Butorphanol reduces the neuronal inflammatory response and apoptosis via inhibition of p38/JNK/ATF2/p53 signaling

xlomafota13 shared this article with you from Inoreader Butorphanol reduces the neuronal inflammatory response and apoptosis via inhibition of p38/JNK/ATF2/p53 signaling Via Experimental and therapeutic medicine Exp Ther Med. 2022 Mar;23(3):229. doi: 10.3892/etm.2022.11151. Epub 2022 Jan 18. ABSTRACT Neuronal cell apoptosis is a complex pathophysiological change that occurs following spinal cord injury (SCI) and affects self-repair. Therefore, preventing neuronal cell apoptosis can promote the recovery of nerve function. The present study aimed to investigate the effects of butorphanol on neuronal inflammatory response and apoptosis. The effects of butorphanol on cell viability and pathway-related protein expression were first assessed using the CCK8 and western blot assays, respectively. Lipopolysaccharide (LPS) was used to establish models. The influences of additional anisomycin, an agonist of MAPK pathway, on cell viability, pathway-related protein expression and lactate dehydrogenase level were determined using the CCK8 assay, western blotting and assay kits, respectively. In addition, the roles of butorphanol and anisomycin in inflammato ry factor levels and cell apoptosis were determined using reverse transcription-quantitative PCR, TUNEL and western blot assays. Butorphanol was found to protect PC12 cells from the action of LPS on viability and effectively upregulated the p38/JNK/activation of transcription factor 2 (ATF2)/p53 protein expression levels. In addition, anisomycin could break the protective role of butorphanol in cell viability and the inhibitory roles in inflammatory response and apoptosis. To sum up, butorphanol reduces neuronal inflammatory response and apoptosis via inhibiting p38/JNK/ATF2/p53 signaling. The present findings may provide a new direction for the treatment for SCI. PMID:35222706 | PMC:PMC8815053 | DOI:10.3892/etm.2022.11151 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.