Tanshinone IIA attenuates demyelination and promotes remyelination in A. cantonensis-infected BALB/c mice

被引:11
作者
Feng, Ying [1 ]
Feng, Feng [4 ]
Zheng, Cunjing [5 ]
Zhou, Zongpu [1 ]
Jiang, Meihua [6 ]
Liu, Zhen [7 ]
Xie, Fukang [5 ]
Sun, Xi [2 ,3 ]
Wu, Zhongdao [2 ,3 ]
机构
[1] South China Univ Technol, Med Sch, Guangzhou, Guangdong, Peoples R China
[2] Sun Yat Sen Univ, Zhongshan Sch Med, Parasitol Dept, Guangzhou, Guangdong, Peoples R China
[3] Minist Educ, Key Lab Trop Dis Control SYSU, Guangzhou, Guangdong, Peoples R China
[4] Sun Yat Sen Univ, Sch Pharmaceut Sci, Dept Pharmacol & Toxicol, Guangzhou, Guangdong, Peoples R China
[5] Sun Yat Sen Univ, Zhongshan Sch Med, Histol & Embryol Dept, Guangzhou, Guangdong, Peoples R China
[6] Sun Yat Sen Univ, Zhongshan Sch Med, Anat Dept, Guangzhou, Guangdong, Peoples R China
[7] Guangzhou First Peoples Hosp, Guangzhou, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
Tanshinone IIA; demyelination; remyelination; microglia polarization; A; cantonensis; CENTRAL-NERVOUS-SYSTEM; ANGIOSTRONGYLUS-CANTONENSIS; MULTIPLE-SCLEROSIS; ACTIVATION; MYELIN; MODEL; CNS; PERSPECTIVES; HEMORRHAGE; THERAPY;
D O I
10.7150/ijbs.35266
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background: Angiostrongylus cantonensis infection can cause demyelination in the central nervous system, and there is no effective treatment. Methods: 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 A. cantonensis-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. Results: 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-1 beta, tumor necrosis factor [TNF]-alpha, 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. Conclusions: Taken together, these results provide evidence that TSIIA combined with AB may be an effective treatment for demyelination caused by A. cantonensis infection and other demyelinating diseases.
引用
收藏
页码:2211 / 2223
页数:13
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