Medical School of South China University of Technology, Guangzhou, China.
The Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou, China.
Int J Biol Sci. 2019 Aug 19;15(10):2211-2223. doi: 10.7150/ijbs.35266. eCollection 2019.
infection can cause demyelination in the central nervous system, and there is no effective treatment.
We used dexamethasone, Tanshinone IIA (TSIIA) and Cryptotanshinone(Two traditional Chinese medicine monomers) in combination with albendazole (AB, a standard anti-helminthic compound) to observe their therapeutic effect on demyelination in -infected mice. Luxol fast blue staining and electron microscope of myelin sheath, Oligodendrocyte (OL) number and myelin basic protein (MBP) expression in brain was detected in above groups.
TSIIA+AB facilitated OL proliferation and significantly increased both myelin sheath thickness and the population of small-diameter axons. In addition, TSIIA treatment inhibited the expression of inflammation-related factors (interleukin [IL]-6, IL-1β, tumor necrosis factor [TNF]-α, inducible nitric oxide synthase [iNOS]) rather than inhibiting eosinophil infiltration in brain. TSIIA also decreased microglial activation and shifted their phenotype from M1 to M2.
Taken together, these results provide evidence that TSIIA combined with AB may be an effective treatment for demyelination caused by infection and other demyelinating diseases.
感染可导致中枢神经系统脱髓鞘,目前尚无有效的治疗方法。
我们使用地塞米松、丹参酮 IIA(TSIIA)和隐丹参酮(两种中药单体)联合阿苯达唑(AB,一种标准的驱虫化合物),观察它们对感染小鼠脱髓鞘的治疗作用。在上述各组中检测了髓鞘质的洛索夫快速蓝染色和电子显微镜、脑内少突胶质细胞(OL)数量和髓鞘碱性蛋白(MBP)的表达。
TSIIA+AB 促进 OL 增殖,显著增加髓鞘厚度和小直径轴突的数量。此外,TSIIA 治疗抑制了炎症相关因子(白细胞介素 [IL]-6、IL-1β、肿瘤坏死因子 [TNF]-α、诱导型一氧化氮合酶 [iNOS])的表达,而不是抑制脑内嗜酸性粒细胞浸润。TSIIA 还减少了小胶质细胞的激活,并将其表型从 M1 转变为 M2。
综上所述,这些结果为 TSIIA 联合 AB 可能是治疗 感染引起的脱髓鞘和其他脱髓鞘疾病的有效方法提供了证据。