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Title: Secondary degeneration after partial optic nerve injury and possible neuroprotective effects of Lycium barbarum (wolfberry)
Authors: Li, HY
Chan, HHL 
Chu, PHW
Chang, RCC
So, KF
Keywords: Lycium barbarum
Optic nerve
Secondary degeneration
Issue Date: 2015
Publisher: Springer
Source: In RCC Chang & KF So (Eds.), Lycium barbarum and human health, p. 135-151. Dordrecht: Springer, 2015 How to cite?
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.
ISBN: 978-94-017-9657-6 (print)
978-94-017-9658-3 (online)
DOI: 10.1007/978-94-017-9658-3_10
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