Mannitol-facilitated entry of vancomycin into the central nervous system inhibits neuroinflammation in a rat model of MRSA intracranial infection by modulating brain endothelial cells
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Mannitol-facilitated entry of vancomycin into the central nervous system inhibits neuroinflammation in a rat model of MRSA intracranial infection by modulating brain endothelial cells |
| Yin Wen, Zhiwei Su, Huishan Zhu, Mengting Liu, Zhuo Li, Shiying Zhang, Shuangming Cai, Jiaqi Tang, Hongguang Ding, Hongke Zeng |
| Figure 4. Mannitol weakened EGL via F-actin depolymerization. A, B: the expression of F-actin decreased over time after mannitol intervention; C: the immunofluorescence signals of syndecan-1 (red) were faded in the Man group compared with the Con group; D, F, G: when pre-treated with Cyt D, the expression of F-actin and syndecan-1 reduced in the Cyt D+Man group compared with the Man group (P<0.05); E, H, I: when pre-treated with Jask, the expression of F-actin and syndecan-1 reduced in the Cyt D+Man group compared with the Man group (P<0.05); J: the immunofluorescence staining images showed that when F-actin was depolymerized with Cyt D, the syndecan-1 further declined, while F-actin was polymerized with Jask, the syndecan-1 remained stable. *P<0.05, ***P<0.001, ****P<0.0001. EGL: endothelial glycocalyx layer; Man: mannitol; Con: control; Cyt D: cytochalasin-D. |
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