Cannabis and Acne AEA simulates lipid production in human sebocytes of sebaceous glands at low concentrations, but induces apoptosis at higher levels, suggesting that this system is under ECS control (Dobrosi et al., 2008). CBD 10–20 mMdid not affect basal lipid synthesis in SZ95 sebocytes, but did block such stimulation by AEA and arachidonate (Biro et al., 2009). Higher doses of CBD (30–50 mM) induced sebocyte apoptosis, which was augmented in the presence of AEA. The effect of CBD to increase Ca++ was blocked by ruthenium red, a TRP-inhibitor. RNA mediated silencing of TRPV1 and TRPV3 failed to attenuate CBD effects, but experiments did support the aetiological role of TRPV4, a putative regulator of systemic osmotic pressure (T. Bíró, 2010, pers. comm.). Given the observed ability of CBD to be absorbed transcutaneously, it offers great promise to attenuate the increased sebum production at the pathological root of acne. Cannabis terpenoids could offer complementary activity. Two citrus EOs primarily composed of limonene inhibited Propionibacterium acnes, the key pathogen in acne (MIC 0.31 mL·mL-1), more potently than triclosan (Kim et al., 2008). Linalool alone demonstrated an MIC of 0.625 mL·mL-1. Both EOs inhibited P. acnes-induced TNF-a production, suggesting an adjunctive anti-inflammatory effect. In a similar manner, pinene was the most potent component of a tea-tree eucalyptus EO in suppression of P. acnes and Staph spp. in another report (Raman et al., 1995). Considering the known minimal toxicities of CBD and these terpenoids and the above findings, new acne therapies utilizing whole CBD-predominant extracts, via multitargeting (Wagner and Ulrich-Merzenich, 2009), may present a novel and promising therapeutic approach that poses minimal risks in comparison to isotretinoin.
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Cannabis and Acne AEA simulates lipid production in human sebocytes of sebaceous glands at low concentrations, but induces apoptosis at higher levels, suggesting that this system is under ECS control (Dobrosi et al., 2008). CBD 10–20 mMdid not affect basal lipid synthesis in SZ95 sebocytes, but did block such stimulation by AEA and arachidonate (Biro et al., 2009). Higher doses of CBD (30–50 mM) induced sebocyte apoptosis, which was augmented in the presence of AEA. The effect of CBD to increase Ca++ was blocked by ruthenium red, a TRP-inhibitor. RNA mediated silencing of TRPV1 and TRPV3 failed to attenuate CBD effects, but experiments did support the aetiological role of TRPV4, a putative regulator of systemic osmotic pressure (T. Bíró, 2010, pers. comm.). Given the observed ability of CBD to be absorbed transcutaneously, it offers great promise to attenuate the increased sebum production at the pathological root of acne. Cannabis terpenoids could offer complementary activity. Two citrus EOs primarily composed of limonene inhibited Propionibacterium acnes, the key pathogen in acne (MIC 0.31 mL·mL-1), more potently than triclosan (Kim et al., 2008). Linalool alone demonstrated an MIC of 0.625 mL·mL-1. Both EOs inhibited P. acnes-induced TNF-a production, suggesting an adjunctive anti-inflammatory effect. In a similar manner, pinene was the most potent component of a tea-tree eucalyptus EO in suppression of P. acnes and Staph spp. in another report (Raman et al., 1995). Considering the known minimal toxicities of CBD and these terpenoids and the above findings, new acne therapies utilizing whole CBD-predominant extracts, via multitargeting (Wagner and Ulrich-Merzenich, 2009), may present a novel and promising therapeutic approach that poses minimal risks in comparison to isotretinoin.