Aging and neurodegenerative diseases share oxidative stress cell damage and depletion of endogenous antioxidants as mechanisms of injury, phenomena that are occurring at different rates in each process. Nevertheless, as the central nervous system (CNS) consists largely of lipids and has a poor catalase activity, a low amount of superoxide dismutase and is rich in iron, its cellular components are damaged easily by overproduction of free radicals in any of these physiological or pathological conditions. Thus, antioxidants are needed to prevent the formation and to oppose the free radicals damage to DNA, lipids, proteins, and other biomolecules. Due to endogenous antioxidant defenses are inadequate to prevent damage completely, different efforts have been undertaken in order to increase the use of natural antioxidants and to develop antioxidants that might ameliorate neural injury by oxidative stress. In this context, natural antioxidants like flavonoids (quercetin, curcumin, luteolin and catechins), magnolol and honokiol are showing to be the efficient inhibitors of the oxidative process and seem to be a better therapeutic option than the traditional ones (vitamins C and E, and β-carotene) in various models of aging and injury in vitro and in vivo conditions. Thus, the goal of the present review is to discuss the molecular basis, mechanisms of action, functions, and targets of flavonoids, magnolol, honokiol and traditional antioxidants with the aim of obtaining better results when they are prescribed on aging and neurodegenerative diseases.

Prospective longitudinal study. To verify the feasibility of performing in vivo quantitative magnetic resonance imaging evaluation of moderate traumatic spinal cord injury (SCI) in rats using a clinical 3T scanner. Animal models of human diseases are essential for translational medicine. Potential treatments of SCI are evaluated in 2 ways: anatomical and functional. Advanced magnetic resonance sequences allow a noninvasive assessment of the spinal cord depicting both. This study describes and validates a very reproducible, feasible, affordable, and reliable method, designed to be applied in commercial 3T equipment, using a novel stereotactic device for spinal cord, leading to a readily available assessment of the progression of damage generated after traumatic SCI in rats. Four Long-Evans female rats were injured with a New York University weight-drop device to produce the SCI by contusion at thoracic level 10. All animals were placed in a fixation system, using a commercial wrist antenna to obtain magnetic resonance imaging data of the relaxometry time, apparent diffusion coefficient, and fractional anisotropy. Three sets of data obtained before SCI and 1 and 4 weeks after injury were compared. The data showed a progressive decline in fractional anisotropy measurements after SCI comparing baseline versus the 1-week period (P < 0.001) and baseline versus the 4-week period (P < 0.019), with a significant progressive increase in apparent diffusion coefficient values and T2 after SCI only in the baseline versus the 4-week period (P < 0.045 and P < 0.024, respectively). Our results helped us to validate a novel method to acquire highly reproducible and reliable quantitative biomarkers of traumatic SCI in vivo by using a 3T clinical MR scanner coupled with a novel stereotactic device for rats. N/A.