Impact of Bupivacaine on malignant proliferation, apoptosis and autophagy o f human colorectal cancer SW480 cells through regulating NF-κB signaling path

To probe into the impact of Bupivacaine on colorectal cancer (CRC) proliferation, apoptosis, and autophagy through regulating the NE-KB signaling pathway. Our work treated CRC cells with Bupivacaine, detected cell vitality through MTT assay, apoptosis through flow cytometry, cell migration through wound healing assay, NF-KB activity through immunofluorescence, inflammatory factor level, including TNF-alpha, IL-1 beta as well as IL-6 through ESLIA, apoptosis factor mRNA expression, including Bcl-2, Bax and caspase-3q through qRT-PCR, and protein expression linking with NF-KB signaling pathway as well as autophagy-related proteins via western blot. In in vivo experiments, we explored the impact of Bupivacaine on tumor volume, tumor and NF-kappa B expression. The results showed that 1 mM Bupivacaine was available to signally inhibit CRC cell vitality, promoted apoptosis rate and apoptosis gene expression, like Bax, and caspase-3, inhibited Bcl-2 expression, inhibited cancer cell migration, promoted autophagy-related protein LC3B II/LC3B I ratio and beclin-1 expression, and inhibited p62 expression. Additionally, it could elevate inflammatory factor level and induce IKK and I kappa B phosphorylation as well as NE-kappa B proteins. In in vivo experiments, Bupivacaine inhibited tumor volume and tumor, as well as NF-kappa B expression. In short, bupivacaine is available to inhibit CRC proliferation through regulating NE-kappa B signaling pathway, promote apoptosis and autophagy, and can be used as a potential drug to treat CRC in the future. [GRAPHICS] .