Table 1.

Role of COX-2, PPAR-γ, and cannabinoid receptors in cannabidiol-mediated apoptotic cell death

Viability (mean ± SEM)DNA fragmentation (mean ± SEM)
A549H460A549H460
Vehicle100% ± 7%100% ± 3%100% ± 6%100% ± 4%
CBD49% ± 9%c17% ± 2%c541% ± 126%b391% ± 80%a
CBD + AM-25150% ± 2%c,e14% ± 2%c,e458% ± 65%b,e409% ± 88%a,e
CBD + AM-63045% ± 5%c,e8% ± 2%c,e679% ± 89%b,e360% ± 6%a,e
CBD + AM-251 + AM-63042% ± 3%c,e12% ± 2%c,e541% ± 35%b,e504% ± 118%b,e
CBD + capsazepine53% ± 3%c,e22% ± 2%c,e599% ± 152%b,e429% ± 67%a,e
Vehicle100% ± 3%100% ± 2%100% ± 10%100% ± 15%
CBD24% ± 7%c41% ± 3%c423% ± 74%c573% ± 65%c
CBD + NS-39882% ± 9%d67% ± 7%d81% ± 6%d170% ± 35%d
CBD + GW966276% ± 4%d67% ± 8%d81% ± 7%d168% ± 30%d
CBD + NS-398 + GW9662112% ± 8%d,f,i90% ± 7%d,g,h56% ± 7%d57% ± 2%d
NS-398112% ± 3%100% ± 1%90% ± 10%115% ± 16%
GW9662104% ± 4%95% ± 4%114% ± 27%98% ± 18%

NOTE: Cells were incubated with cannabidiol (3 μmol/L) or vehicle for 48 hours (WST-1 test) or 18 hours (DNA fragmentation) following a 1-hour pretreatment with AM-251 (CB1 antagonist; 1 μmol/L), AM-630 (CB2 antagonist; 1 μmol/L), capsazepine (TRPV1 antagonist; 1 μmol/L), NS-398 (COX-2 inhibitor; 1 μmol/L), or GW9662 (PPAR-γ antagonist; 10 μmol/L). Values are mean ± SEM of n = 6–12 (WST), n = 3–8 (DNA fragmentation of GW9662- and NS-398–treated cells), n = 8 (DNA fragmentation of cells treated with AM-251, AM-630, and capsazepine) experiments.

Abbreviation: CBD, cannabidiol.

  • ↵aP < 0.05.

  • ↵bP < 0.01.

  • ↵cP < 0.001 vs. vehicle.

  • ↵dP < 0.001 vs. CBD.

  • ↵enot significant vs. CBD.

  • ↵fP < 0.05.

  • ↵gP < 0.01 for CBD + NS-398 + GW9662 vs. CBD + NS-398.

  • ↵hP < 0.05.

  • ↵iP < 0.01 for CBD + NS-398 + GW9662 vs. CBD + GW9662.