Ageing is associated with a general reduction of physiological function and a reduction of muscle mass and strength. Endocrine factors such as myostatin, activin A, growth and differentiation factor 11 (GDF-11) and their inhibitory peptides influence muscle mass in health and disease. We hypothesised that myocytes cultured in plasma from older and younger individuals would show an ageing effect, with reduced proliferation and differentiation in older environments. C2C12 myoblasts were grown as standard and stimulated with media conditioned with 5% plasma from healthy male participants that were either younger (n = 6, 18–35 years of age) or older (n = 6, >57 years of age). Concentration of plasma myostatin (total and free), follistatin-like binding protein (FLRG), GDF-11 and activin A were quantified by ELISA. Both FLRG and activin A were elevated in older individuals (109.6 and 35.1% increase, respectively), whilst myostatin (free and total) and GDF-11 were not. Results indicated that plasma activin A and FLRG were increased in older vs. younger participants, GDF11 and myostatin did not differ. Myoblasts in vitro showed no difference in proliferation rate between ages, however scratch closure was greater in younger vs. older plasma stimulated myoblasts (78.2 vs. 87.2% of baseline scratch diameter, respectively). Myotube diameters were larger in cells stimulated with younger plasma than with older at 24 and 48 h, but not at 2 h. A significant negative correlation was noted between in vivo plasma FLRG concentration and in vitro myotube diameter 48 h following plasma stimulation (r2 = 0.392, p = 0.030). Here we show that myoblasts and myotubes cultured in media conditioned with plasma from younger or older individuals show an ageing effect, and further this effect moderately correlates with circulating FLRG concentration in vivo. The effect of ageing on muscle function may not be innate to the tissue, but involve a general cellular environment change. Further work is needed to examine the effect of increased FLRG concentration on muscle function in ageing populations.

Quality control has been a significant issue in herbal medicine since herbs became widely used to heal. Modern technologies have improved the methods of evaluating the quality of medicinal herbs but the methods of adulterating them have also grown in sophistication. In this paper we undertook a comprehensive literature search to identify the key analytical techniques used in the quality control of herbal medicine, reviewing their uses and limitations. We also present a new tool, based on mitochondrial profiling, that can be used to measure medicinal herbal quality. Besides being fundamental to the energy metabolism required for most cellular activities, mitochondria play a direct role in cellular signalling, apoptosis, stress responses, inflammation, cancer, ageing, and neurological function, mirroring some of the most common reasons people take herbal medicines. A fingerprint of the specific mitochondrial effects of medicinal herbs can be documented in order to assess their potential efficacy, detect adulterations that modulate these effects and determine the relative potency of batches. Furthermore, through this method it will be possible to assess whole herbs or complex formulas thus avoiding the issues inherent in identifying active ingredients which may be complex or unknown. Thus, while current analytical methods focus on determining the chemical quality of herbal medicines, including adulteration and contamination, mitochondrial functional analysis offers a new way of determining the quality of plant derived products that is more closely linked to the biological activity of a product and its potential clinical effectiveness.

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The application of near infrared (NIR)-light to living systems has been suggested as a potential method to enhance tissue repair, decrease inflammation, and possibly mitigate cancer therapy-associated side effects. In this study, we examined the effect of exposing three cell lines: breast cancer (MCF7), non-cancer breast cells (MCF10A), and lung fibroblasts (IMR-90), to 734 nm NIR-light for 20 minutes per day for six days, and measuring changes in cellular senescence. Positive senescent populations were induced using doxorubicin. Flow cytometry was used to assess relative levels of senescence together with mitochondria-related variables. Exposure to NIR-light significantly increased the level of senescence in MCF7 cells (13.5%; P<0.01), with no observable effects on MCF10A or IMR-90 cell lines. NIR-induced senescence was associated with significant changes in mitochondria homeostasis, including raised ROS level (36.0%; P<0.05) and mitochondrial membrane potential (14.9%; P<0.05), with no changes in mitochondrial Ca2+. These results suggest that NIR-light exposure can significantly arrest the proliferation of breast cancer cells via inducing senescence, while leaving non-cancerous cell lines unaffected.