Journal of Capital Medical University ›› 2011, Vol. 32 ›› Issue (4): 501-508.doi: 10.3969/j.issn.1006-7795.2011.04.013

• 神经元退行性变的实验研究 • Previous Articles     Next Articles

Influence of peptidoglycan on BV2 cells after endocytosis of amyloid protein β oligomers

JIANG Xin1, XIANG Rong-cai2, BAI Li-juan1, ZHANG He-min1, CHEN Xiao-hong1, MA En-long3   

  1. 1. Department of Neurology, The People’s Hospital of Liaoning Province, Shenyang 110016, China;2. Department of Biophysics, College of Basic Medical Sciences, China Medical University, Shenyang 110012, China;3. Department of Pharmacy, School of Pharmacy, Shenyang Pharmaceutical University, Shenyang 110016, China
  • Received:2011-03-30 Revised:1900-01-01 Online:2011-08-21 Published:2011-08-21

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Abstract: Objective To investigate the influences and mechanisms of the pro-inflammatory medium of peptidoglycan(PGN) on BV2 cells after endocytosis of amyloid protein β(Aβ) oligomers. Methods BV2 cells were cultivated by cell passage method, instead of neurons and microglia separately. Aβ1-42 oligomers were prepared according to Klein WL (2002). The endocytosis amount of Aβ in BV2 cells was determined by immunofluorescence staining. The expression of phosphorylated p38 mitogen-activated protein kinase(p-p38MAPK), p38MAPK protein of BV2 cells in each group was determined by Western blotting method, and mouse homologue formyl peptide receptor 2(mFPR2)mRNA by PCR method. Results The endocytosis of Aβ42 oligomer increased after BV2 cells was activated by PGN, which could be inhibited by mFPR2. PGN could lead to the increase of mFPR2 mRNA expression in BV2 cells in relation with concentration and time, which could be inhibited by SB202190-p38MAPK. When the expression of SB202190 increased, the inhibition increased. Compared with 0 μmol/L, concentration of each group was inhibited more significantly, for 1 μmol/L group(P<0.05), for 10, 20, 30 μmol/L groups(P <0.01). After PGN activated BV2 cells, the activation of p38MAPK phosphorylation at each time point was significantly different from the control group(P<0.01). Conclusion The endocytosis of Aβ42 oligomer increased after BV2 cells was activated by PGN, which can be inhibited by mFPR2, so it is speculated that endocytosis of Aβ in BV2 cells may have relation with the expression of mFPR2. PGN could lead to the increase of mFPR2 mRNA expression in BV2 cells, which may participate in the endocytosis of Aβ after BV2 cells are activated. PGN can lead to the increase of p38MAPK expression in BV2, and its inhibitor can decrease the expression of mFPR2 mRNA, which may be the mechanism of endocytosis of Aβ after BV2 cells are activated.

Key words: peptidoglycan, microglia, Aβ1-42 oligomer, p38 mitogen-activated protein kinase, formyl peptide receptor/mouse homologue formyl peptide receptor

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