PMC

SP1 overexpression reverses the pro-apoptotic effect of cannabidiol in vivo. A. The tumors of four groups were isolated and compared. B. Tumor growth curve of Sham group, Cannabidiol + Lv-OE-SP1 group, Cannabidiol + Lv-OE-NC group and Cannabidiol group (n=4 per group). Tumor volume was measured every few days. C. Tumor weight was measured at the end of the experiment. D-G. The protein levels of BAX, Bcl2, cleaved caspase-3 and CBX2 in the Sham group, Cannabidiol group, Cannabidiol + Lv-OE-SP1 group, and Cannabidiol + Lv-OE-NC group. The data shown are mean ± SD. **P<0.01 vs. Sham; #P<0.05, ##P<0.01 vs. Cannabidiol + Lv-OE-NC.

CBD = cannabidiol, EEG = electroencephalogram.

Cannabidiol (10 mg/kg) treatment enhances social interaction preferences but reduces the social novelty sniffing preference of male C57BL/6J mice. (A) Cannabidiol and vehicle treated mice did not differ in social interaction preference. However only cannabidiol treated C57BL/6J mice spent significantly more time in chambers with strangers than novel objects (*p < 0.05). (B) Cannabidiol treated mice also spent more time sniffing strangers than novel objects (*p = 0.05), while vehicle controls did not. (C) In social novelty tests cannabidiol and vehicle treated mice did not differ significantly in preference. Yet vehicle treated mice tended to prefer novel strangers in chamber dwelling time measurements (p = 0.06) while cannabidiol treated mice did not. (D) By measurements of sniffing time, cannabidiol and vehicle treated mice did not differ in social novelty preference. Within groups cannabidiol treated mice lacked preference for social novelty exhibited by vehicle treated C57BL/6J males (*p < 0.005). Sample sizes were 10 mice per group; data shown are mean ±95% CI, small squares are individual values.

a Target-mediated drug–drug interactions of cannabidiol with cannabinoid and 5-hydroxytryptamine 1A receptors . b Target-mediated drug–drug interactions of cannabidiol with 5-hydroxytryptamine 2A receptors . c Target-mediated drug–drug interactions of cannabidiol with 5-hydroxytryptamine 3A receptors . d Target-mediated drug–drug interactions of cannabidiol with prostaglandin G/H synthase 1 and 2 inhibitors . e Target-mediated drug–drug interactions of cannabidiol with Cytochrome P450 1B1 and 3A5 inhibitor . f Target-mediated drug–drug interactions of cannabidiol with Cytochrome P450 2D6 and 3A7 inhibitor . g Target-mediated drug–drug interactions of cannabidiol with Cytochrome P450 1A2 inhibitor . The red dotted lines indicate CBD’s mechanism/actions as listed in red boxes. The blue double-headed arrows indicate the possible targets and interactions of CBD with other targets/mechanisms as listed in blue boxes. Green single-headed arrows indicate the drugs that act on these targets, as listed in green boxes. Such drugs may have additive/synergistic or antagonistic effects if given concomitantly with CBD.