（Ba，Ca）（Ti，Sn）O3基压电陶瓷通过调节小胶质细胞IL-6/JAK2/STAT3信号通路促进神经保护
{"_":"(Ba,Ca)(Ti,Sn)O-based piezoelectric ceramics promotes neuroprotection by regulating microglial IL-6/JAK2/STAT3 signaling pathway.","sub":["3"]}
摘要(中文译文)
探讨(Ba,Ca)(Ti,Sn)O基压电陶瓷(BCTS)是否通过抑制小胶质细胞中IL-6/JAK2/STAT3信号通路发挥神经保护作用。采用扫描电子显微镜(SEM)和能量色散X射线光谱(EDX)分析BCTS的表面形貌和元素分布，通过X射线衍射(XRD)测定物相组成，并通过接触角分析测量亲水性。采用免疫荧光(IF)、Western blot和ELISA评估BV2损伤模型及脊髓损伤大鼠中小胶质细胞标志物和炎症因子的表达。进行行为学测试以评估脊髓损伤大鼠的运动功能恢复情况。将PC12细胞与BCTS-CM(经BCTS处理的BV2细胞上清液)共培养，以评估IL-6/JAK2/STAT3信号通路的表达及其对LDH释放、抗氧化酶活性、凋亡蛋白和β-III-微管蛋白表达的影响。BCTS呈现纯钙钛矿相、晶粒致密堆积及良好的亲水性。BCTS不影响BV2细胞活力，但抑制LPS诱导的M1型小胶质细胞活化，降低TNF-α、IL-1β和IL-6的表达。同时，BCTS促进M2型小胶质细胞极化，上调IL-4、IL-10和TGF-β1。在PC12细胞中，BCTS-CM提高细胞存活率、抗氧化活性、Bcl-2和β-III-微管蛋白表达，同时降低LDH释放、MDA含量、BAX和Cleaved Caspase-3表达。BCTS诱导的神经保护作用是通过抑制IL-6/JAK2/STAT3信号通路介导的，证据在于补充IL-6可抵消这种保护作用，而与单独使用BCTS-CM相比，AG490处理进一步增强了这种保护作用。在脊髓损伤大鼠模型中，BCTS抑制损伤部位小胶质细胞和炎症因子的表达，同时改善BBB评分并降低网格行走测试中的错误率。(Ba,Ca)(Ti,Sn)O基压电陶瓷通过抑制小胶质细胞IL-6分泌，从而阻止神经元中IL-6/JAK2/STAT3信号通路的激活，发挥神经保护作用。
Abstract
To investigate whether (Ba,Ca)(Ti,Sn)O-based piezoelectric ceramics (BCTS) provide neuroprotection by inhibiting the IL-6/JAK2/STAT3 signaling pathway in microglia. BCTS surface morphology and elemental distribution were analyzed using Scanning Electron Microscopy (SEM) and Energy Dispersive X-ray Spectroscopy (EDX), phase composition was determined via X-ray diffraction (XRD), and hydrophilicity was measured through contact angle analysis. Immunofluorescence (IF), Western blot, and ELISA were employed to evaluate the expression of microglial markers and inflammatory factors in the BV2 injury model and in spinal cord injury rats. Behavioral tests were conducted to evaluate motor function recovery in spinal cord injury rats. PC12 cells were cultured with BCTS-CM (supernatant from BCTS-treated BV2 cells) to assess the IL-6/JAK2/STAT3 signaling pathway expression and its effects on LDH release, antioxidant enzyme activity, apoptotic proteins, and β-III-tubulin expression. BCTS exhibited a pure perovskite phase, densely packed grains, and favorable hydrophilicity. It did not affect BV2 cell viability but inhibited LPS-induced M1 microglial activation, reducing the expression of TNF-α, IL-1β, and IL-6. Simultaneously, BCTS promoted M2 microglial polarization, upregulating IL-4, IL-10, and TGF-β1. In PC12 cells, BCTS-CM increased cell survival, antioxidant activities, Bcl-2, and β-III-tubulin expression, while decreasing LDH release, MDA content, BAX and Cleaved Caspase-3 expression. BCTS-induced neuroprotection is mediated by the suppression of the IL-6/JAK2/STAT3 signaling pathway, as evidenced by the fact that IL-6 supplementation counteracts this protection while AG490 treatment further reinforces it compared to BCTS-CM alone. In the spinal cord injury rat model, BCTS inhibited the expression of microglia and inflammatory factors at the injury site, while improving the BBB score and reducing the error rate in the grid walking test. (Ba,Ca)(Ti,Sn)O-based piezoelectric ceramics exhibit neuroprotective effects by inhibiting IL-6 secretion from microglia, thereby preventing the activation of the IL-6/JAK2/STAT3 signaling pathway in neurons.
如何引用
AMA
Haiwang Song, Geng Tang, Yumei Li, Baofei Sun, Zijiang Yu, Mudan Zhang, et al. {"_":"(Ba,Ca)(Ti,Sn)O-based piezoelectric ceramics promotes neuroprotection by regulating microglial IL-6/JAK2/STAT3 signaling pathway.","sub":["3"]}. Frontiers in cellular neuroscience. 2026; doi:10.3389/fncel.2026.1793008.
APA
Haiwang Song, Geng Tang, Yumei Li, Baofei Sun, Zijiang Yu, Mudan Zhang, et al (2026). {"_":"(Ba,Ca)(Ti,Sn)O-based piezoelectric ceramics promotes neuroprotection by regulating microglial IL-6/JAK2/STAT3 signaling pathway.","sub":["3"]}. Frontiers in cellular neuroscience. https://doi.org/10.3389/fncel.2026.1793008
GB/T 7714
Haiwang Song, Geng Tang, Yumei Li, Baofei Sun, Zijiang Yu, Mudan Zhang, et al. {"_":"(Ba,Ca)(Ti,Sn)O-based piezoelectric ceramics promotes neuroprotection by regulating microglial IL-6/JAK2/STAT3 signaling pathway.","sub":["3"]}[J]. Frontiers in cellular neuroscience, 2026 doi:10.3389/fncel.2026.1793008.
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