Silencing TRPV4 partially reverses the neurotoxic effects caused by excess Ketamine

Excessive use of Ketamine (KET) has a neurotoxic effect on the brain. This study explored Transient Receptor Potential Vanilloid 4 (TRPV4) KET-induced neurotoxicity in hippocampus. We extracted and identified rat hippocampal neuronal cells. The neurons were treated with different concentrations (0, 0.1, 1, 10, 100, 300 1000 μmol/L) KET (6, 12 24 hr). Cell viability was detected by cell counting Kit-8 (CCK-8), TRPV4 expression quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) western blot. After silencing TRPV4, we tested apoptosis. contents superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA), catalase (CAT) colorimetry, TNF-α, IL-1β, IL-6 reactive oxygen species (ROS) Enzyme-Linked ImmunoSorbent Assay (ELISA). Finally, levels apoptosis-related proteins Bcl-2, Bax Cleaved caspase-3, phosphorylated-p65 (p-65), p65, phosphorylated-IκBα (p-IκBα) IκBα qRT-PCR inhibited dose-dependent manner, up-regulated expression. SiTRPV4 inhibits decrease promotes reduced MDA ROS content, increased SOD, GSH CAT levels. release proinflammatory factors IL-1β also siTRPV4. In addition, siTRPV4 Bcl-2 neurons, down-regulated activation inflammatory pathway. Silencing partially reverses effects induced through regulating p65/IκBα