Show pageBacklinksCite current pageExport to PDFFold/unfold allBack to top This page is read only. You can view the source, but not change it. Ask your administrator if you think this is wrong. A study investigated the effects of a synthetic [[cannabinoid receptor]] [[agonist]] [[WIN55,212-2]] (WIN) on VaD, and molecular mechanisms of the effects. VaD model was induced by 2-[[vessel occlusion]] (2VO). Spatial reference learning was evaluated by the [[Morris water maze]], and recognition memory was assessed using the novel object recognition test. Autophagy-related proteins [microtubule-associated protein 1 light chain 3 (LC-3) and Beclin-1] were examined by immunohistochemistry and Western blot. [[Caspase]]-3 was detected by Western blot. Inflammatory factors, tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β), were estimated by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. VaD increased the levels of LC-3, Beclin-1, and inflammatory factors, which were reversed by chronic treatment with WIN. WIN decreased the expression of Capase-3, and improved the learning and memory impairment of VaD rats. These data indicate that WIN exerts a neuroprotective effect on the cognitive deficits of VaD rats, which may be associated with the suppression of excessive [[autophagy]] and inflammation ((Wang DP, Yin H, Kang K, Lin Q, Su SH, Hai J. The potential protective effects of cannabinoid receptor agonist WIN55,212-2 on cognitive dysfunction is associated with the suppression of autophagy and inflammation in an experimental model of vascular dementia. Psychiatry Res. 2018 Jun 14;267:281-288. doi: 10.1016/j.psychres.2018.06.012. [Epub ahead of print] PubMed PMID: 29945070. )). win55_212-2.txt Last modified: 2025/04/29 20:23by 127.0.0.1