Dendrobium nobile Alkaloids Protects against H2O2-Induced Neuronal Injury by Suppressing JAK-STATs Pathway Activation in N2A Cells.

Abstract

The purpose of this study was to investigate the preventive effect and mechanism of Dendrobium alkaloids (DNLA) on oxidative stress-related death in neuronal cells. Our results demonstrated that DNLA has a direct neuroprotective effect through oxidative stress in N2A cells induced by hydrogen peroxide (H2O2). CCK8, lactate dehydrogenase (LDH), intracellular Ca2+, intracellular reactive oxygen species (ROS), and mitochondrial membrane potential (MMP) were used to evaluate the mechanism of DNLA neutralization by H2O2-induced injury. Results presented in the paper indicate that treatment with DNLA (35 ng/mL) significantly attenuated decreases in cell viability, release of LDH, and apoptosis after H2O2-induced neuronal injury. Furthermore, DNLA significantly reduced intracellular Ca2+ up-regulation, ROS production, and inhibited mitochondrial depolarization. Moreover, DNLA treatment significantly downregulated expressions of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-6, nitric oxide synthase, janus kinase-signal transducer and activators of transcription (JAK-STATs) signaling in N2A cells, all of which were H2O2-induced. Taken together, our findings suggested that DNLA may inhibit the expression of pro-inflammatory and pro-apoptotic factors by blocking JAK-STATs signaling after oxidative stress injury. This research provides a potential experimental basis for further application of DNLA to prevent various human nervous system diseases caused by oxidative stress.