Schisandrin B attenuates the inflammatory response, oxidative stress and apoptosis induced by traumatic spinal cord injury via inhibition of p53 signaling in adult rats.

Schisandrin B is an active monomer of the Chinese magnolia vine (Schisandra chinensis) that can reduce transaminase activity in liver cells, inhibit lipid peroxidation, enhance antioxidant status, has protective effects in the liver and has antitumor effects. The present study investigated the potential protective effects of schisandrin B on the p53 signaling pathway in attenuating the inflammatory response, oxidative stress and apoptosis induced by traumatic spinal cord injury (TSCI) in adult rats. Behavioral examination, inclined plate test and spinal cord water content were used to evaluate the protective effect of schisandrin B in TSCI rats. The expression levels of superoxide dismutase (SOD), malondialdehyde (MDA), nuclear factor (NF)­κB subunit p65 and tumor necrosis factor (TNF)­α were examined using ELISA kits. Western blot analysis was performed to analyze the protein expression of caspase­3 and phosphorylated (p)­p53 in TSCI rats. In the present study, schisandrin B improved behavioral examination results and the maximum angle of inclined plate test, and inhibited spinal cord water content in rats with TSCI. Notably, schisandrin B reduced the activation of traumatic injury­associated pathways, including SOD, MDA, NF­κB p65 and TNF­α, in TSCI rats. In addition, schisandrin B suppressed the TSCI­induced expression of caspase­3 and p­p53 in TSCI rats. These results indicated that schisandrin B may attenuate the inflammatory response, oxidative stress and apoptosis in TSCI rats by inhibiting the p53 signaling pathway in adult rats.

Effect of neural stem cell transplantation combined with erythropoietin injection on axon regeneration in adult rats with transected spinal cord injury.

We investigated the effect of neural stem cells (NSC) and erythropoietin (EPO) on axon regeneration in adult rats with transected spinal cord injury, and provided an experimental basis for clinical treatment. Forty Wistar rats with T10-transected spinal cord injury were randomly divided into four groups of ten rats: a control group (group A), an NSC-transplant group (group B), an NSC-transplant and EPO group (group C), and an EPO group (group D). Biotinylated dextran amines (BDA) anterograde corticospinal cord neuronal tracing and Fluoro-Gold (FG) retrograde tracing were carried out at the 8th week after operation to observe the regeneration of nerve fibers. The Basso, Beattie, and Bresnahan (BBB) locomotor score was used to evaluate restoration. 1) BDA and FG immunofluorescence staining: in group C, a large number of regenerated axons were observed and some penetrated the injured area. In group B, only a small number of regenerated axons were observed and none penetrated the injured area. In group D, only sporadic regenerated nerve fibers were observed occasionally, while in group A, no axonal regeneration was observed. In group C, a small number of cones and axons emitted yellow fluorescence, and no FG-labeled cells were observed in the other groups. 2) The BBB scores for group C were higher than those for the other groups, and the differences were statistically significance (P < 0.05). NSC transplantation combined with EPO intraperitoneal injection may benefit axon regeneration in rats with transected spinal cord injury, and accelerate the functional recovery of the hindlimb locomotor.

Glucocorticoid induced autophagy in N1511 chondrocyte cells.

OBJECTIVE: To determine whether autophagy was involved in chondrocyte cells post Glucocorticoids (GCs) treatment. MATERIALS AND METHODS: LC3-GFP reporter plasmid transfection and western blotting analysis were conducted to determine the autophagic vesicles and autophagy-associated molecules in the N1511 chondrocyte cells post dexamethasone (Dex) treatment. And the N1511 cell viability was also determined by MTT assay. RESULTS: We found that autophagy was induced in the N1511 chondrocyte cells post treatment with Dex of 5 µM to 1 mM, and the autophagy-induction by Dex could be inhibited by 3 MA and RU486, a GC antagonist. And the autophagy induced by the high dose of Dex (200 µM or 1 mM) was associated with a reduction of N1511 cell viability. CONCLUSIONS: These results suggested that GCs could induce autophagy, as might contribute to the viability reduction of chondrocyte cells.