The development and in vivo validation of an external fixation device with standardized micromotion for accelerating fracture healing.

Micromotion can accelerate fracture healing, with critical parameters being range of motion, frequency of motion, duration of motion, as well as initial timing of the motion. However, these parameters of micromotion have not been optimized. It is because in previous studies large animals were used. The displacement among fracture fragments caused by animal activity brings a considerable systemic error to experimental data. Also, the sample size is limited by time and cost. Thus, the rat with femur fracture can be a good animal model in investigating this problem as its advantages on high consistency of experimental results, short convalescence, and low maintenance cost. The challenge in using a small animal model in the micromotion study include 1) highly specific stiffness of the fixator; 2) lightweight fixator to bring less interference to animal's activity; 3) high accuracy on measurement method. This study aims to solve this problem by integrating 1) an aluminum fixator with a solid construction; 2) a modularized experimental device with dismountable parts; 3) a non-contact measurement model based on video identification technology. Our preliminary validation results confirmed the reliability and reproducibility of the external fixation device used in the investigation on the effect of applied micromotion on bone healing.

The role of ginsenoside Rb1, a potential natural glutathione reductase agonist, in preventing oxidative stress-induced apoptosis of H9C2 cells.

BACKGROUND: Oxidative stress-induced cardiomyocytes apoptosis is a key pathological process in ischemic heart disease. Glutathione reductase (GR) reduces glutathione disulfide to glutathione (GSH) to alleviate oxidative stress. Ginsenoside Rb1 (GRb1) prevents the apoptosis of cardiomyocytes; however, the role of GR in this process is unclear. Therefore, the effects of GRb1 on GR were investigated in this study. METHODS: The antiapoptotic effects of GRb1 were evaluated in H9C2 cells by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, annexin V/propidium iodide staining, and Western blotting. The antioxidative effects were measured by a reactive oxygen species assay, and GSH levels and GR activity were examined in the presence and absence of the GR inhibitor 1,3-bis-(2-chloroethyl)-1-nitrosourea. Molecular docking and molecular dynamics simulations were used to investigate the binding of GRb1 to GR. The direct influence of GRb1 on GR was confirmed by recombinant human GR protein. RESULTS: GRb1 pretreatment caused dose-dependent inhibition of tert-butyl hydroperoxide-induced cell apoptosis, at a level comparable to that of the positive control N-acetyl-L-cysteine. The binding energy between GRb1 and GR was positive (-6.426 kcal/mol), and the binding was stable. GRb1 significantly reduced reactive oxygen species production and increased GSH level and GR activity without altering GR protein expression in H9C2 cells. Moreover, GRb1 enhanced the recombinant human GR protein activity in vitro, with a half-maximal effective concentration of ≈2.317 µM. Conversely, 1,3-bis-(2-chloroethyl)-1-nitrosourea co-treatment significantly abolished the GRb1's apoptotic and antioxidative effects of GRb1 in H9C2 cells. CONCLUSION: GRb1 is a potential natural GR agonist that protects against oxidative stress-induced apoptosis of H9C2 cells.