Effects of a Thermal Agent and Physical Activity on Muscle Tendon Stiffness, as Well as the Effects Combined With Static Stretching.

CONTEXT: A recent review or article reported that thermal agents (TA) or physical activity (PA) can increase range of motion (ROM) and that the combination of TA with stretching is superior to performing stretching only. However, since ROM is affected by the psychological factors, it is questionable whether these studies measured the effect of these interventions on muscle flexibility. By measuring muscle stiffness, the authors attempted to evaluate the effect these interventions on muscle flexibility. OBJECTIVE: To compare the individual effects of TA and PA on muscle flexibility, as well as their effectiveness when combined with static stretching (SS). DESIGN: Crossover trial. SETTING: University research laboratory. PARTICIPANTS: 15 healthy men without a history of orthopedic disease in their lower limbs. INTERVENTIONS: 15 minutes of 3 different conditions: hot pack as TA, pedaling exercise as PA, and the control group with no TA or PA intervention, followed by 3 min of SS for the hamstrings. MAIN OUTCOME MEASURES: Joint angle and passive torque of the knee during passive elongation were obtained prior to interventions, after 3 kinds of intervention, and after SS. From these data, muscle-tendon-unit (MTU) stiffness of the hamstrings was calculated. RESULTS: Although knee-joint ROM increased with both TA and PA (P < .05), there were no significant differences in MTU stiffness between pre- and postintervention measurements for either of the interventions (TA, P = .477; PA, P = .377; control, P = .388). However, there were similar significant decreases in MTU stiffness between postintervention and post-SS for all conditions (P < .01). CONCLUSIONS: TA and PA did not decrease MTU stiffness, and combining these interventions with SS did not provide additional decreases in MTU stiffness compared with performing SS alone.

The neuroprotective effect of hesperidin in NMDA-induced retinal injury acts by suppressing oxidative stress and excessive calpain activation.

We found that hesperidin, a plant-derived bioflavonoid, may be a candidate agent for neuroprotective treatment in the retina, after screening 41 materials for anti-oxidative properties in a primary retinal cell culture under oxidative stress. We found that the intravitreal injection of hesperidin in mice prevented reductions in markers of the retinal ganglion cells (RGCs) and RGC death after N-methyl-D-aspartate (NMDA)-induced excitotoxicity. Hesperidin treatment also reduced calpain activation, reactive oxygen species generation and TNF-α gene expression. Finally, hesperidin treatment improved electrophysiological function, measured with visual evoked potential, and visual function, measured with optomotry. Thus, we found that hesperidin suppressed a number of cytotoxic factors associated with NMDA-induced cell death signaling, such as oxidative stress, over-activation of calpain, and inflammation, thereby protecting the RGCs in mice. Therefore, hesperidin may have potential as a therapeutic supplement for protecting the retina against the damage associated with excitotoxic injury, such as occurs in glaucoma and diabetic retinopathy.

Mallotus philippinensis bark extracts promote preferential migration of mesenchymal stem cells and improve wound healing in mice.

In the present study, we report the effects of the ethanol extract from Mallotus philippinensis bark (EMPB) on mesenchymal stem cell (MSC) proliferation, migration, and wound healing in vitro and in a mouse model. Chemotaxis assays demonstrated that EMPB acted an MSC chemoattractant and that the main chemotactic activity of EMPB may be due to the effects of cinnamtannin B-1. Flow cytometric analysis of peripheral blood mononuclear cells in EMPB-injected mice indicated that EMPB enhanced the mobilization of endogenous MSCs into blood circulation. Bioluminescent whole-animal imaging of luciferase-expressing MSCs revealed that EMPB augmented the homing of MSCs to wounds. In addition, the efficacy of EMPB on migration of MSCs was higher than that of other skin cell types, and EMPB treatment improved of wound healing in a diabetic mouse model. The histopathological characteristics demonstrated that the effects of EMPB treatment resembled MSC-induced tissue repair. Taken together, these results suggested that EMPB activated the mobilization and homing of MSCs to wounds and that enhancement of MSC migration may improve wound healing.