Research on Mechanism of miR-106a Nanoparticles Carrying Dexmedetomidine in Regulating Recovery and Metabolism of Nerve Cells in Hypoxia-Reoxygenation Injury

Abstract

We studied the mechanism of miR-106a nanoparticles carrying dexmedetomidine (DEX) in regulating the recovery and metabolism of nerve cells in hypoxia-reoxygenation injury. Hippocampus neuron model in hypoxia-reoxygenation injury was prepared in vitro. Study groups were randomly divided into control set, ischemic reperfusion (IR) set, dexmedetomidine (DEX) set, miR-106a-nanoparticles (NPs) set and set of dexmedetomidine (DEX) and miR-106a-NPs. We studied miR-106a expression, proliferative and apoptotic activity, secretion of IL-6 and tumor necrosis factor (TNF)-α, quantity of Phosphocreatine (PCr), adenosine triphosphate (ATP) and total adenine nucleotide, and also content of reactive oxygen species (ROS) and superoxide dismutases (SOD). Expressions of of Bax, Bcl-2 and NF-κB were also detected. Results showed that the expression of miR-106a in hippocampus neuron was reduced, while proliferation was reduced and apoptotic activity was increased. The secretions of IL-6 and TNF-α were increased, while the quantities of Phosphocreatine (PCr), adenosine triphosphate (ATP) and total adenine nucleotide were reduced. Bax expression was also increased and Bcl-2 expression was reduced. Moreover, ROS content was increased and SOD activity was reduced, while the NF-κB presentation was increased. The above-mentioned changes could be reversed in IR set, DEX set and miR-106a-NPs set. The action was more notable in the DEX and miR-106a-NPs sets. Finally, the proliferation in hippocampus neuron in hypoxia-reoxygenation injury could be prompted and apoptosis could be restrained by DEX and miR-106a-NPs. The secretion of inflammatory factors could be restrained through restraining the inflammatory pathway and oxidative stress. The energy metabolism could therefore be improved effectively and recovery of nerve cells in HBI could be improved.