page_title: WIN 55,212-2
hierarchical_section_title: WIN 55,212-2
caption_attribution_description: English: Figure 8. Cannabinoid receptor activation reduces invasiveness. A significant reduction in the number of invaded cells was seen after treatment with WIN (p = 0.0081; A). A near-complete reversal of the reduced invasiveness was seen when the cells were pre-incubated with AM251 or a combination of AM251 and AM630 (A). This was not found with AM630 alone (A). WIN induced a significant decrease in MMP-2 levels (p = 0.026; B) which was partially reversible by a combination of AM251 and AM630 (B). Actin cytoskeleton staining with phalloidin demonstrated that control PSC showed the normal cellular structure (C&amp;D) but that WIN induced a more round and smaller PSC phenotype (E&amp;F). Original magnification: x 40 (C&amp;E), x 80 (D&amp;F). Nuclear stain: DAPI. White bars: control; black bars: WIN55,212-2±AM251/AM630. Data are shown as mean±SEM.Русский: Агонист каннабиноидных рецепторов снижает характеристики воспаления в панкреатических звездчатых клетках.
context_page_description: WIN 55,212-2 is a chemical described as an aminoalkylindole derivative, which produces effects similar to those of cannabinoids such as tetrahydrocannabinol but has an entirely different chemical structure.
  WIN 55,212-2 is a potent cannabinoid receptor agonist that has been found to be a potent analgesic in a rat model of neuropathic pain. It activates p42 and p44 MAP kinase via receptor-mediated signaling.
  At 5 μM WIN 55,212-2 inhibits ATP production in sperm in a CB₁ receptor-dependent fashion.
  WIN 55,212-2, along with HU-210 and JWH-133, may prevent the inflammation caused by amyloid beta proteins involved in Alzheimer's disease, in addition to preventing cognitive impairment and loss of neuronal markers. This anti-inflammatory action is induced through agonist action at cannabinoid receptors, which prevents microglial activation that elicits the inflammation. Additionally, cannabinoids completely abolish neurotoxicity related to microglial activation in rat models.
  WIN 55,212-2 is a full agonist at the CB₁ cannabinoid receptor and has much higher affinity than THC for this receptor. WIN 55,212-2 is also an agonist of the PPARα and PPARγ nuclear receptors.
context_section_description: WIN 55,212-2 is a chemical described as an aminoalkylindole derivative, which produces effects similar to those of cannabinoids such as tetrahydrocannabinol (THC) but has an entirely different chemical structure.
  WIN 55,212-2 is a potent cannabinoid receptor agonist that has been found to be a potent analgesic in a rat model of neuropathic pain. It activates p42 and p44 MAP kinase via receptor-mediated signaling.
  At 5 μM WIN 55,212-2 inhibits ATP production in sperm in a CB₁ receptor-dependent fashion.
  WIN 55,212-2, along with HU-210 and JWH-133, may prevent the inflammation caused by amyloid beta proteins involved in Alzheimer's disease, in addition to preventing cognitive impairment and loss of neuronal markers. This anti-inflammatory action is induced through agonist action at cannabinoid receptors, which prevents microglial activation that elicits the inflammation. Additionally, cannabinoids completely abolish neurotoxicity related to microglial activation in rat models.
  WIN 55,212-2 is a full agonist at the CB₁ cannabinoid receptor (Kᵢ = 1.9 nM) and has much higher affinity than THC (Kᵢ = 41 nM) for this receptor. WIN 55,212-2 is also an agonist of the PPARα and PPARγ nuclear receptors.
  WIN 55,212-2 reduces voluntary wheel running in laboratory mice, but with effects that depend on both genetic background and sex.
  In the United States, all CB₁ receptor agonists of the 3-(1-naphthoyl)indole class such as WIN 55,212-2 are Schedule I Controlled Substances. WIN 55,212-2 is illegal in the UK.
caption: Pancreatic stellate cells. The cells in the lower frame are under the action of WIN 55,212-2. They are thought to assume a more "quiescent" phenotype. From Michalski et al., 2008.[2]
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