Effects of Bu Shen Yi sui capsule on NogoA/NgR and its signaling pathways RhoA/ROCK in mice with experimental autoimmune encephalomyelitis

Abstract Background Axon growth inhibitory factors NogoA/Nogo receptor (NgR) and its signaling pathways RhoA/Rho kinase (ROCK) play a critical role in the repair of nerve damage in multiple sclerosis (MS). Bu Shen Yi Sui Capsule (BSYSC) is an effective Chinese formula utilized to treat MS in clinica...

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Main Authors: Ling Fang, Yongqiang Wang, Qi Zheng, Tao Yang, Peiyuan Zhao, Hui Zhao, Qiuxia Zhang, Yuanyuan Zhao, Fang Qi, Kangning Li, Zhenzhen Chen, Junling Li, Nan Zhang, Yongping Fan, Lei Wang
Format: Article
Language:English
Published: BMC 2017-07-01
Series:BMC Complementary and Alternative Medicine
Subjects:
Online Access:http://link.springer.com/article/10.1186/s12906-017-1847-4
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author Ling Fang
Yongqiang Wang
Qi Zheng
Tao Yang
Peiyuan Zhao
Hui Zhao
Qiuxia Zhang
Yuanyuan Zhao
Fang Qi
Kangning Li
Zhenzhen Chen
Junling Li
Nan Zhang
Yongping Fan
Lei Wang
author_facet Ling Fang
Yongqiang Wang
Qi Zheng
Tao Yang
Peiyuan Zhao
Hui Zhao
Qiuxia Zhang
Yuanyuan Zhao
Fang Qi
Kangning Li
Zhenzhen Chen
Junling Li
Nan Zhang
Yongping Fan
Lei Wang
author_sort Ling Fang
collection DOAJ
description Abstract Background Axon growth inhibitory factors NogoA/Nogo receptor (NgR) and its signaling pathways RhoA/Rho kinase (ROCK) play a critical role in the repair of nerve damage in multiple sclerosis (MS). Bu Shen Yi Sui Capsule (BSYSC) is an effective Chinese formula utilized to treat MS in clinical setting and noted for its potent neuroprotective effects. In this study, we focus on the effects of BSYSC on promoting nerve repair and the underlying mechanisms in mice with experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Methods The EAE mouse model was induced by injecting subcutaneously with myelin oligodendrocyte glycoprotein (MOG) 35–55 supplemented with pertussis toxin. BSYSC was orally administrated at dose of 3.0 g/kg once a day for 40 days. The levels of protein gene product (PGP) 9.5, p-Tau, growth associated protein (GAP) -43, KI67 and Nestin in the brain or spinal cord on 20 and 40 day post-induction (dpi) were detected via immunofluorescence and Western blot analysis. Furthermore, NogoA/NgR and RhoA/ROCK signaling molecules were studied by qRT-PCR and Western blot analysis. Results Twenty or 40 days of treatment with BSYSC increased markedly PGP9.5 and GAP-43 levels, reduced p-Tau in the brain or spinal cord of mice with EAE. In addition, BSYSC elevated significantly the expression of KI67 and Nestin in the spinal cord 40 dpi. Further study showed that the activation of NogoA/NgR and RhoA/ROCK were suppressed by the presence of BSYSC. Conclusions BSYSC could attenuate axonal injury and promote repair of axonal damage in EAE mice in part through the down-regulation of NogoA/NgR and RhoA/ROCK signaling pathways.
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spelling doaj.art-e24d19e5df1043a780e4cab7bc93a41d2022-12-22T00:23:34ZengBMCBMC Complementary and Alternative Medicine1472-68822017-07-0117111210.1186/s12906-017-1847-4Effects of Bu Shen Yi sui capsule on NogoA/NgR and its signaling pathways RhoA/ROCK in mice with experimental autoimmune encephalomyelitisLing Fang0Yongqiang Wang1Qi Zheng2Tao Yang3Peiyuan Zhao4Hui Zhao5Qiuxia Zhang6Yuanyuan Zhao7Fang Qi8Kangning Li9Zhenzhen Chen10Junling Li11Nan Zhang12Yongping Fan13Lei Wang14School of Traditional Chinese Medicine, Beijing Key Lab of TCM Collateral Disease Theory Research, Capital Medical UniversitySchool of Traditional Chinese Medicine, Beijing Key Lab of TCM Collateral Disease Theory Research, Capital Medical UniversitySchool of Traditional Chinese Medicine, Beijing Key Lab of TCM Collateral Disease Theory Research, Capital Medical UniversityBeijing Tian Tan Hospital, Capital Medical UniversitySchool of Traditional Chinese Medicine, Beijing Key Lab of TCM Collateral Disease Theory Research, Capital Medical UniversitySchool of Traditional Chinese Medicine, Beijing Key Lab of TCM Collateral Disease Theory Research, Capital Medical UniversitySchool of Traditional Chinese Medicine, Beijing Key Lab of TCM Collateral Disease Theory Research, Capital Medical UniversityCore Facility Center, Capital Medical UniversitySchool of Traditional Chinese Medicine, Beijing Key Lab of TCM Collateral Disease Theory Research, Capital Medical UniversityBeijing Tian Tan Hospital, Capital Medical UniversitySchool of Traditional Chinese Medicine, Beijing Key Lab of TCM Collateral Disease Theory Research, Capital Medical UniversitySchool of Traditional Chinese Medicine, Beijing Key Lab of TCM Collateral Disease Theory Research, Capital Medical UniversitySchool of Traditional Chinese Medicine, Beijing Key Lab of TCM Collateral Disease Theory Research, Capital Medical UniversityBeijing Tian Tan Hospital, Capital Medical UniversitySchool of Traditional Chinese Medicine, Beijing Key Lab of TCM Collateral Disease Theory Research, Capital Medical UniversityAbstract Background Axon growth inhibitory factors NogoA/Nogo receptor (NgR) and its signaling pathways RhoA/Rho kinase (ROCK) play a critical role in the repair of nerve damage in multiple sclerosis (MS). Bu Shen Yi Sui Capsule (BSYSC) is an effective Chinese formula utilized to treat MS in clinical setting and noted for its potent neuroprotective effects. In this study, we focus on the effects of BSYSC on promoting nerve repair and the underlying mechanisms in mice with experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Methods The EAE mouse model was induced by injecting subcutaneously with myelin oligodendrocyte glycoprotein (MOG) 35–55 supplemented with pertussis toxin. BSYSC was orally administrated at dose of 3.0 g/kg once a day for 40 days. The levels of protein gene product (PGP) 9.5, p-Tau, growth associated protein (GAP) -43, KI67 and Nestin in the brain or spinal cord on 20 and 40 day post-induction (dpi) were detected via immunofluorescence and Western blot analysis. Furthermore, NogoA/NgR and RhoA/ROCK signaling molecules were studied by qRT-PCR and Western blot analysis. Results Twenty or 40 days of treatment with BSYSC increased markedly PGP9.5 and GAP-43 levels, reduced p-Tau in the brain or spinal cord of mice with EAE. In addition, BSYSC elevated significantly the expression of KI67 and Nestin in the spinal cord 40 dpi. Further study showed that the activation of NogoA/NgR and RhoA/ROCK were suppressed by the presence of BSYSC. Conclusions BSYSC could attenuate axonal injury and promote repair of axonal damage in EAE mice in part through the down-regulation of NogoA/NgR and RhoA/ROCK signaling pathways.http://link.springer.com/article/10.1186/s12906-017-1847-4Experimental autoimmune encephalomyelitisMultiple sclerosisBu Shen Yi sui capsulePGP9.5P-tauGap-43
spellingShingle Ling Fang
Yongqiang Wang
Qi Zheng
Tao Yang
Peiyuan Zhao
Hui Zhao
Qiuxia Zhang
Yuanyuan Zhao
Fang Qi
Kangning Li
Zhenzhen Chen
Junling Li
Nan Zhang
Yongping Fan
Lei Wang
Effects of Bu Shen Yi sui capsule on NogoA/NgR and its signaling pathways RhoA/ROCK in mice with experimental autoimmune encephalomyelitis
BMC Complementary and Alternative Medicine
Experimental autoimmune encephalomyelitis
Multiple sclerosis
Bu Shen Yi sui capsule
PGP9.5
P-tau
Gap-43
title Effects of Bu Shen Yi sui capsule on NogoA/NgR and its signaling pathways RhoA/ROCK in mice with experimental autoimmune encephalomyelitis
title_full Effects of Bu Shen Yi sui capsule on NogoA/NgR and its signaling pathways RhoA/ROCK in mice with experimental autoimmune encephalomyelitis
title_fullStr Effects of Bu Shen Yi sui capsule on NogoA/NgR and its signaling pathways RhoA/ROCK in mice with experimental autoimmune encephalomyelitis
title_full_unstemmed Effects of Bu Shen Yi sui capsule on NogoA/NgR and its signaling pathways RhoA/ROCK in mice with experimental autoimmune encephalomyelitis
title_short Effects of Bu Shen Yi sui capsule on NogoA/NgR and its signaling pathways RhoA/ROCK in mice with experimental autoimmune encephalomyelitis
title_sort effects of bu shen yi sui capsule on nogoa ngr and its signaling pathways rhoa rock in mice with experimental autoimmune encephalomyelitis
topic Experimental autoimmune encephalomyelitis
Multiple sclerosis
Bu Shen Yi sui capsule
PGP9.5
P-tau
Gap-43
url http://link.springer.com/article/10.1186/s12906-017-1847-4
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