concanavalin a/cannabis

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[Cannabinoid receptor 2 deletion promotes proliferation and activation of hepatic macrophages in mice with acute liver injury induced by concanavalin A].

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Objective To investigate the effect of cannabinoid receptor 2 (CB2) gene deletion on liver macrophages in mice with acute liver injury induced by concanavalin A (ConA). Methods The mice with gene deletion were identified by PCR. Twenty 8-week-old wild-type C57BL/6J male mice were randomly divided

Selective CB1 cannabinoid receptor antagonist, SR141716A, attenuates liver injury induced by Concanavalin A.

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OBJECTIVE The aim of this study was to investigate the hepatoprotective activity of a selective cannabinoid receptor 1 (CB1) antagonist, SR141716A, in a Concanavalin A (Con A)-induced mouse liver injury model and to determine whether SR141716A has an effect on the production of inflammatory

Protective effects of specific cannabinoid receptor 2 agonist GW405833 on concanavalin A-induced acute liver injury in mice.

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Cannabinoid receptor 2 (CB2R) is highly expressed in immune cells and plays an important role in regulating immune responses. In the current study, we investigated the effects of GW405833 (GW), a specific CB2R agonist, on acute liver injury induced by concanavalin A (Con A). In animal experiments,

Marijuana and immunity: tetrahydrocannabinol mediated inhibition of lymphocyte blastogenesis.

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The effects of delta-9-tetrahydrocannabinol (THC) and its major metabolite, 11-OH delta-9-tetrahydrocannabinol (11-OH THC) on mitogen driven lymphocyte blastogenic transformation (LBT) were studied. THC inhibited LBT responses to the T lymphocyte mitogens phytohemagglutinin and concanavalin A but

Age-related suppression of murine lymphoid cell blastogenesis by marijuana components.

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Marijuana components modulate a variety of immune response parameters. The cannabinoids delta 9-tetrahydrocannabinol (THC) and 11-hydroxy-tetrahydrocannabinol (11 OH-THC) are known to depress the in vitro proliferative response of murine lymphoid cells to the mitogens concanavalin A (Con A) and

Age-associated differences in cannabinoid-induced suppression of murine spleen, lymph node and thymus cell blastogenic responses.

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The effects of delta 9-tetrahydrocannabinol (THC) and 11-OH THC on the proliferative responses of murine thymus, spleen and lymph node cells were examined. Specifically, weanling and adult mouse lymphocytes were stimulated in vitro with the T-cell mitogens concanavalin A and phytohemagglutinin.

Relative involvement of cannabinoid CB(1) and CB(2) receptors in the Delta(9)-tetrahydrocannabinol-induced inhibition of natural killer activity.

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We demonstrated that in vivo administration of Delta(9)-tetrahydrocannabinol in mice (15 mg/kg s.c.) significantly inhibited natural killer cell (NK) cytolytic activity without affecting Concanavalin A (ConA)-induced splenocyte proliferation. Moreover, we investigated the effect of in vivo

The effects of cannabinoids and cannabispiro compounds on Escherichia coli adhesion to tissue culture cells and on leukocyte functions in vitro.

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delta 9-Tetrahydrocannabinol, cannabidiol, cannabidiolic acid, tetrahydrocannabidiolic acid, cannabispirol, acetylcannabispirol, cannabispirone, and cannabispirenone in a low concentration did not affect the adhesion of Escherichia coli on cultured HEp-2 cells. Cannabinoids at 10(-6) M increased the

Maternal exposure to the synthetic cannabinoid HU-210: effects on the endocrine and immune systems of the adult male offspring.

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Natural and synthetic cannabinoid receptor agonists have been described to exert profound effects on both the neuroendocrine integration and the functional responses of the immune system. In the present study, Wistar rats were exposed to the highly potent cannabinoid agonist HU-210 (1, 5 and 25

A novel synthetic cannabinoid derivative inhibits inflammatory liver damage via negative cytokine regulation.

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The therapeutic potential of cannabinoids has been described previously for several inflammatory diseases, but the molecular mechanisms underlying the anti-inflammatory properties of cannabinoids are not well understood. In this study, we investigated the mechanism of action of a novel synthetic

Attenuation of experimental autoimmune hepatitis by exogenous and endogenous cannabinoids: involvement of regulatory T cells.

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Immune-mediated liver diseases including autoimmune and viral hepatitis are a major health problem worldwide. Natural cannabinoids such as Delta(9)-tetrahydrocannabinol (THC) effectively modulate immune cell function, and they have shown therapeutic potential in treating inflammatory diseases. We

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