Short Communication Neuroprotective effects of Lycium barbarum Lynn on protecting retinal ganglion cells in an ocular hypertension model of glaucoma Hiu-Chi Chan a , Raymond Chuen-Chung Chang a,b,c , Angel Koon-Ching Ip a , Kin Chiu a , Wai-Hung Yuen e , Sze-Yong Zee d, ⁎ , Kwok-Fai So a,b,c, ⁎ a Department of Anatomy, Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR b Central Laboratory of the Institute of Molecular Technology for Drug Discovery and Synthesis, The University of Hong Kong, Pokfulam, Hong Kong SAR c State Key Laboratory of Brain and Cognitive Sciences, The University of Hong Kong, Pokfulam, Hong Kong SAR d Department of Botany, Faculty of Science, The University of Hong Kong, Pokfulam, Hong Kong SAR e Department of Chemistry and Open Laboratory of Chemical Biology of the Institute of Molecular Technology for Drug Discovery and Synthesis, The University of Hong Kong, Pokfulam, Hong Kong SAR Received 7 March 2006; revised 8 May 2006; accepted 23 May 2006 Available online 11 October 2006 Abstract Glaucoma is one of the major neurological disorders in eye leading to irreversible blindness in elderly. Increase in intraocular pressure (IOP) has been considered to be the major risk factor for the progressive loss of retinal ganglion cells (RGCs) in retina. While attenuation of IOP has been a major pharmaceutical target, reduction of IOP cannot prevent progressive loss of RGCs. In this regard, urgent need for alternative treatment has to be investigated. Anti-aging medicinal herb Lycium barbarum L. has been used for centuries in Eastern World to protect the eyes and maintain good health. Using an ocular hypertension (OH) model in rat by laser photocoagulation of episcleral and limbal veins, we attempted to investigate whether L. barbarum can promote RGCs survival against elevated IOP. Oral administration of L. barbarum in Sprague-Dawley rats (250–280 g) significantly reduced the loss of RGCs, although elevated IOP was not significantly altered. Rats fed with the 1 mg/kg extract could nearly totally escape from pressure-induced loss of RGCs. In conclusion, this is the first in vivo report showing the therapeutic function of L. barbarum against neurodegeneration in the retina of rat OH model. The results demonstrate that this extract may be a potential candidate for the development of neuroprotective drug against the loss of RGCs in glaucoma. © 2006 Elsevier Inc. All rights reserved. Keywords: Neuroprotection; L. barbarum; Glaucoma; Macrophage; Microglia Glaucoma is widely recognized as a neurodegenerative disease, characterized by optic nerve atrophy and progressive loss of vision from the periphery towards the central vision field (Quigley et al., 1981; Laquis et al., 1998; Gazzard et al., 2002; Foster et al., 2002). Death of retinal ganglion cells (RGCs) can attribute to visual loss in glaucoma patients (Flammer et al., 2002; Harwerth et al., 2002). Elevation of the intraocular pressure (IOP) has been considered to be a major pathological factor leading to the death of RGCs in glaucoma (Goldblum and Mittag, 2002; Wax and Tezel, 2002; Wein and levin, 2002). As a general practice, treatments of glaucoma usually focus on reducing the IOP. However, inhibition on the degeneration of RGCs can be accomplished to a certain extent only. Therefore, effort has been made to find out other neurotoxic factors in glaucoma. Glutamate released from the injured or dead neurons and nitric oxide (NO) (Neufeld et al., 1999; Haefliger et al., 1999) triggered by glutamate excitotoxicity threatening the survival of neighboring neurons have been reported to induce progressive degeneration of RGCs. Knowing that the extracts of anti-aging herbs, Lycium barbarum, exhibit cytoprotective effects on many cell types including neurons (Wang et al., 2002; Luo et al., 2004; Yu et al., 2005, 2006), we aim to investigate whether this kind of extract can protect RGCs in an animal experimental model of ocular hypertension. Experimental Neurology 203 (2007) 269 – 273 www.elsevier.com/locate/yexnr ⁎ Corresponding authors. S.-Y. Zee is to be contacted at Level 5, The International Centre, Zhuhai Campus of Beijing Normal University, Jinfeng Road, Tangjiwan, Xiangzhou District, Zhuhai, China; K.-F. So, 1/F Laboratory Block, Faculty of Medicine, The University of Hong Kong, 21 Sassoon Road, Pokfulam, Hong Kong SAR. Fax: +852 2817 0857. E-mail addresses: syzee@hkbu.edu.hk (S.-Y. Zee), hrmaskf@hkccu.hku.hk (K.-F. So). 0014-4886/$ - see front matter © 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.expneurol.2006.05.031