Myostatin and plasticity of skeletal muscle tissue

Skeletal muscle is an extremely plastic tissue for its ability to respond to different stimuli such as physiological variation and external stress. Muscle hypertrophy involves an increase in muscle mass, changes in myofibril composition and adaptation of metabolic pathways. Plasticity of skeletal muscle in response to exercise training is also caused by proliferation and differentiation of the satellite muscle stem cells in response to various growth and differentiation factors. This process is mainly mediated by myokines secreted during skeletal muscle contraction. Myokines are proteins that act as hormones both locally in the muscle and/or in an endocrine manner in other organs, mainly liver, brain and adipose tissue. Myostatin, known as growth differentiation factor-8, a myokine member of transforming growth factor-b (TGF-b) superfamily, can act on muscle cells in an autocrine manner leading to inhibition of muscle myogenesis. Muscle myostatin expression and its plasma concentration are downregulated after acute and long-term physical exercise thus allowing muscle hypertrophy. In addition, myostatin is correlated to obesity and insulin resistance for its ability to affect energy metabolism and insulin-sensitivity in muscle cells, respectively. These findings reveal that myostatin may have potential therapeutic applications to treat muscle atrophy diseases in humans. Even in sports, drugs able to inhibit myostatin expression can lead athletes to increase their sport performance. Here, we present a brief overview of myostatin and its role in biological mechanisms involved in exercise-induced plasticity of skeletal muscle

Circadian rhythms, physical activity and longevity

Human health implies complex mechanisms and involves diseases prevention aimed at ensuring a psycho-physical wellbeing homoeostasis. The search for longevity can be related to the slowdown in aging, and psycho-physical wellbeing is often related to the lifestyle, mainly to the human physical activity and nutrition. Circadian rhythms are processes that affect the behaviour, physiology and metabolism of mammals across cyclic periods of 24 hours. These rhythms are regulated by multiple physiological systems, whose key elements are the alternation between light and dark and between food consumption and periods of fasting. Therefore, during evolution, a constant adaptation to natural rhythms by humans has been established towards the surrounding environment determining periods of food consumption and periods of fasting coinciding with rest. Recent sociological surveys have shown that there is a slight increase in the number of people who devote themselves to a constant physical/sport activity, but this is an ephemeral percentage compared to the dramatic increase in the incidence of diseases related to aging such as obesity and diabetes, easily preventable with healthy lifestyles. Therefore, the connection between circadian rhythms, physical activity and lifestyles represents an important feature involved in human longevity. Here, a survive of the biological mechanisms, implied in this behaviour, is presented

DONEPEZIL DERIVATIVES AS DUAL ACETYLCHOLINESTERASE AND b-SECRETASE 1 INHIBITORS FOR THE TREATMENT OF ALZHEIMER’S DISEASE

Introduction: This work is focused on the study of the inhibition activity exerted by some donepezil derivatives, on the acetlycholinesterase and b-secretase 1 (Bace-1) activities, potentially useful as dual inhibitors for the treatment of Alzheimer’s disease (AD). Results: The Authors report the effect produced by some donepezil derivatives on the enzymatic activity of acetlycholinesterase and Bace-1. Conclusion: In vitro AChE activity inhibition represent an useful approach to identity molecular candidates for a more appropriate AD therapy

Effects of physical exercise and plant polyphenols on human mitochondrial health

Physical activity combined with a polyphenols rich diet have been recently emerged as a non-pharmacological approach able to prevent and/or ameliorate symptoms that are related to the disfunctions of energy-related health processes, in particular during aging. In this article we first described the key role of mitochondrial functions in energy production systems that are activated during different types of physical activity. Then, we have reported some relevant and recent aspects concerning aging-related mitochondrial disfunctions involved in several human diseases, providing an overview of the most relevant in vivo and in vitro studies. These studies aimed to the identification of molecular mechanisms causing mitochondrial disfunctions including mitochondrial DNA mutations, radical oxygen species (ROS) generation and oxidative stress, that led to aging-related sarcopenia. These results explored the major approaches used for the prevention and the treatments of mitochondrial diseases. In particular, we have highlighted the effects of physical exercise and plant polyphenols on mitochondrial function in the aerobic mechanism of ATP synthesis. In fact, the secretion of myokines from contracting skeletal muscle allows the modulation of various metabolic processes and can improve mitochondria cell and bioenergetic functions. Polyphenol intake has been shown to counteract several aging-related alterations including inflammation and oxidative stress, and therefore we describe the effects of these molecules, also in pure form, as food integration, and we have also summarized their effects on mitochondrial functions. Finally, we have reviewed the state of art of these strategies focusing on both physical exercise and plant polyphenols-rich diet based approaches on skeletal muscle mitochondrial health in humans that aim to prevent and counteract aging-related diseases

Dietary Protein and Physical Exercise for the Treatment of Sarcopenia

Sarcopenia is a multifactorial age-related disorder that causes a decrease in muscle mass, strength, and function, leading to alteration of movement, risk of falls, and hospitalization. This article aims to review recent findings on the factors underlying sarcopenia and the strategies required to delay and counteract its symptoms. We focus on molecular factors linked to ageing, on the role of low-grade chronic and acute inflammatory conditions such as cancer, which contributes to the onset of sarcopenia, and on the clinical criteria for its diagnosis. The use of drugs against sarcopenia is still subject to debate, and the suggested approaches to restore muscle health are based on adequate dietary protein intake and physical exercise. We also highlight the difference in the amount and quality of amino acids within animal- and plant-based diets, as studies have often shown varying results regarding their effect on sarcopenia in elderly people. In addition, many studies have reported that non-pharmacological approaches, such as an optimization of dietary protein intake and training programs based on resistance exercise, can be effective in preventing and delaying sarcopenia. These approaches not only improve the maintenance of skeletal muscle function, but also reduce health care costs and improve life expectancy and quality in elderly people

GREEN TEA POLYPHENOLS AFFECT INVASIVENESS OF HUMAN GASTRIC MKN-28 CELLS BY INHIBITION OF LPS OR TNF-ΑLPHA INDUCED MATRIX METALLOPROTEINASE-9/2

Green tea polyphenols have been identified as molecules responsible for the beneficial effects showed by the green tea against oxidative stress and cancer risk. We investigated the effects of green tea polyphenol extracts (GTPs) on oxidative stress and cell invasiveness in human gastric MKN-28 cancer cells. The pre-treatment with 10–4 M catechin equivalents of GTPs exerts a protective effect on xanthine-xanthine oxidase induced cell cytotoxicity, thus confirming the anti-oxidant properties of GTPs. The effect of GTPs was also extended on the cell invasive ability induced by TNF-lpha or LPS. Results demonstrated that demonstrated that GTPs exposure (10–6 M) prevents the increase in cell invasiveness induced by the inflammatory agents. In addition, the treatment with GTPs prevented the TNF-lpha or LPS induced Matrix Metalloproteinases (MMP)-9/2 up-regulation. In conclusion, our results demonstrated that GTPs reduced the oxidative stress and the invasive potential of gastric MKN-28 cancer cells thus confirming the protective role of these polyphenols against the metastatic process in gastric cancer

Annurca Apple Polyphenol Extract Affects Acetyl- Cholinesterase and Mono-Amine Oxidase In Vitro Enzyme Activity

In this study, we explored the ability of Annurca apple flesh polyphenol extract (AFPE) to affect the activity of key enzymes involved in neurodegenerative disorders—in particular, Acetyl- and Butirryl-cholinesterases, and type A and B monoamine oxidase. The effect of AFPE on enzyme activity was analyzed by in vitro enzyme assays, and the results showed concentration-dependent enzyme inhibition, with IC50 values corresponding to 859 ± 18 µM and 966 ± 72 µM for AChE and BuChE respectively, and IC50 corresponding to 145 ± 3 µM and 199 ± 7 µM for MAO-A and MAO-B, respectively, with a preference for MAO-A. Moreover, in this concentration range, AFPE did not affect the viability of human neuroblastoma SH-SY5Y and fibroblast BJ-5ta cell lines, as determined by an MTT assay. In conclusion, our results demonstrate that AFPE shows the new biological properties of inhibiting the activity of enzymes that are involved in brain functions, neurodegenerative disorders, and agin

EXERCISE-INDUCED MUSCLE DAMAGE (EIMD) AND NATURAL POLYPHENOLS

Although it is well known that physical activity contributes to a healthy life style, unaccustomed exercise or high eccentric muscle contraction lead to exercise-induced muscle damage (EIMD) inducing pains and affecting exercise training in athletes. Several approaches, including nutrition based on a polyphenols-rich diet or supplementation, have been showed to prevent and/or reduce muscle damage in athletes after physical exercise. In this manuscript we addressed the effect of natural polyphenols as antioxidant and anti- inflammatory agent that are used on recovery of EIMD in athletes