Life sciences
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Evidence suggests that task-specific gait training improves locomotor impairments in people with incomplete spinal cord injury (SCI); however, plastic changes in brain areas remain poorly understood. The aim of this study was to examine the possible effects of a task-specific overground gait training on locomotor recovery and neuroplasticity markers in the cortex, cerebellum, and lumbar spinal cord in an experimental model of incomplete-SCI. ⋯ Task-specific overground gait training improves locomotor recovery in a rat model of incomplete thoracic-SCI. Furthermore, training promotes motor cortex plasticity, evidenced for increasing expression of the neuroplasticity markers that may support the functional recovery.
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Sepsis is a leading cause of death and disability worldwide. Autophagy may play a protective role in sepsis-induced myocardial dysfunction (SIMD). The present study investigated whether valproic acid (VPA), a class I histone deacetylase (HDAC) inhibitor, can attenuate SIMD by accelerating autophagy. ⋯ This study found that VPA attenuates SIMD through myocardial autophagy acceleration by increasing PTEN expression and inhibiting the AKT/mTOR pathway. These findings preliminarily suggest that VPA may be a potential approach for the intervention and treatment of SIMD.
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To observe the effect of dexmedetomidine (DEX) on mitochondrial apoptosis of hippocampal neurons in hypoxia/reoxygenation (H/R) brain injury in developing rats, and to investigate its regulatory mechanism on HIF-1α/p53 signaling pathway. ⋯ DEX alleviates H/R-induced brain injury and mitochondrial apoptosis in developing rats through α2 receptor, which may be related to activation of HIF-1α/p53 signaling pathway to up-regulate the expression of Ngb.
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Mitochondrial dysfunction has been regarded as one of the hallmarks of cerebral ischemia-reperfusion injury. In previous studies, we have provided evidence that the extracellular signaling pathway (ERK) 1/2 inhibitor PD98059 improved the neurological deficits by modulating antioxidant and anti-apoptotic activities in rats subjected to cardiac arrest/cardiopulmonary resuscitation (CA/CPR). Since oxidative stress can activate mitochondria-dependent apoptosis and autophagy, we further explored the effects of PD98059 on mitochondria involved with apoptosis and autophagy in rat CA model. ⋯ PD98059 protects the brain against mitochondrial-mediated apoptosis and autophagy at 24 h post-resuscitation in rats subjected to CA/CPR, which is linked with the downregulation of Drp1 expression.
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Airway mucin overproduction is the hallmark risk factor of asthma, which is associated with the reduction of lung function. An aberrant mucin expression is responsible for airway obstruction due to its high viscous characteristics. Among the mucins discovered, MUC5AC is the prime mucin of airway epithelia. ⋯ Currently, flavonoids, glycoside and steroids like natural compounds have acquired great attention due to their anti-inflammatory and mucoregulatory effects. Most importantly, many natural compounds have shown their potential effects as the modulator of mucin expression, secretion, and production. Therefore, targeting airway MUC5AC expression and production represents an auspicious area of research for the development of drugs against various respiratory diseases.