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ABSTRACT: The active component of Wolfberry (Lycium barbarum), lycium barbarum polysaccharides (LBP), has been shown to be neuroprotective to retinal ganglion cells (RGCs) against ocular
hypertension (OH). Aiming to study whether this neuroprotection is mediated via modulating immune cells in the retina, we
used multiphoton confocal microscopy to investigate morphological changes of microglia in whole-mounted retinas. Retinas under
OH displayed slightly activated microglia. One to 100mg/kg LBP exerted the best neuroprotection and elicited moderately activated
microglia in the inner retina with ramified appearance but thicker and focally enlarged processes. Intravitreous injection
of bacterial endotoxin lipopolysaccharide (LPS) decreased the survival of RGCs at 4weeks, and the activated microglia exhibited
amoeboid appearance as fully activated phenotype. When activation of microglia was attenuated by intravitreous injection of
macrophage/microglia inhibitory factor, protective effect of 10mg/kg LBP was attenuated. The results implicated that neuroprotective
effects of LBP were partly due to modulating the activation of microglia.
Journal of ocular biology, diseases, and informatics 04/2012; 2(3):127-136.
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ABSTRACT: The active component of Wolfberry (Lycium barbarum), lycium barbarum polysaccharides (LBP), has been shown to be neuroprotective to retinal ganglion cells (RGCs) against ocular hypertension (OH). Aiming to study whether this neuroprotection is mediated via modulating immune cells in the retina, we used multiphoton confocal microscopy to investigate morphological changes of microglia in whole-mounted retinas. Retinas under OH displayed slightly activated microglia. One to 100 mg/kg LBP exerted the best neuroprotection and elicited moderately activated microglia in the inner retina with ramified appearance but thicker and focally enlarged processes. Intravitreous injection of bacterial endotoxin lipopolysaccharide (LPS) decreased the survival of RGCs at 4 weeks, and the activated microglia exhibited amoeboid appearance as fully activated phenotype. When activation of microglia was attenuated by intravitreous injection of macrophage/microglia inhibitory factor, protective effect of 10 mg/kg LBP was attenuated. The results implicated that neuroprotective effects of LBP were partly due to modulating the activation of microglia.[This corrects the article on p. in vol. .].
Journal of Ocular Biology Diseases and Informatics 09/2009; 2(3):127-136.
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ABSTRACT: The active component of Wolfberry (Lycium barbarum), lycium barbarum polysaccharides (LBP), has been shown to be neuroprotective to retinal ganglion cells (RGCs) against ocular hypertension (OH). Aiming to study whether this neuroprotection is mediated via modulating immune cells in the retina, we used multiphoton confocal microscopy to investigate morphological changes of microglia in whole-mounted retinas. Retinas under OH displayed slightly activated microglia. One to 100 mg/kg LBP exerted the best neuroprotection and elicited moderately activated microglia in the inner retina with ramified appearance but thicker and focally enlarged processes. Intravitreous injection of lipopolysaccharide decreased the survival of RGCs at 4 weeks, and the activated microglia exhibited amoeboid appearance as fully activated phenotype. When activation of microglia was attenuated by intravitreous injection of macrophage/microglia inhibitory factor, protective effect of 10 mg/kg LBP was attenuated. The results implicated that neuroprotective effects of LBP were partly due to modulating the activation of microglia.
Journal of Ocular Biology Diseases and Informatics 07/2009; 2(2):47-56.
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ABSTRACT: In the goldfish, norepinephrine (NE) inhibits growth hormone (GH) secretion through activation of pituitary alpha(2)-adrenergic receptors. Interestingly, a GH rebound is observed after NE withdrawal, which can be markedly enhanced by prior exposure to gonadotropin-releasing hormone (GnRH). Here we examined the mechanisms responsible for GnRH potentiation of this "postinhibition" GH rebound. In goldfish pituitary cells, alpha(2)-adrenergic stimulation suppressed both basal and GnRH-induced GH mRNA expression, suggesting that a rise in GH synthesis induced by GnRH did not contribute to its potentiating effect. Using a column perifusion approach, GnRH given during NE treatment consistently enhanced the GH rebound following NE withdrawal. This potentiating effect was mimicked by activation of PKC and adenylate cyclase (AC) but not by induction of Ca(2+) entry through voltage-sensitive Ca(2+) channels (VSCC). Furthermore, GnRH-potentiated GH rebound could be alleviated by inactivation of PKC, removal of extracellular Ca(2+), blockade of VSCC, and inhibition of Ca(2+)/calmodulin (CaM)-dependent protein kinase II (CaMKII). Inactivation of AC and PKA, however, was not effective in this regard. These results, as a whole, suggest that GnRH potentiation of GH rebound following NE inhibition is mediated by PKC coupled to Ca(2+) entry through VSCC and subsequent activation of CaMKII. Apparently, the Ca(2+)-dependent cascades are involved in GH secretion during the rebound phase but are not essential for the initiation of GnRH potentiation. Since GnRH has been previously shown to have no effects on cAMP synthesis in goldfish pituitary cells, the involvement of cAMP-dependent mechanisms in GnRH potentiation is rather unlikely.
AJP Endocrinology and Metabolism 02/2007; 292(1):E203-14. · 4.75 Impact Factor
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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.
Experimental Neurology 02/2007; 203(1):269-73. · 4.70 Impact Factor
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Hiu-chi. Chan
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ABSTRACT: Title from title frame. Thesis (M. Phil.)--University of Hong Kong, 2004. Text (Electronic book). Mode of access: World Wide Web.
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ABSTRACT: (Uncorrected OCR) Abstract of thesis entitled GOU QI ZI PROTECTS RAT RETINAL GANGLION CELLS FROM NEURODEGENERATION UPON EXPERIMENTAL GLAUCOMA: A NEURO-IMMUNE MECHANISM Submitted by ChanHiu Chi for the degree of Master of Philosophy at The University of Hong Kong in August 2003 Gou Qi Zi (Lycium barbarum Lynn fli'ifff':-"), a traditional Chinese medicine, is recorded for improving visual acuity such as the protection of damaged pigmented epithelium in light-induced phototoxicity and in age-related macular degeneration. The immunopotentiating effect of Gou Qi Zi and its active ingredients has been demonstrated in Gou Qi Zi-treated patients and in animal studies. It was reported that enhanced immune response in the central nervous system (CNS) facilitates the neuronal survival in CNS trauma. Administration of Gou Qi Zi extracts may preserve damaged retinal neurons by stimulating the immunoactivity in eye. In this study, we examined (1) the efficacy of Gou Qi Zi in enhancing the survival of retinal ganglion cells (RGCs), the retinal neurons for the transmission of visual impulses, in Sprague-Dawley rats with experimental glaucoma; and (2) the relationship between the neuroprotective effect and the immunostimulating effect of Gou Qi Zi. It was found that 17 % of RGCs degenerated following ocular hypertension for 2 weeks. Survival of RGCs was enhanced entirely in the ocular hypertensive rats with daily oral administration of optimal dosage of Gou Qi Zi extracts (8 ml/kg fresh juice, 10 mglkg commercially available Gou Qi Zi extract and 1 mglkg 70蚓 extracted watersoluble fraction). Immunohistochemical analysis has shown that microglial cells in the retina of the treated animals were activated. However, the neuroprotective effect of Gou Qi Zi was reduced when the microglial activity was suppressed by intravitreous injection of microglia-inhibiting factor or when the animals were thymectomized at neonatal stage. Microglial activity was also retarded in the thymectomized animals. This indicated that microglial activity and the presence of thymus, which is the origin of endogenous T cells, were required for the Gou Qi Zimediated neuroprotection, and thus, immune cells were involved in the particular neuroprotective mechanism. Here in this study, we have provided for the first time of some preliminary evidences to show that Gou Qi Zi is neuroprotective to damaged RGCs in hypertensive eyes and that the neuroprotective mechanism of Gou Qi Zi was partially directed through the immune system. The finding on the immune-related neuroprotective mechanism of Gou Qi Zi may also indicate the clinical application of Gou Qi Zi in preventing RGC degeneration.
http://sunzi.lib.hku.hk/hkuto/record/B29387450.
