Cannabinoid CB2 Receptor Mediates Nicotine-Induced Anti-Inflammation in N9 Microglial Cells Exposed to β Amyloid via Protein Kinase C

Figure 7

Hypothetical model of CB2 receptor mediates nicotine-induced neuroprotection against Aβ toxicity in microglia. Nicotine exposure increases microglial CB2 receptor expression, which then shifts microglial M1 to M2 state, leading to the result that less TNF-α and IL-6 and more BDNF are released from the cells, and the process is mediated by PKC. Then the nicotine-induced anti-inflammation may happen, resulting in anti-Aβ effect and neuroprotection.