It has been suggested that cannabis might treat psoriasis, due to the anti-inflammatory properties of its cannabinoids, and the regulatory effects of THC (tetra hydro cannabinon) on the immune system. The adverse effects of cannabis might be overcome by use of more specific cannabinoid receptor medications, to inhibit keratinocyte proliferation.
Endocannabinoids are lipophilic compounds derived from membrane phospholipids; they do not need to be stored in synaptic vesicles like other neurotransmitters. In the brain, they are produced by neurons at their sites of action and act on demand, generating a transient, rapid effect before being hydrolyzed and inactivated. Because of their lipophilic nature and the mechanism of their synthesis and release, endocannabinoids are considered as local neuromodulators. First two endocannabinoids, AEA and 2-arachidonoyl-glycerol (2-AG).
Endocannabinoid receptors are highly expressed in the brain, and have been also found in organs and tissues of the body involved in energy homeostasis, such as adipose tissue, liver, gastrointestinal tract, and skeletal muscle (Outside the brain, endocannabinoids also appear to be produced on demand and act on cells in a paracrine or autocrine manner.
Endocannabenoid system has the following functions : Energy balance, immune modulator, stress recovery, metabolic homeostasis and food intake .
It’s reported that Cannabinoids inhibit human keratinocyte proliferation through a non-CB1/CB2 mechanism and have a potential therapeutic value in the treatment of psoriasis. Cannabinoids from cannabis (Cannabis sativa) are anti-inflammatory and have inhibitory effects on the proliferation of a number of tumorigenic cell lines, some of which are mediated via cannabinoid receptors. Cannabinoid (CB) receptors are present in human skin and anandamide, an endogenous CB receptor ligand, inhibits epidermal keratinocyte differentiation. The cannabinoids tested all inhibited keratinocyte proliferation in a concentration-dependent manner .
Also it’s reported in other study that anandamide regulates keratinocyte differentiation by inducing DNA methylation in a CB1 Receptor-dependent manner . AEA is able to inhibit keratinocyte differentiation by modifying the gene expression profile of these cells by decreasing gene transcription by inducing DNA methylation .Moreover inhibition of DNA methylation prevents the effects of AEA on gene expression. AEA can induce DNA methylation of keratinocyte-differentiating genes by increasing the activity of DNA methyltransferase (DNMT) activity which mediated by CB1R .
0 التعليقات:
إرسال تعليق