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      Shexiang Baoxin Pill, a Formulated Chinese Herbal Mixture, Induces Neuronal Differentiation of PC12 Cells: A Signaling Triggered by Activation of Protein Kinase A

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          Abstract

          Background: Shexiang Baoxin Pill (SBP) is a well-known composite formula of traditional Chinese medicine (TCM), which is commonly used today in treating cardiovascular diseases. SBP consists of seven materials thereof, including Moschus, extract of Ginseng Radix et Rhizoma, Bovis Calculus Artifactus, Cinnamomi Cortex, Styrax, Bufonis Venenum, and Borneolum Syntheticum. Here, we are investigating the potential roles of SBP in inducing neuron differentiation, i.e., seeking possible application in neurodegenerative diseases.

          Methods: Water and ethanol extracts of SBP, denoted as SBP water and SBP EtOH, respectively, as well as its individual herbal materials, were standardized and applied onto cultured rat pheochromocytoma PC12 cells. The potential effect of SBP extracts in neuronal differentiation was suggested by following parameters: (i) induction of neurite outgrowth of PC12 cells, (ii) increase of neurofilament expression, and (iii) activation of transcription of neurofilament.

          Results: The treatments of SBP water and SBP EtOH, or extracts from individual herbal materials, with or without low concentration of nerve growth factor (NGF), could potentiate the differentiation of cultured PC12 cells. The differentiation was indicated by increase of neurite outgrowth, as well as expression of neurofilaments. In addition, application of H89, a protein kinase A (PKA) inhibitor, suppressed the SBP-induced neurofilament expressions, as well as the phosphorylation of cAMP-responsive element binding protein (CREB) in cultures.

          Conclusion: SBP is proposed to possess trophic activity in modulating neuronal differentiation of PC12 cells, and this induction is shown to be mediated partly by a cAMP-PKA signaling pathway. These results indicate the neurite-promoting SBP could be useful in developing potential drug in treating or preventing neurodegenerative diseases.

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          Current advances in using neurotrophic factors to treat neurodegenerative disorders

          April Weissmiller, Chengbiao Wu (2012)
          Neurotrophic factors are best known for their roles in both development and continued maintenance of the nervous system. Their strong potential to elicit pro-survival and pro-functional responses in neurons of the peripheral and central nervous system make them good drug candidates for treatment of a multitude of neurodegenerative disorders. However, significant obstacles remain and need to be overcome before translating the potential of neurotrophins into the therapeutic arena. This article addresses current efforts and advances in resolving these challenges and provides an overview of roadmaps for future translational research and neurotrophin-based drug developments.
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            Neuronal intermediate filaments.

            Karyn Cleveland, Wen-Chung Lee (1995)
            Neurofilaments (NFs) are the most abundant structural components in large-diameter myelinated axons. Assembled as obligate heteropolymers requiring NF-L and substoichiometric amounts of NF-M and/or NF-H, NF investment into axons is essential for establishment of axonal caliber, itself a key determinant of conduction velocity. Use of transgenic mice to increase axonal accumulation of NFs or to express mutant NFs subunits has proven that aberrant organization or assembly of NFs is sufficient to cause disease arising from selective dysfunction and degeneration of motor neurons. Because aberrant accumulation of NFs is a common pathology in a series of motor neuron diseases-including amyotrophic lateral sclerosis-NF misaccumulation, and the resultant disruption in axonal transport, is probably a key intermediate in the pathogenesis of these diseases.
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              Up-regulation of neurotrophic factors by cinnamon and its metabolite sodium benzoate: therapeutic implications for neurodegenerative disorders.

              Avik Roy, Kalipada Pahan, B Sweder van Asbeck … (2013)
              This study underlines the importance of cinnamon, a widely-used food spice and flavoring material, and its metabolite sodium benzoate (NaB), a widely-used food preservative and a FDA-approved drug against urea cycle disorders in humans, in increasing the levels of neurotrophic factors [e.g., brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3)] in the CNS. NaB, but not sodium formate (NaFO), dose-dependently induced the expression of BDNF and NT-3 in primary human neurons and astrocytes. Interestingly, oral administration of ground cinnamon increased the level of NaB in serum and brain and upregulated the levels of these neurotrophic factors in vivo in mouse CNS. Accordingly, oral feeding of NaB, but not NaFO, also increased the level of these neurotrophic factors in vivo in the CNS of mice. NaB induced the activation of protein kinase A (PKA), but not protein kinase C (PKC), and H-89, an inhibitor of PKA, abrogated NaB-induced increase in neurotrophic factors. Furthermore, activation of cAMP response element binding (CREB) protein, but not NF-κB, by NaB, abrogation of NaB-induced expression of neurotrophic factors by siRNA knockdown of CREB and the recruitment of CREB and CREB-binding protein to the BDNF promoter by NaB suggest that NaB exerts its neurotrophic effect through the activation of CREB. Accordingly, cinnamon feeding also increased the activity of PKA and the level of phospho-CREB in vivo in the CNS. These results highlight a novel neutrophic property of cinnamon and its metabolite NaB via PKA - CREB pathway, which may be of benefit for various neurodegenerative disorders.
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                Author and article information

                Contributors
                Journal
                Journal ID (nlm-ta): Front Pharmacol
                Journal ID (iso-abbrev): Front Pharmacol
                Journal ID (publisher-id): Front. Pharmacol.
                Title: Frontiers in Pharmacology
                Publisher: Frontiers Media S.A.
                ISSN (Electronic): 1663-9812
                Publication date (Electronic): 09 October 2019
                Publication date Collection: 2019
                Volume: 10
                Electronic Location Identifier: 1130
                Affiliations
                [1] 1Shenzhen Key Laboratory of Edible and Medicinal Bioresources, HKUST Shenzhen Research Institute , Shenzhen, China
                [2] 2Division of Life Science and Center for Chinese Medicine and State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology , Kowloon, Hong Kong
                [3] 3Shanghai Hutchison Pharmaceuticals Ltd , Shanghai, China
                [4] 4Shanghai Engineering Research Center for Innovation of Solid Preparation of TCM , Shanghai, China
                Author notes

                Edited by: Rong-Rong He, Jinan University, China

                Reviewed by: Phan Chia Wei, University of Malaya, Malaysia; Lu Yan, Institute of Botany, China; Chinese Academy of Sciences, China; Huangquan Lin, The Chinese University of Hong Kong, Hong Kong

                *Correspondence: Karl W. K. Tsim, botsim@ 123456ust.hk

                This article was submitted to Ethnopharmacology, a section of the journal Frontiers in Pharmacology

                Article
                DOI: 10.3389/fphar.2019.01130
                PMC ID: 6794430
                PubMed ID: 31649530
                SO-VID: d505c482-38f3-4c2c-8d72-e182aed33ba5
                Copyright © Copyright © 2019 Xu, Zheng, Xia, Liu, Chan, Hu, Duan, Dong, Zhan, Shang and Tsim
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                Date received : 23 April 2019
                Date accepted : 30 August 2019
                Page count
                Figures: 9, Tables: 0, Equations: 0, References: 45, Pages: 15, Words: 6288
                Categories
                Subject: Pharmacology
                Subject: Original Research

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: alzheimer’s disease,shexiang baoxin pill,chinese medicine,neuronal differentiation,protein kinase a,camp-responsive element binding protein
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: alzheimer’s disease, shexiang baoxin pill, chinese medicine, neuronal differentiation, protein kinase a, camp-responsive element binding protein

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