Abstract
Background and objectives:Neuroinflammation is closely associated with various diseases including neuropathic pain. Microglia are immune cells in the central nervous system which are the main players of immunity and inflammation. Since microglia are activated by nerve injury, and they produce proinflammatory mediators to cause neuropathic pain, targeting activated microglia is considered to be a strategy for treating neuropathic pain. Activation of the cannabinoid CB2 receptor is known to have anti-inflammatory effects in microglia. ABK5-1 is a CB2 subtype selective agonist which inhibits IL-1β and IL-6 production in the microglia cell line BV-2. The purpose of the current study is to further analyze anti-inflammatory effects of ABK5 in terms of different cytokines and the possible pathway involved in the effect in the BV-2 cell line.Methods:A cytokine array was performed to screen the effect of ABK5-1 on forty inflammatory mediators in BV-2 cells. Changes of the inflammatory mediators was further supported by mRNA analysis, and a possible signaling molecule that involved the observation was evaluated by western blot.Results:Stimulating BV-2 cells by lipopolysaccharide increased expression of eleven inflammatory mediators, and ABK5-1 treatment resulted in more than a 50% decrease of sICAM1, IL-6, and RANTES. Real-time PCR results showed a decrease of G-CSF, ICAM1, MCP-1, MIP-1α, and MIP-1β mRNA levels. Western blot analysis showed that ABK5-1 inhibited LPS-induced ERK phosphorylation, which can be a mechanism of ABK5-1-mediated anti-inflammatory effect.Conclusions:Our current results support the possibility that ABK5-1 is an anti-inflammatory drug for microglia.
Highlights
Cannabis has been used for centuries for medical reasons and is known to have various beneficial impact such as antiinflammation and analgesic effects [1], while it may cause some unwanted effects. ∆9-tetrahydrocannabinol (THC) is a well-studied component of cannabis which is known to cause these effects by binding both subtypes of cannabinoid receptors, CB1 and CB2
Real-time PCR results showed a decrease of Granulocyte colony-stimulating factor (G-CSF), ICAM1, monocyte chemotactic protein 1 (MCP-1), macrophage inflammatory proteins (MIP)-1α, and MIP-1β mRNA levels
Western blot analysis showed that ABK5-1 inhibited LPS-induced ERK phosphorylation, which can be a mechanism of ABK5-1-mediated anti-inflammatory effect
Summary
Cannabis has been used for centuries for medical reasons and is known to have various beneficial impact such as antiinflammation and analgesic effects [1], while it may cause some unwanted effects. ∆9-tetrahydrocannabinol (THC) is a well-studied component of cannabis which is known to cause these effects by binding both subtypes of cannabinoid receptors, CB1 and CB2. ∆9-tetrahydrocannabinol (THC) is a well-studied component of cannabis which is known to cause these effects by binding both subtypes of cannabinoid receptors, CB1 and CB2. Since CB1 is mainly expressed in the central nervous system (CNS) and involved in control of neurotransmitter release [3,4]. While it expected to be a good target for some diseases, unwanted psychoactive. ABK5-1 is a CB2 subtype selective agonist which inhibits IL-1β and IL-6 production in the microglia cell line BV-2. The purpose of the current study is to further analyze anti-inflammatory effects of ABK5 in terms of different cytokines and the possible pathway involved in the effect in the BV-2 cell line
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
