Poster presentationWe have shown neuronal apoptosis in the hippocampus of rats exposed to chronic intermittent hypoxia
mimicking severe conditions of obstructive sleep apnea (OSA) syndrome in patients [1]. Lycium barbarum
polysaccharides (LBP), active biological ingredients of traditional Chinese herbal medicine Goji, have
been shown to possess cytoprotective properties [2].
The aim of this study was to examine the protective effects of LBP against neuronal apoptosis in the
hippocampus in a severe OSA rodent model. We hypothesized that oral administration of LBP ameliorates
neuronal apoptosis in the rat hippocampus induced by chronic intermittent hypoxia.
Adult SD rats were randomly divided into 4 experimental groups, namely: (i) normoxic control (Nx);
(ii) Nx treated with LBP; hypoxic groups treated with either (iii) LBP or (iv) vehicle. The hypoxic groups
were kept in a normobaric chamber with inspired oxygen alternating from 21 to 5 ± 0.5% oxygen per
minute for 8 hr/day for 7 days, whereas Nx groups was maintained in room air for 7 days. LBP (1mg/kg)
were orally fed to the rats 2 hours prior the daily hypoxic treatment. Rats were sacrificed and the
hippocampus was harvested for measurements of oxidative marker, malondialdehyde (MDA), apoptotic
cell death using TUNEL assay, protein expression levels of antioxidant enzymes, and inflammatory
cytokines by Western blot.
There were significantly more TUNEL positive –labeling cells in the CA regions and dentate gyrus of
the hippocampus in the vehicle-treated hypoxic group than those of the Nx control and LBP-treated
groups. In addition, levels of MDA and the protein expressions of cleaved caspase 3 and inflammatory
cytokines were increased in the vehicle-treated hypoxic group when compared to the Nx groups and were
lowered by the LBP treatment. Intriguingly, there were significantly more PCNA-labeling cells in the
dentate gyrus of the hippocampus in the LBP-treated hypoxic groups than those of the other groups.
Also, the protein expression of cyclin D1 was increased in the hypoxic groups when compared to the Nx
groups.
In conclusion, oral administration of LBP significantly ameliorates oxidative stress, inflammation and
neuronal apoptosis with enhanced proliferative activities in the hippocampus of rats exposed to chronic
intermittent hypoxia. Thus, LBP may be proposed as a health supplement to mitigate neurological deficits
in OSA patients, for which awaits future studies to delineate the neuroprotective mechanism of LBP.
[Studies supported by research grants (HKU 7510/06M, HKU 766110M) from RGC and funding
(201007176007, SFPBR 200911159072) from HKU]
[1] Hung, M.W., et al. (2008) J Pineal Res 44: 214-221.
[2] Chang, R.C., et al. (2008). Cell Mol Neurobiol 28: 643-652.published_or_final_versio
