Table 4.
PEC | Ld | Spleen cells | Curcumin (μM) | IFNγ (pg/ml) | Nitrite (μM) | % Infection | Amastigotes/infected macrophage | ||||
---|---|---|---|---|---|---|---|---|---|---|---|
BALB/c | |||||||||||
+ | − | − | 0 | 67.0±2.5 | 2.3±0.1 | NA | NA | ||||
+ | + | − | 0 | 104.5±2.5 | 2.2±0.1 | 90.6±1.2 | 10.0±0.8 | ||||
− | − | + | 0 | 318.0±113.6 | 0.00±0.2 | NA | NA | ||||
− | + | + | 0 | 724.7±32.2 | 4.7±1.7 | NA | NA | ||||
+ | + | + | 0 | 1268.2±56.3 | 38.3±1.4 | 36.3±3.1 | 2.3±0.0 | ||||
+ | + | + | 5 | 1134.0±17.5 | 17.9±1.0 | 51.0±1.0 | 3.9±0.1 | ||||
+ | + | + | 7.5 | 848.2±86.4 | 8.2±0.6 | 65.3±1.5 | 7.8±0.4 | ||||
+ | + | + | 10 | 632.8±72.9 | 2.5±0.2 | 81.0±2.6 | 8.8±0.4 | ||||
C3H/He | |||||||||||
+ | − | − | 0 | 96.2±0.1 | 1.7±0.0 | NA | NA | ||||
+ | + | − | 0 | 114.5±0.1 | 0.9±0.1 | 87.0±2.0 | 7.5±0.4 | ||||
− | − | + | 0 | 358.0±10.0 | 0.2±0.1 | NA | NA | ||||
− | + | + | 0 | 1271.3±0.1 | 4.9±0.2 | NA | NA | ||||
+ | + | + | 0 | 2225.0±208.8 | 41.4±0.2 | 26.6±2.1 | 2.1±0.1 | ||||
+ | + | + | 5 | 1682.3±89.8 | 20.2±1.5 | 44.3±2.1 | 3.7±0.2 | ||||
+ | + | + | 7.5 | 1606.5±24.8 | 16.2±0.8 | 65.3±3.1 | 5.2±0.4 | ||||
+ | + | + | 10 | 679.0±30.3 | 5.6±0.8 | 80.3±2.1 | 7.1±0.2 |
IFNγ, interferon-γ.
Nonelicited PEC were cultured with L. donovani (Ld) promastigotes in wells that contained cover slips for a period of 16–20 h; then curcumin and splenocytes from mice that had been infected with Leishmania were added. On day 5, the amount of nitric oxide was determined with Griess reagent, and the cover slips were stained with propidium iodide to enumerate the percent of infected macrophages and number of amastigotes per macrophage under a fluorescence microscope. The amount of IFNγ in the supernatant was determined by ELISA 72 h after addition of curcumin and primed splenocytes. The brackets indicate the groups compared in the ANOVA, which showed that the effect of curcumin was significant (P < 0.001).