Figure 5
From: Heme oxygenase-1 derived carbon monoxide suppresses Aβ1–42 toxicity in astrocytes
Aβ1-42toxicity involves peroxynitrite formation. (a) Separate fluorescence images of astrocytes loaded with the ONOO– sensitive dye, 2-[6-(4′-amino) phenoxy-3H-xanthen-3-on-9-yl]benzoic acid (APF). Cells were either untreated or exposed to 500 nM Aβ1-42 for 24 h. (b) Mean±S.E.M. (taken from 5-10 recordings) APF fluorescence detected in astrocytes without treatment, or following a 24 h treatment with either 100–1000 nM Aβ1–42 or reverse peptide (500 nM), as indicated. *P<0.05; **P<0.01 as compared with control. (c) Effect on cell viability of 24 h exposure of astrocytes to Aβ1–42 alone (100–1000 nM, white bars) or Aβ1–42 in the additional presence of 500 μM L-NAME (grey bars). Bars represent the mean±S.E.M. data of cells from 6 repeats (each performed in duplicate) with cells from different preparations. Significance: ***P<0.001 as compared either with respective controls, or between drug treatment or no treatment, as indicated. (d) as (c), except that cells were exposed either to Aβ1–42 alone (100–1000 nM, white bars) or Aβ1–42 in the additional presence of 50 μM FeTPPs (grey bars). Bars represent the mean±S.E.M. data of cells from 3 repeats. Significant difference: ***P<0.001 effects of peptide alone compared to control, or between amyloid peptide with or without FeTPPS at each amyloid concentration, as indicated
