科研之友
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摘要
Two hallmarks of Alzheimer diseases are the continuous inflammatory process, and the brain deposit of Amyloid b (A beta), a cytotoxic protein. The intracellular accumulation of A beta(25-35) fractions, in the absence of Heat Shock proteins (Hsps), could be responsible for its cytotoxic activity. As, pro-inflammatory mediators and nitric oxide control the expression of Hsps, our aim was to investigate the effect of A beta(25-35) on the concentration of IL-1 beta, TNF-alpha and nitrite levels, and their relation to pHSF-1, Hsp-60, -70 and -90 expressions, in the rat C6 astrocyte cells. Interleukin-specific ELISA kits, immunohistochemistry with monoclonal anti-Hsp and anti pHSF-1 antibodies, and histochemistry techniques, were used. Our results showed that A beta(25-35) treatment of C6 cells increased, significantly and consistently the concentration of IL-1 beta, TNF-alpha and nitrite 3 days after initiating treatment. The immunoreactivity of C6 cells to Hsp-70 reached its peak after 3 days of treatment followed by an abrupt decrease, as opposed to Hsp-60 and -90 expressions that showed an initial and progressive increase after 3 days of A beta(25-35) treatment. pHSF-1 was identified throughout the experimental period. Nevertheless, progressive and sustained cell death was observed during all the treatment times and it was not caspase-3 dependent. Our results suggest that Hsp-70 temporary expression serves as a trigger to inhibit casapase-3 pathway and allow the expression of Hsp-60 and -90 in C6 astrocytoma cells stimulated with A beta(25-35).
- 出版日期2013-10
