Figure 3

From: Amyloid proteotoxicity initiates an inflammatory response blocked by cannabinoids

Figure 3

Eicosanoids, endocannabinoids and RAGE modulate Aβ toxicity. MC65 cells induced (Δtet) to make Aβ in the presence or absence of the indicated compounds and cell viability and/or intracellular Aβ levels monitored at day 2 or 2.5 following induction. 5H (5-HETE, 500 nmol/l); 5Hp (5-HETE peroxide, 500 nmol/l); 12H (12 HETE, 500 nmol/l); D2 (PGD2, 500 nmol/l); E2 (PDE2, 10 μmol/l); AEA (arachidonoyl ethanolamide, 1 μmol/l); THC (tetrahydrocannabinol, 50 nmol/l); Q-3 (Q-3 carboxamide, 100 nmol/l); 404 (AM404, 1 μmol/l); 630 (AM630, 10 nmol/l); 251 (AM251, 1 μmol/l). (a) Cell viability at 2 days; (b) cell viability at 3 days; (c) cell viability at 2.5 days; (d) Aβ at 2 days; (e) THC dose response, cell viability; (f) THC dose response, intracellular Aβ at 2 days. (g) MC65 cells were incubated with or without the RAGE inhibitor (RI) FPS-ZMII (1 μmol/l) with (+) and without (−) tet. Cell viability assayed on day 4 (h) The amount of IL8 assayed on day 3 following Aβ induction. (i) Aβ expression was monitored on day 3 (j) Cells were treated with RAGE siRNA or control siRNA and cell viability assayed after 2 days. (k) IL-8 was assayed on day 3, (l) Phospho NFkB, RAGE and Aβ expression were assayed on day 3. Aβ, beta amyloid; SiRNA, small interfering RNA.