile, the results of immunofluorescence verified the fluorescence intensity of TrKB in neurons increased. And all above effects were reduced by treated hUCMSCs-Exos with BDNF inhibitors. hUCMSC-Exos effectively reduced the apoptosis rate of retinal neurons by activating the BDNF-TrkB pathway in a HG environment. CONCLUSION: In the HG environment, hUCMSC-Exos could carry BDNF into rat retinal neurons, inhibiting neuronal apoptosis by activating the BDNF-TrkB pathway.

中文翻译：

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人脐带间充质干细胞源性外泌体通过脑源性神经营养因子/TrkB通路对高血糖大鼠视网膜神经元的保护作用

目的：探讨人脐带间充质干细胞（hUCMSC）来源的外泌体（hUCMSC-Exos）是否通过激活脑源性神经营养因子（BDNF）-TrkB通路来保护高血糖（HG）条件下的大鼠视网膜神经元。方法：采用差速超速离心法收集hUCMSC-Exos，并用透射电镜观察。使用酶联免疫吸附测定（ELISA）来定量 hUCMSC-Exos 中的 BDNF，并使用蛋白质印迹来鉴定 hUCMSC-Exos 的表面标记。大鼠视网膜神经元分为4组。此外，还测量了视网膜神经元中的细胞活力、细胞凋亡和 TrkB 蛋白表达。结果：hUCMSCs和分离的hUCMSC-Exos均成功培养。通过透射电子显微镜观察，所有 hUCMSC-Exos 的直径均为 30 至 150 nm，并具有磷脂双分子膜结构。ELISA结果显示hUCMSCs-Exos的BDNF浓度为2483.16±281.75。hUCMSCs-Exos有效降低视网膜神经元凋亡率，提高神经元存活率，同时免疫荧光结果证实神经元中TrKB荧光强度增加。使用 BDNF 抑制剂处理 hUCMSCs-Exos 后，所有上述影响均得到降低。hUCMSC-Exos 通过激活 HG 环境中的 BDNF-TrkB 通路，有效降低视网膜神经元的凋亡率。结论：在HG环境下，hUCMSC-Exos可以携带BDNF进入大鼠视网膜神经元，通过激活BDNF-TrkB通路抑制神经元凋亡。