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Secondary Degeneration After Partial Optic Nerve Injury and Possible Neuroprotective Effects of Lycium Barbarum (Wolfberry)

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Lycium Barbarum and Human Health

Abstract

Secondary degeneration occurs commonly in a range of neurodegenerative diseases, including glaucoma. Partial optic nerve transection (PONT) model was established in the last decade and was good for studying secondary degeneration in retinas and optic nerves. The results from the published papers about PONT showed that the mechanisms—apoptosis, necrosis, autophagy, oxidative stress, calcium overload, mitochondria, activation of c-jun, water channel change, and glial cells (microglia, astrocytes and oligodendrocytes)—were involved in secondary degeneration after PONT. In addition to the cell bodies and the axons of retinal ganglion cells (RGCs), other cells in the layers outside the ganglion cell layer were also affected according to the measurement of multifocal electroretinogram (mfERG) by our group. Lycium barbarum (L. barbarum) is a traditional medicine in the oriental world and has long been used as a functional food and for medicinal purposes. The data from our group and others showed that the polysaccharides extracted from L. barbarum (LBP) were neuroprotective in different animal models, including the PONT model. Our results showed that LBP could inhibit secondary degeneration of the cell bodies of RGCs rather than primary degeneration as well as preserve the function of retinas measured by mfERG. These effects are related with the antioxidant function of LBP, inhibition of c-jun N-terminal kinase (JNK) pathway in the retinas after PONT. Other possible mechanisms involved in LBP’s neuroprotective effects for secondary degeneration are immunomodulatory effects, preservation of synapses, and modulation of autophagy.

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Authors and Affiliations

  1. GHM Institute of CNS Regeneration and Guangdong Key Laboratory of Brain Function and Diseases, Jinan University, Guangzhou, People’s Republic of China

    Hong-Ying Li, Raymond Chuen-Chung Chang & Kwok-Fai So PhD

  2. Department of Anatomy, Jinan University School of Medicine, Guangzhou, People’s Republic of China

    Hong-Ying Li

  3. Department of Ophthamology, The University of Hong Kong, Hong Kong, People’s Republic of China

    Hong-Ying Li & Kwok-Fai So PhD

  4. The State Key Laboratory of Brain and Cognitive Science and the Research Centre of Heart, Brain, Hormone and Healthy Aging, The University of Hong Kong, Hong Kong, People’s Republic of China

    Hong-Ying Li, Raymond Chuen-Chung Chang & Kwok-Fai So PhD

  5. Department of Anatomy, The University of Hong Kong, Hong Kong, People’s Republic of China

    Raymond Chuen-Chung Chang & Kwok-Fai So PhD

  6. Laboratory of Experimental Optometry (Neuroscience), School of Optometry, The Hong Kong Polytechnic University, Hong Kong, People’s Republic of China

    Henry HL Chan & Patrick HW Chu

Authors
  1. Hong-Ying Li
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  2. Henry HL Chan
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  3. Patrick HW Chu
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  4. Raymond Chuen-Chung Chang
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  5. Kwok-Fai So PhD
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Corresponding author

Correspondence to Kwok-Fai So PhD .

Editor information

Editors and Affiliations

  1. Department of Anatomy, LKS Faculty of Medicine the University of Hong Kong, Hong Kong, China

    Raymond Chuen-Chung Chang

  2. Department of Anatomy, LKS Faculty of Medicine the University of Hong Kong, Hong Kong, China

    Kwok-Fai So

Conclusions

Conclusions

In neurodegenerative diseases and other diseases of CNS, secondary degeneration of neurons and glial cells occurred. Protection of neurons and glial cells died from secondary degeneration is a promising direction for therapy of these diseases. PONT model is a useful tool to study the mechanisms of secondary degeneration and to screen the neuroprotective drugs for secondary degeneration since it can separate primary degeneration from secondary degeneration in location. Until now, the mechanisms of secondary degeneration after PONT could be apoptosis, necrosis, and autophagy. Oxidative stress, calcium overload, mitochondria dysfunction, JNK pathway, change of water channel, microglia and macrophages, astrocytes, and oligodendrocytes were involved in the secondary degeneration after PONT. LBP could delay secondary degeneration of RGCs and outer retinas and improve the function of retinas by inhibiting oxidative stress and activation of JNK pathway after PONT. Other possible neuroprotective mechanisms of LBP for secondary degeneration include immunomodulatory effects, preserving synapses, modulating autophagy, and modulating signal processing.

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Li, HY., Chan, H., Chu, P., Chang, RC., So, KF. (2015). Secondary Degeneration After Partial Optic Nerve Injury and Possible Neuroprotective Effects of Lycium Barbarum (Wolfberry). In: Chang, RC., So, KF. (eds) Lycium Barbarum and Human Health. Springer, Dordrecht. https://doi.org/10.1007/978-94-017-9658-3_10

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  • DOI: https://doi.org/10.1007/978-94-017-9658-3_10

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  • Publisher Name: Springer, Dordrecht

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  • Online ISBN: 978-94-017-9658-3

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