Cakir, MuratTekin, SuatDoganyigit, ZuleyhaErden, YavuzSoyturk, MerveCigremis, YilmazSandal, Suleyman2024-08-042024-08-0420190024-32051879-0631https://doi.org/10.1016/j.lfs.2018.11.058https://hdl.handle.net/11616/98553Aim: Cannabinoid system has various physiological roles such as neurogenesis, synaptic plasticity and emotional state regulation in the body. The presence of cannabinoid type 2 receptor (CB2), a member of the cannabinoid system, was detected in different regions of the brain. CB2 receptor plays a role in neuroinflammatory and neurodegenerative processes. We aimed to determine the possible effect of CB2 agonist JWH-133 in Okadaic acid (OKA)-induced neurodegeneration model mimicking Alzheimer's Disease (AD) through tau pathology. Materials and methods: In this study, 40 Sprague Dawley male rats were divided into 4 groups (Control, Sham, OKA, OKA + JWH-133). Bilateral intracerebroventricular (icv) injection of 200 ng OKA was performed in the OKA group. In the OKA + JWH-133 group, injection of JWH-133 (0.2 mg/kg) was performed intraperitoneally for 13 days different from the group of OKA. Morris water maze test was used to evaluate the spatial memory. Levels of caspase-3, phosphorylated tau (ser396), amyloid beta (A beta), tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) levels in brain cortex; and the hippocampus regions were examined by immunohistochemical methods. Key findings: In the OKA group, caspase-3, phosphorylated tau (ser396), A beta, IL-1 beta levels were higher in the cortex and hippocampus than in the other groups. The implementation of the JWH-133 reversed the increments in these parameters, and also prevented spatial memory impairment.eninfo:eu-repo/semantics/closedAccessAlzheimer's diseaseOkadaic acidCannabinoid type 2 receptorJWH-133Article21725333050055210.1016/j.lfs.2018.11.0582-s2.0-85057559841Q1WOS:000454622400004Q2