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      Tanshinone IIA Promotes Axonal Regeneration in Rats with Focal Cerebral Ischemia Through the Inhibition of Nogo-A/NgR1/RhoA/ROCKII/MLC Signaling

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          The aim of this study was to evaluate the neuroprotective effect of tanshinone IIA (TSA) on focal cerebral ischemia in rats and to investigate whether it was associated with Nogo-A/NgR1/RhoA/Rho-associated protein kinase 2 (ROCKII)/myosin light chain (MLC) signaling.


          In this study, focal cerebral ischemia animal model was used. Neurological deficit scores and infarction volume were investigated to evaluate the neuroprotection of TSA. Hematoxylin-eosin staining, Nissl staining, and immunofluorescence staining were conducted to detect ischemic changes in brain tissue and changes in neurofilament protein 200 (NF200) and growth-associated protein-43 (GAP-43) expression, respectively. Western blotting and qRT-PCR analyses were used to detect the expression levels of NF200, GAP-43 and Nogo-A/NgR1/RhoA/ROCKII/MLC pathway-related signaling molecules.


          TSA treatment can improve the survival rate of rats, reduce the neurological score and infarct volume, and reduce neuron damage. In addition, TSA also increased axon length and enhanced expression of NF200 and GAP-43. Importantly, TSA significantly attenuated the expression of Nogo-A, NgR1, RhoA, ROCKII, and p-MLC, and thus inhibiting the activation of this signaling pathway.


          TSA promoted axonal regeneration by inhibiting the Nogo-A/NgR1/RhoA/ROCKII/MLC signaling pathway, thereby exerting neuroprotective effects in cerebral ischemia rats, which provided support for the clinical application of TSA in stroke treatment.

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          Most cited references 25

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          Timeliness of tissue-type plasminogen activator therapy in acute ischemic stroke: patient characteristics, hospital factors, and outcomes associated with door-to-needle times within 60 minutes.

          The benefits of intravenous tissue-type plasminogen activator (tPA) in acute ischemic stroke are time dependent, and guidelines recommend an arrival to treatment initiation (door-to-needle) time of ≤60 minutes. Data from acute ischemic stroke patients treated with tPA within 3 hours of symptom onset in 1082 hospitals participating in the Get With the Guidelines-Stroke Program from April 1, 2003, to September 30, 2009 were studied to determine frequency, patient and hospital characteristics, and temporal trends in patients treated with door-to-needle times ≤60 minutes. Among 25 504 ischemic stroke patients treated with tPA, door-to-needle time was ≤60 minutes in only 6790 (26.6%). Patient factors most strongly associated with door-to-needle time ≤60 minutes were younger age, male gender, white race, or no prior stroke. Hospital factors associated with ≤60 minute door-to-needle time included greater annual volumes of tPA-treated stroke patients. The proportion of patients with door-to-needle times ≤60 minutes varied widely by hospital (0% to 79.2%) and increased from 19.5% in 2003 to 29.1% in 2009 (P 60 minutes. Fewer than one-third of patients treated with intravenous tPA had door-to-needle times ≤60 minutes, with only modest improvement over the past 6.5 years. These findings support the need for a targeted initiative to improve the timeliness of reperfusion in acute ischemic stroke.
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            Therapeutic Benefit of Intravenous Administration of Bone Marrow Stromal Cells After Cerebral Ischemia in Rats

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              Nogo limits neural plasticity and recovery from injury.

              The expression of Nogo-A and the receptor NgR1 limits the recovery of adult mammals from central nervous system injury. Multiple studies have demonstrated efficacy from targeting this pathway for functional recovery and neural repair after spinal cord trauma, ischemic stroke, optic nerve injury and models of multiple sclerosis. Recent molecular studies have added S1PR2 as a receptor for the amino terminal domain of Nogo-A, and have demonstrated shared components for Nogo-A and CSPG signaling as well as novel Nogo antagonists. It has been recognized that neural repair involves plasticity, sprouting and regeneration. A physiologic role for Nogo-A and NgR1 has been documented in the restriction of experience-dependent plasticity with maturity, and the stability of synaptic, dendritic and axonal anatomy. Copyright © 2014 Elsevier Ltd. All rights reserved.

                Author and article information

                Drug Des Devel Ther
                Drug Des Devel Ther
                Drug Design, Development and Therapy
                15 July 2020
                : 14
                : 2775-2787
                [1 ]Department of Chinese Medicine Diagnostics, Hebei University of Chinese Medicine , Shijiazhuang, Hebei 050200, People’s Republic of China
                [2 ]Department of Rehabilitation Medicine, The Second Hospital of Hebei Medical University , Shijiazhuang, Hebei 050000, People’s Republic of China
                [3 ]College of Integrated Chinese and Western Medicine, Hebei University of Chinese Medicine , Shijiazhuang, Hebei 050200, People’s Republic of China
                [4 ]Department of Chinese Medicine, The Third Hospital of Hebei Medical University , Shijiazhuang, Hebei 050051, People’s Republic of China
                [5 ]Department of Respiratory Diseases, Hebei Province Hospital of Traditional Chinese Medicine , Shijiazhuang, Hebei 050000, People’s Republic of China
                [6 ]College of Integrated Chinese and Western Medicine, Hebei Medical University , Shijiazhuang, Hebei 050017, People’s Republic of China
                Author notes
                Correspondence: Yali Wang Department of Chinese Medicine Diagnostics, Hebei University of Chinese Medicine , Luquan Xingyuan Road 3, Shijiazhuang, Hebei050200, People’s Republic of China Email lvyihongni1988@163.com
                © 2020 Wang et al.

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                Page count
                Figures: 8, Tables: 1, References: 29, Pages: 13
                Original Research


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