Globally, traditional and herbal teas are a prominent dietary source of polyphenols, and represent a class of bioactive molecules that are closely associated with a variety of health benefits. Most consumers prepare tea using tea bags, although there is little information about whether this production step alters the content of the final product. The study purpose was to investigate the effect of steep time and tea type on the polyphenol content and predicted antioxidant capacity of commercially available tea bag products, including Green, Orange Pekoe, Red Roiboos, Peppermint, and Chamomile. Total polyphenol content (TPC), antioxidant capacity (1,1-diphenyl-2-picrylhydrazyl inhibition), and total predicted antioxidant capacity were measured in aliquots sampled every minute for 10 min. Polyphenols were extracted into solution in a nonlinear fashion, with~80-90% of the TPC appearing within 5 min of tea bag immersion. Moreover, a significant range in TPC values was observed between products, with true teas containing at least two-fold greater polyphenol content than the herbal varieties. Our results are consistent with previous work using loose-leaf tea products and demonstrates that tea bag products are an effective source of polyphenols that may offer health benefits relating to their constituent antioxidant activity.
The sarco(endo)plasmic reticulum Ca2+ ATPase (SERCA) restores intracellular Ca2+ ([Ca2+]i) to resting levels after muscle contraction, ultimately eliciting relaxation. SERCA pumps are highly susceptible to tyrosine (T)‐nitration, impairing their ability to take up Ca2+ resulting in reduced muscle function and increased [Ca2+]i and cellular damage. The mitochondrial antioxidant enzyme, superoxide dismutase 2 (SOD2), converts superoxide radicals into less reactive H2O2. Heterozygous deletion of SOD2 (Sod2+/−) in mice increases mitochondrial oxidative stress; however, the consequences of reduced SOD2 expression in skeletal and cardiac muscle, specifically the effect on SERCA pumps, has yet to be investigated. We obtained soleus, extensor digitorum longus (EDL), and left ventricle (LV) muscles from 6 to 7 month‐old wild‐type (WT) and Sod2+/− female C57BL/6J mice. Ca2+‐dependent SERCA activity assays were performed to assess SERCA function. Western blotting was conducted to examine the protein content of SERCA, phospholamban, and sarcolipin; and immunoprecipitation experiments were done to assess SERCA2a‐ and SERCA1a‐specific T‐nitration. Heterozygous SOD2 deletion did not alter SERCA1a or SERCA2a expression in the soleus or LV but reduced SERCA2a in the EDL compared with WT, though this was not statistically significant. Soleus muscles from Sod2+/− mice showed a significant reduction in SERCA’s apparent affinity for Ca2+ when compared to WT, corresponding with significantly elevated SERCA2a T‐nitration in the soleus. No effect was seen in the EDL or the LV. This is the first study to investigate the effects of SOD2 deficiency on muscle SERCA function and shows that it selectively impairs SERCA function in the soleus.
Higher bone mineral density (BMD) is often associated with greater consumption of black tea (BT). However, the dose-response of BT on mineralization in an osteoblast cell model has not yet been studied. The study objective was to determine the dose-dependent response of BT in Saos-2 cells and investigate changes to several proteins involved in the mineralization process. Mineralization was induced in the presence of BT at concentrations that represent levels likely achieved through daily consumption (0.1, 0.5, 0.75, 1 lg gallic acid equivalents [GAE]/mL) or through supplementation (2, 5, or 10 lg GAE/mL). BT exerted a positive dose-response on bone mineralization, peaking at 1 lg GAE/mL of BT (P < .05). Cellular activity was significantly greater than control with exposure to 2-10 lg GAE/mL of BT (at 24 h) (P < .05) and 1-10 lg GAE/mL (at 48 h) (P < .05), with a peak at 5 lg GAE/mL at 24 and 48 h (P < .05). Protein expression of alkaline phosphatase and ectonucleotide pyrophosphatase/phosphodiesterase-1 were unchanged, whereas a moderate dose of BT (0.75 lg GAE/mL) resulted in greater expression of osteopontin compared with the highest dose (10 lg GAE/mL) (P < .05). Doses of BT from 0.5 to 10 lg GAE/mL resulted in higher antioxidant capacity compared with control (P < .05). In summary, the higher antioxidant capacity, enhanced cell viability, and upregulated mineralization suggest that consumption of BT may have a positive effect on BMD at levels obtained through consumption of tea.
Duchenne muscular dystrophy (DMD) is a severe muscle wasting disorder that leads to early mortality. We examined the pathogenic contribution of glycogen synthase kinase 3 (GSK3) to DMD using the mdx model. GSK3 is a serine/threonine kinase that has been implicated in other muscular dystrophies and our initial results showed that overactivation of GSK3 may contribute to increased disease severity found in DBA/2J (D2) mdx mice vs C57BL/10 mdx mice. In support of this, treating D2 mdx mice with the GSK3 inhibitor, tideglusib (10 mg/kg/day), increased muscle mass, strength, and fatigue resistance. We also found elevated proportions of oxidative fibers and increased utrophin mRNA, while muscle necrosis and oxidative stress were reduced. Finally, young D2 mdx mice displayed early diastolic dysfunction, and this was blunted with tideglusib treatment, an effect attributed to lowered oxidative stress and fibrosis. This study highlights the therapeutic potential of tideglusib and GSK3 inhibition for DMD.
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