by in About CBD 11 February 2019

Anti-inflammatory and analgesic effect of CBD

The ability of CBD to stimulate adenosine A2 receptors is considered to be the main mechanism of anti-inflammatory activity. In a study of CBD in acute lung injury in rats, a single cannabidiol dose of 20mg / kg given prior to the induction of LPS-induced acute lung damage (lipopolysaccharide) reduced the migration of leukocytes (in particular neutrophils) to the lungs, decreased albumin in the fluid after bronchoalveolar lavage, reduces the activity of myeloperoxidase in lung tissues and the production of proinflammatory cytokines (TNF and IL-6) and chemokines (MCP-1 and MIP-2). In addition, the adenosine A2A receptor is involved in the anti-inflammatory effect of cannabidiol on acute lung injury induced by LPS [11]. It is confirmed that CBD has analgesic and anti-inflammatory effects in inflammation and joint pain of various etiology or even rheumatoid (Rheumatoid arthritis). It was also discovered that the mechanism of anti-inflammatory activity does not have to bind to the endocannabinoid system (stimulating CB1 or CB2 receptors) but also works through glycine receptors (GlyR) [1]. Experimental evidence suggests that prostaglandin E2 (PGE2), a critical mediator of central and peripheral pain sensitization, selectively inhibits the α3 GlyR function [2,3]. It works in the opposite direction to cannabidiol, which stimulates these receptors. It was found that the suppression of inhibition of GlyRs α3 receptors by PGE2 may be associated with the anti-inflammatory action of CBD and reduce inflammatory pain.

This indicates the additional effect of cannabinoids on our body through stimulation or inhibition of other systems of our body, not only the endocannabinoid system, which significantly broadens the horizons of cannabinoids impact on our health. In an ex vivo study, draining lymph node cells from CBD-treated mice showed decreased production of IFN-γ (Interferon belonging to type II-plays an essential role as a mediator of immune response) [8]. CBD, through combined immunological and anti-inflammatory actions, has a strong anti-arthritic effect in rats. In addition, the influence of CBD on the regulation of the immune system and the number of lymphatic cells T [9,10] has been proven.

 

How can we use it?

Inflammation almost always brings along pain. Treatment of a patient with inflammation should then include the treatment of pain. Fortunately, CBD has anti-inflammatory, immunosuppressive and painkilling effects.
Several preclinical studies have shown that CBD has analgesic properties [4,5,6]. In addition, CBD at a dose of 10 mg / kg has been shown to abrogate hyperalgesia (i.e., excessive pain sensitivity) induced by carrageenan against a thermal stimulus in rats [5]. Other clinical evidence points to the effectiveness of CBD in the treatment of neuropathic pain symptoms [7]. This gives us the opportunity to use cannabinoids to fight pain in the future. At present, NSAIDs (non-steroidal anti-inflammatory drugs) are the most common group of painkillers. They have a lot of side effects (including peptic action in the stomach) and interact with other drugs (eg medicines for hypertension). Replacing NSAIDs with drugs with a much smaller number of side effects would be a great solution in the fight against pain.
Immunosuppression associated with CBD supplementation combined with its anti-inflammatory and analgesic effects may find its application in Multiple Sclerosis, Rheumatoid Arthritis, sudden and chronic inflammation, joint injuries with inflammation or chronic muscle or joint pain. However, the anti-inflammatory effect does not have to be associated only with arthritis and muscle inflammation. They can definitely be used in inflammation of the skin or acne.

 

References and research used in the article:

1.   Cannabinoids suppress inflammatory and neuropathic pain by targeting α3 glycine receptors. Wei Xiong, Tanxing Cui, Kejun Cheng, Fei Yang, Shao-Rui Chen, Dan Willenbring, Yun Guan, Hui-Lin Pan, Ke Ren, Yan Xu and Li Zhang.
2.   PGE(2) selectively blocks inhibitory glycinergic neurotransmission onto rat superficial dorsal horn neurons. Ahmadi S, Lippross S, Neuhuber WL, Zeilhofer HU. Nat Neurosci. 2002 Jan; 5(1):34-40.
3.   GlyR alpha3: an essential target for spinal PGE2-mediated inflammatory pain sensitization. Harvey RJ, Depner UB, Wässle H, Ahmadi S, Heindl C, Reinold H, Smart TG, Harvey K, Schütz B, Abo-Salem OM, Zimmer A, Poisbeau P, Welzl H, Wolfer DP, Betz H, Zeilhofer HU, Müller U. Science. 2004 May 7; 304(5672):884-7.
4.       Costa B, Colleoni M, Conti S, Parolaro D, Franke C, Trovato AE, Giagnoni G. Oral anti-inflammatory activity of cannabidiol, a non-psychoactive constituent of cannabis, in acute carrageenan-induced inflammation in the rat paw. Naunyn Schmiedebergs Arch Pharmacol 2004;369:294–9.
5.       Costa B, Giagnoni G, Franke C, Trovato AE, Colleoni M. Vanilloid TRPV1 receptor mediates the antihyperalgesic effect of the nonpsychoactive cannabinoid, cannabidiol, in a rat model of acute inflammation. Br J Pharmacol 2004;143:247–50.
6.       Costa B, Trovato AE, Comelli F, Giagnoni G, Colleoni M. The non-psychoactive cannabis constituent cannabidiol is an orally effective therapeutic agent in rat chronic inflammatory and neuropathic pain. Eur J Pharmacol 2007;556:75–83.
7.       Wade DT, Robson P, House H, Makela P, Aram J. A preliminary controlled study to determine whether whole-plant cannabis extracts can improve intractable neurogenic symptoms. Clin Rehabil 2003;17:21–9.
8.       The nonpsychoactive cannabis constituent cannabidiol is an oral anti-arthritic therapeutic in murine collagen-induced arthritis. A. M. Malfait, R. Gallily, P. F. Sumariwalla,  A. S. Malik, E. Andreakos, R. Mechoulam, and M. Feldmann
9.       Cannabidiol (CBD) Induces Functional Tregs in Response to Low-Level T Cell Activation. Saphala Dhital, John V. Stokes, Nogi Park, Keun-Seok Seo, and Barbara L.F. Kaplan.
10.   Cannabidiol, a non-psychoactive cannabinoid, leads to EGR2-dependent anergy in activated encephalitogenic T cells. Ewa Kozela, Ana Juknat, Nathali Kaushansky, Avraham Ben-Nun, Giovanni Coppola, and Zvi Vogel
11.   Cannabidiol, a non-psychotropic plant-derived cannabinoid, decreases inflammation in a murine model of acute lung injury: Role for the adenosine A2A receptor. AlisonRibeiro,VivianeFerraz-de-Paula, Milena L.Pinheiro, Luana B.Vitoretti, Domenica P.Mariano-Souza, Wanderley M.Quinteiro-Filho, Adriana T.Akamine, Vinícius I.Almeida, JoãoQuevedo, FelipeDal-Pizzol, Jaime E.Hallak, Antônio W.Zuardi, José A.Crippa, JoãoPalermo-Neto

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