Abstract This study aimed to explore the effects of Yiqi Huoxue Recipe (YQHXF) on the pathological changes, Th-17 lymphocyte infiltration, nucleus pulposus cell apoptosis, and the expression of extracellular matrix related proteins in degenerative intervertebral disc of rats. Thirty SD rats were randomly divided into 5 groups (Sham, Model, Low YQHXF, Medium YQHXF, and High YQHXF). In this paper, the annulus fibrosus was broken and arranged disorderly, nucleus pulposus cells apoptosis was increased, and the intervertebral discs were infiltrated by a large number of inflammatory cells in model group rats. However, YQHXF treatment group significantly attenuated these effects. Annulus fibrosus puncture caused increase in Th-17 lymphocyte infiltration and inflammatory factors in the model group, however, those effects were inhibited by YQHXF intervention. YQHXF treatment significantly reduced nucleus pulposus cell apoptosis, which was increased in the model group. The down-regulation of SOX-9 phosphorylation, type II collagen, BMP-2 and the up-regulation of β-catenin, MMP-3, MMP-13 and ADAMTS5 were found in the model group compared with sham group. However, those changes were significantly attenuated by YQHXF treatment. YQHXF could alleviate intervertebral disc degeneration in rats by reducing Th-17 lymphocyte infiltration, inhibiting nucleus pulposus cell apoptosis and promoting SOX-9/β-catenin-mediated ECM synthesis

Naringin (Nar) has been reported to exert potential hepatoprotective effects against acetaminophen (APAP)-induced injury. Mitochondrial dysfunction plays an important role in APAP-induced liver injury. However, the protective mechanism of Nar against mitochondrial damage has not been elucidated. Therefore, the aim of this study was to investigate the hepatoprotective effects of Nar against APAP and the possible mechanisms of actions. Primary rat hepatocytes and HepG2 cells were utilized to establish an in vitro model of APAP-induced hepatotoxicity. The effect of APAP and Nar on cell viability was evaluated by a CCK8 assay and detection of the concentrations of alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase. The cellular concentrations of biomarkers of oxidative stress were measured by ELISA. The mRNA expression levels of APAP-related phase II enzymes were determined by real-time PCR. The protein levels of Nrf2, phospho (p)-AMPK/AMPK, and biomarkers of mitochondrial dynamics were determined by western blot analysis. The mitochondrial membrane potential (MMP) was measured by high-content analysis and confocal microscopy. JC-1 staining was performed to evaluate mitochondrial depolarization. Nar pretreatment notably prevented the marked APAP-induced hepatocyte injury, increases in oxidative stress marker expression, reductions in the expression of phase II enzymes, significant loss of MMP, mitochondrial depolarization, and mitochondrial fission in vitro. In conclusion, Nar alleviated APAP-induced hepatocyte and mitochondrial injury by activating the AMPK/Nrf2 pathway to reduce oxidative stress in vitro. Applying Nar for the treatment of APAP-induced liver injury might be promising.

Effects of forming pores in Zr70Cu30 metallic glass on the deformation behaviour is investigated through molecular dynamics simulations. The formation of pores leads to only a small reduction in strength, but dramatically enhanced plasticity in compression. The large plasticity of glass is attributed to the large effective free space induced by forming pores. It can also promote formation of crystalline phases in the amorphous matrix during deformation. Simulation reproduces the images of the evolution of pores in the metallic glass. The simulation results are in good agreement with experimental results.