Reversal of apoptotic resistance by Lycium barbarum glycopeptide 3 in aged T cells

Biomedical and Environmental Sciences : BES
Long-Guo YuanQi-Yang He

Abstract

To study whether Lycium barbarum glycopeptide 3 (LBGP3) affects T cell apoptosis in aged mice. LBGP3 was purified with DEAE cellulose and Sephadex columns. Apoptotic "sub-G1 peak" was detected by flow cytometry and DNA ladder was resolved by agarose gel electrophoresis. Levels of IFN-gamma and IL-10 were measured with specific kits and mRNA expression was detected by RT-PCR. Apoptosis-related proteins of FLIP, FasL, and Bcl-2 were determined by Western blotting. LBGP3 was purified from Fructus Lycii water extracts and identified as a 41 kD glycopeptide. Treatment with 200 microg/mL LBGP3 increased the apoptotic rate of T cells from aged mice and showed a similar DNA ladder pattern to that in young T cells. The reversal of apoptotic resistance was involved in down-regulating the expression of Bcl-2 and FLIP, and up-regulating the expression of FasL. Lycium barbarum glycopeptide 3 reverses apoptotic resistance of aged T cells by modulating the expression of apoptosis-related molecules.

References

Jan 1, 1992·Cytometry·Z DarzynkiewiczF Traganos
Oct 8, 1992·Nature·R P BissonnetteD R Green
Oct 1, 1994·International Immunology·T TakahashiS Nagata
Jan 13, 2000·Current Opinion in Immunology·A V Chervonsky
Apr 3, 2002·Inflammation Research : Official Journal of the European Histamine Research Society ... [et Al.]·R A FlavellR J Davis
May 23, 2006·Nature Immunology·Robert L Coffman

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