Engineered Heterochronic Parabiosis in 3D Microphysiological System for Identification of Muscle Rejuvenating Factors.

Exposure of aged mice to a young systemic milieu revealed remarkable rejuvenation effects on aged tissues, including skeletal muscle. Although some candidate factors have been identified, the exact identity and the underlying mechanisms of putative rejuvenating factors remain elusive, mainly due to the complexity of in vivo parabiosis. Here, we present an in vitro muscle parabiosis system that integrates young- and old-muscle stem cell vascular niche on a three-dimensional microfluidic platform designed to recapitulate key features of native muscle stem cell microenvironment. This innovative system enables mechanistic studies of cellular dynamics and molecular interactions within the muscle stem cell niche, especially in response to conditional extrinsic stimuli of local and systemic factors. We demonstrate that vascular endothelial growth factor (VEGF) signaling from endothelial cells and myotubes synergistically contribute to the rejuvenation of the aged muscle stem cell function. Moreover, with the adjustable on-chip system, we can mimic both blood transfusion and parabiosis and detect the time-varying effects of anti-geronic and pro-geronic factors in a single organ or multi-organ systems. Our unique approach presents a complementary in vitro model to supplement in vivo parabiosis for identifying potential anti-geronic factors responsible for revitalizing aging organs.

The elevation training mask induces modest hypoxaemia but does not affect heart rate variability during cycling in healthy adults.

This study examined the acute effects of the elevation training mask (ETM) on haemodynamics and heart rate variability (HRV) at rest, during cycling, and during recovery in healthy adults. Fifteen healthy male (N=9) and female (N=6) adults (27.0 ± 1.14 years) completed two trials with the mask (MASK) and without the mask (CON). The 40-minute cycling exercise protocol included 10-minute phases of (1) rest, (2) 50% of VO2peak cycling, (3) 70% of VO2peak cycling, and (4) recovery. Blood pressure and pulse oximetry saturation (SPO2) were measured at each phase. An Actiwave-Cardio ECG monitor (CamNtech, UK) was used to measure HRV variables including time and frequency domains. A greater response in systolic blood pressure (p=.035) was observed at rest while SPO2 (p=.033) was lower during high-intensity cycling (70% of VO2peak) in the MASK trial. The HRV indices were not different between trials during cycling. However, heart rate (p=.047) was greater while inter-beat interval and sympathovagal balance (the ratio between low-frequency and high-frequency components; ln LF/HF, p=.01) were lower in the MASK than the CON trials during recovery. Wearing an ETM during high-intensity cycling (70% of VO2peak) induces modest hypoxaemia. Although this device did not affect HRV changes during cycling, it seems to delay the cardiac-autonomic recovery from exercise. Healthy adults may be required to perform high-intensity exercise with an ETM to simulate a hypoxic environment, but future studies are needed to determine whether repeated exposure to this condition provides similar benefits as altitude training.

Terrein reduces age-related inflammation induced by oxidative stress through Nrf2/ERK1/2/HO-1 signalling in aged HDF cells.

This study investigated whether multiple bioactivity of terrein such as anti-inflammatory and anti-oxidant inhibits age-related inflammation by promoting an antioxidant response in aged human diploid fibroblast (HDF) cells. HDF cells were cultured serially for in vitro replicative senescence. To create the ageing cell phenotype, intermediate stage (PD31) HDF cells were brought to stress-induced premature senescence (SIPS) using hydrogen peroxide (H2 O2). Terrein increased cell viability even with H2O2 stress and reduced inflammatory molecules such as intracellular adhesion molecule-1 (ICAM-1), cyclooxygenase-2 (COX-2), interleukin-1beta (IL-1ß) and tumour necrosis factor-alpha (TNF-α). Terrein reduced also phospho-extracellular kinase receptor1/2 (p-EKR1/2) signalling in aged HDF cells. SIPS cells were attenuated for age-related biological markers including reactive oxygen species (ROS), senescence associated beta-galactosidase (SA ß-gal.) and the aforementioned inflammatory molecules. Terrein induced the induction of anti-oxidant molecules, copper/zinc-superoxide defence (Cu/ZnSOD), manganese superoxide dismutase (MnSOD) and heme oxygenase-1 (HO-1) in SIPS cells. Terrein also alleviated reactive oxygen species formation through the Nrf2/HO-1/p-ERK1/2 pathway in aged cells. The results indicate that terrein has an alleviative function of age-related inflammation characterized as an anti-oxidant. Terrein might be a useful nutraceutical compound for anti-ageing.

PPARγ delivered by Ch-GNPs onto titanium surfaces inhibits implant-induced inflammation and induces bone mineralization of MC-3T3E1 osteoblast-like cells.

OBJECTIVES: To deliver the efficacy and safety of Ch-GNPs (Chitosan gold nanoparticles) conjugated anti-inflammatory molecules peroxisome proliferator activated receptor gamma (PPARγ) on implant surface titanium (Ti) to reduce implant-induced inflammation. MATERIALS AND METHODS: The Ch-GNPs were conjugated with the PPARγ cDNA through a coacervation process. Conjugation was cast over Ti surfaces by dipping, and cells were seeded on different sizes (6 × 6 × 0.1 cm and 1 × 1 × 0.1 cm; n = 3) of Ti surfaces. The size of Ch-GNPs and surface characterization of Ti was performed using UV-vis spectroscopy, TEM (Transmission electron microscopy) and EDX (energy-dispersive X-ray). The DNA conjugation and transfection capacity of Ch-GNPs were simultaneously confirmed by agarose gel electrophoresis, ß-galactosidase staining, and immunoblotting. RESULTS: The Ch-GNPs were well dispersed and spherical in shape, with average size around 10-20 nm. Ti surfaces coated with Ch-GNPs/LacZ, as transfection efficacy molecule, showed strong ß-galactosidase staining in MC-3T3 E1 cells. Cells cultured on Ch-GNPs/PPARγ-coated Ti surfaces were able to inhibit implant-induced inflammation by simultaneously suppressing the expression of tumor necrosis factor- alpha (TNF-α), interleukin-1 beta (IL-1ß), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and matrix metalloproteinase-2 (MMP-2). The inhibition mechanism of Ch-GNPs/PPARγ was due to inhibition of both reactive oxygen species (ROS) and nitric oxide (NO) secretion (n = 3; P < 0.05). In addition, Ch-GNPs/PPARγ was able to increase expression of bone morphogenetic protein (BMP-7) and runt-related transcription factor-2 (RUNX-2). Furthermore, alkaline phosphatase activity (ALP) was also increased than that in control (n = 3; P < 0.01). Whereas, expression of receptor activator of NF-κB ligand (RANKL) was decreased. CONCLUSIONS: The novel gene delivery materials, like Ch-GNPs, can carry the PPARγ cDNA into the required areas of the implant surfaces, thus aiding to inhibit inflammation and promote osteoblast function. Thus, the PPARγ on implant surfaces may promote its clinical application on peri-implantitis or periodontitis like diseases.

Fomitoside-K from Fomitopsis nigra induces apoptosis of human oral squamous cell carcinomas (YD-10B) via mitochondrial signaling pathway.

In this study, a new lanostane triterpene glycoside (fomitoside-K) having biologically active molecules was isolated from a mushroom Fomitopsis nigra to test its anticancer activity on human oral squamous cell carcinomas (YD-10B). We focused on the effect of fomitoside-K on apoptosis, the mitochondria-mediated death pathway and the accumulation of reactive oxygen species (ROS) in YD-10B cells. Fomitoside-K could induce a dose and time-dependent apoptosis in YD-10B cells as characterized by cell morphology, cell cycle arrest, inhibition of survivin, activation of poly(ADP-ribose) polymerase (PARP), caspase-3, -9 and an increased expression ratio of Bax/Bcl-2. The mitochondria membrane potential loss and cytochrome c (Cyt C) release from mitochondria to cytosol were observed during the induction. Moreover, fomitoside-K caused dose-dependent elevation of intracellular ROS level and increase phosphorylation of c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) in YD-10B cells. To further investigate the mechanisms, we examined the effects of ROS scavenger N-acetyl-L-cysteine (NAC) and selective inhibitors for mitogen activated protein kinase (MAPK) pathways on the cell death. The fomitoside-K induced cell death by ROS was significantly inhibited by NAC, ERK (PD98059) and JNK inhibitor (SP600125). In addition, fomitoside-K has a synergistic effect with adriamycin in suppressing the growth of YD-10B cells. These data suggest that fomitoside-K induces apoptosis in YD-10B cells through the ROS-dependent mitochondrial dysfunction pathway and provides a mechanistic framework for further exploring the use of fomitoside-K against the proliferation of human oral cancer.

c-myb mediates inflammatory reaction against oxidative stress in human breast cancer cell line, MCF-7.

Emerging evidence suggests that oncogenes play an important role in the inflammatory reactions in cancer cells, but the precise molecular and cellular mechanisms linking the oncogenes to inflammation is unclear. This study examined the contribution of proto-oncogene c-myb to inflammation in MCF-7 breast cancer cells. An inflammatory response was elicited directly by the cells using an in vitro culture system whereby the cells were exposed to H(2) O(2) . Upon exposure to H(2) O(2) , the cells showed a local inflammatory response, as evidenced by matrix metalloproteinases (MMPs) and ICAM-1 expression. Significant up-regulation of the proto-oncogene c-myb also was observed under inflammatory conditions. c-myb, overexpressed in the cells by transducing with Ad/c-myb, showed an increase in MMPs and ICAM-1 expression under H(2) O(2) stimulation. Despite H(2) O(2) stimulation, the c-myb down-regulated cells by c-myb siRNA inhibit the expression of MMPs and ICAM-1. Among the MAPKs, ERK1/2 and SAPK/JNK were activated by the H(2) O(2) treatment. Interestingly, the H(2) O(2) -induced activation of ERK1/2 and SAPK/JNK was inhibited by siRNA c-myb. These results suggest that breast cancer cells may play a significant role in sustaining and amplifying the inflammation process through the activation of c-myb, which results in the activation of the ERK1/2 and SAPK/JNK pathway. This condition highlights the potential link between inflammation and its involvement in promoting breast cancer proliferation.

c-myb has a character of oxidative stress resistance in aged human diploid fibroblasts: regulates SAPK/JNK and Hsp60 pathway consequently.

This study examined whether c-myb acts as a survival molecule in aged cells. A previous in vitro ageing model suggested that aged cells have a higher cell capacity for survival after exposure to oxidative stress, which involves blockage of the translocation of Hsp60 from the mitochondria to the cytoplasm followed by SAPK/JNK inactivation, than young cells. In human diploid fibroblasts (HDFs), c-myb expression increased gradually with ageing, and this increase had a significant influence on the cell survival capacity after exposure to oxidative stress. To clarify the role of c-myb in oxidative stress, young cells under 21 passages, which lacked c-myb expression, were transfected with adenovirus-mediated c-myb for express c-myb. These c-myb-over-expressed young cells showed increased cell viability upon exposure to oxidative stress to a similar extent to that of the aged cells. In addition, these c-myb-over-expressed young cells did not exhibit SAPK/JNK activation, Hsp60 displacement and cytochrome C release, as was observed in aged cells. The aged cells that had c-myb suppressed using siRNA c-myb showed reduced cell viability and increased apoptosis in a manner to that observed in young cells. From this study, c-myb blocked SAPK/JNK and Hsp60 translocation upon exposure to oxidative stress. This result suggests that c-myb might act as a modulator of cell survival in the ageing process by suppressing apoptosis in aged cells.

PPARgamma inhibits inflammatory reaction in oxidative stress induced human diploid fibloblast.

The ageing of an inevitable life function is an unavoidable regressive physical process. Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor family. PPARgamma plays an important role in regulating several metabolic pathways. Recently, PPARgamma has been implicated in inflammatory responses and age-related diseases. The aim of this study was to determine the anti-inflammatory reaction of PPARgamma in an induced ageing progress. The late passage of human diploid fibroblasts (HDF), an in vitro ageing model, reveals the biological index materials of ageing. Aged cells showed decreased PPARgamma expression and elevated levels of intracellular adhesion molecule-1 (ICAM-1), an inflammatory molecule. To induce the aged cell phenotype, the middle stage of HDF cells (PD31) were induced stress induced premature senescence (SIPS) with 200 microM H(2)O(2) for 2 h. SIPS-HDF cells showed high levels of ICAM-1, extracellular signal regulated kinase (ERK1/2) activity and matrix metallomatrix protease (MMP-2, -9) activity, and low levels of PPARgamma expression. A reconstitution of SIPS HDF cells with Ad/PPARgamma resulted in the downregulation of ICAM-1, ERK1/2, MMP-2 and -9, and normalized growth of SIPS-HDF cells. Moreover, PPARgamma in aged HDF cells reduced pro-inflammatory molecules and eliminated the formation of reactive oxygen species (ROS) through the ERK1/2 pathway. These results strongly suggest that PPARgamma plays a key role in age-related inflammation and may have clinical applications as a molecular target in the treatment of age-related inflammation.

Enhancement of osteoblast biocompatibility on titanium surface with Terrein treatment.

Titanium is biocompatible with bodily tissues. However, the formation of ROS on the titanium surfaces might have negative response of the activity of the surroundings cells. Terrein was isolated from Penicullium sp. 20135 and found to reduce the effects of LPS-induced inflammation. This study examined the role of Terrein on the biocompatibility of titanium to determine if it can help improve osseointegration. MC-3T3 E1 cells were grown on titanium surfaces. The biocompatibility of Terrein was examined by adding it directly to the culture media at the indicated concentration. The cells on the titanium surface produced excessive ROS and decreased the activity of Cu/Zn SOD and Mn SOD. Moreover, the cells had higher activity towards oxidative stress molecules, such as MAPK, FAK and iNOS expression. In addition, MC-3T3 E1 osteoblast-like cells promoted osteoclast differentiation but reduced osteoblast differentiation and mineralization on the titanium surface. Interestingly, the cells given the Terrein treatment showed higher resistance towards oxidative stress through the up-regulation of ERK1/2 and FAK activity but the down-regulation of SAPK/JNK and iNOS activity. Moreover, Terrein promoted osteoblast differentiation and bone mineralization to elevate the activity of ALP, SPARC and down-regulate RANKL expression after blocking NF-κB translocation from the cytosol to the nucleus. In conclusion, the presence of Terrein on titanium surfaces increases osteoblast cell growth without inflammation. Moreover, Terrein, as a putative antioxidant agent, may enhance osseointegration by decreasing the level of ROS and having a potentially synergistic effect on osteoblast differentiation.

Superoxide-mediated oxidative stress accelerates skeletal muscle atrophy by synchronous activation of proteolytic systems.

The maintenance of skeletal muscle mass depends on the overall balance between the rates of protein synthesis and degradation. Thus, age-related muscle atrophy and function, commonly known as sarcopenia, may result from decreased protein synthesis, increased proteolysis, or simultaneous changes in both processes governed by complex multifactorial mechanisms. Growing evidence implicates oxidative stress and reactive oxygen species (ROS) as an essential regulator of proteolysis. Our previous studies have shown that genetic deletion of CuZn superoxide dismutase (CuZnSOD, Sod1) in mice leads to elevated oxidative stress, muscle atrophy and weakness, and an acceleration in age-related phenotypes associated with sarcopenia. The goal of this study is to determine whether oxidative stress directly influences the acceleration of proteolysis in skeletal muscle of Sod1-/- mice as a function of age. Compared to control, Sod1-/- muscle showed a significant elevation in protein carbonyls and 3-nitrotyrosine levels, suggesting high oxidative and nitrosative protein modifications were present. In addition, age-dependent muscle atrophy in Sod1-/- muscle was accompanied by an upregulation of the cysteine proteases, calpain, and caspase-3, which are known to play a key role in the initial breakdown of sarcomeres during atrophic conditions. Furthermore, an increase in oxidative stress-induced muscle atrophy was also strongly coupled with simultaneous activation of two major proteolytic systems, the ubiquitin-proteasome and lysosomal autophagy pathways. Collectively, our data suggest that chronic oxidative stress in Sod1-/- mice accelerates age-dependent muscle atrophy by enhancing coordinated activation of the proteolytic systems, thereby resulting in overall protein degradation.

Oxidative stress resistance through blocking Hsp60 translocation followed by SAPK/JNK inhibition in aged human diploid fibroblasts.

The stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) pathway is a well-known senescence-related stress activated protein kinase. Multiple environmental stresses induce programmed cell death, such as apoptosis. Normal human diploid fibroblast (HDF) cells have a limited life span in vitro, halting proliferation after a fixed number of cell divisions. Aged passage HDF showed resistance to oxidative stress involving heat shock proteins (Hsp60) through a mechanism involving the translocation of Hsp60 from the mitochondria to the cytosol. The present study showed that the translocation of Hsp60 from the mitochondria to the cytosol followed by high levels of p-SAPK/JNK activation as a result of oxidative stress was observed in the young cells only. The inhibition of SAPK/JNK activation by SP600125 under oxidative stress almost completely blocked the translocation of Hsp60 in both young and aged cells. This suggests that aged HDF cells are resistant to oxidative stress by blocking the translocation of Hsp60 from the mitochondria to the cytosol followed by SAPK/JNK inhibition. Overall, the mechanism of resistance by oxidative stress in aged cells is induced by blocked of the translocation of Hsp60 followed by SAPK/JNK inactivation.

Critical Limb Ischemia Induces Remodeling of Skeletal Muscle Motor Unit, Myonuclear-, and Mitochondrial-Domains.

Critical limb ischemia, the most severe form of peripheral artery disease, leads to extensive damage and alterations to skeletal muscle homeostasis. Although recent research has investigated the tissue-specific responses to ischemia, the role of the muscle stem cell in the regeneration of its niche components within skeletal muscle has been limited. To elucidate the regenerative mechanism of the muscle stem cell in response to ischemic insults, we explored cellular interactions between the vasculature, neural network, and muscle fiber within the muscle stem cell niche. Using a surgical murine hindlimb ischemia model, we first discovered a significant increase in subsynaptic nuclei and remodeling of the neuromuscular junction following ischemia-induced denervation. In addition, ischemic injury causes significant alterations to the myofiber through a muscle stem cell-mediated accumulation of total myonuclei and a concomitant decrease in myonuclear domain size, possibly to enhance the transcriptional and translation output and restore muscle mass. Results also revealed an accumulation of total mitochondrial content per myonucleus in ischemic myofibers to compensate for impaired mitochondrial function and high turnover rate. Taken together, the findings from this study suggest that the muscle stem cell plays a role in motor neuron reinnervation, myonuclear accretion, and mitochondrial biogenesis for skeletal muscle regeneration following ischemic injury.

Pax9 mediated cell survival in oral squamous carcinoma cell enhanced by c-myb.

Paired box gene 9 (Pax9) and c-myb are transcription factors that regulate the expression of the genes involved in mediating cell proliferation, resistance to apoptosis, and migration. However, the function of Pax9 in oral squamous cell carcinoma (OSCC) is virtually unknown. This study examined the anti-apoptotic roles of Pax9 and c-myb, and clarified interaction between the two genes in KB cells. Inhibition of Pax9 caused the induction of apoptosis with enhanced cleavage of caspase-3 and PARP, accelerated Bax, and reduced Bcl-2 expression. Transducing c-myb cells with adenovirus c-myb (Ad/c-myb) were induced cell growth and inhibited apoptosis, but dominant-negative myb cells (Ad/DN-myb) were not affected. Pax9 was upregulated in the Ad/c-myb cells with simultaneous decrease in the Ad/DN-myb infection. However, c-myb remained unaffected in the Pax9 small interfering RNA (siRNA) transfected cells. Moreover, the Pax9 siRNA transfected cells and Ad/DN-myb infected cells were able to arrest the cell cycle at the G(0) phase. This suggests that Pax9 and c-myb expression in KB cells is essential for cell growth, and survival is enhanced by c-myb. Disrupting the function of c-myb and Pax9 could be a potential target for cancer treatment.

Optimization of antibacterial activity by Gold-Thread (Coptidis Rhizoma Franch) against Streptococcus mutans using evolutionary operation-factorial design technique.

This study was conducted to find the optimum extraction condition of Gold-Thread for antibacterial activity against Streptococcus mutans using The evolutionary operation-factorial design technique. Higher antibacterial activity was achieved in a higher extraction temperature (R2 = -0.79) and in a longer extraction time (R2 = -0.71). Antibacterial activity was not affected by differentiation of the ethanol concentration in the extraction solvent (R2 = -0.12). The maximum antibacterial activity of clove against S. mutans determined by the EVOP-factorial technique was obtained at 80 degrees C extraction temperature, 26 h extraction time, and 50% ethanol concentration. The population of S. mutans decreased from 6.110 logCFU/ml in the initial set to 4.125 logCFU/ml in the third set.

Acute effects of Kinesio taping on muscle function and self-perceived fatigue level in healthy adults.

This study investigated the acute effects of Kinesio taping (KT) on muscular power, strength, endurance, and self-perceived fatigue level. This is a randomized, partial double-blind, crossover trial. Eighteen healthy adults (7 males [23.86 ± 1.68 years] and 11 females [24.82 ± 3.71 years]) were enrolled in this study. All subjects underwent three different trials which included no tap (NT), placebo tap (PT), and KT. Idividuals were assessed for peak and mean power, muscular strength and endurance, and self-perceived fatigue after each condition. The results revealed no significant differences in all variables (p > 0.05) except muscular endurance (F = 5.775, p = 0.007). Muscular endurance in the NT (58.28 ± 12.18 reps/min) condition was significantly higher than that in the KT (52.83 ± 11.76 reps/min) condition. These results suggest that KT on rectus femoris and the patella of the lower limb does not improve muscular function and self-perceived fatigue level. KT is unlikely to enhance exercise performance capacity in healthy adults.

Metabolites distinguishing visceral fat obesity and atherogenic traits in individuals with overweight.

OBJECTIVE: To screen the metabolomes of both overweight subjects with low visceral fat area (LFO) and high visceral fat area (HFO) to identify potential metabolites that are associated with the different metabolic characteristics. METHODS: The metabolic characteristics of 112 overweight (25 kg/m2 ≤ BMI < 30 kg/m2 ) Korean individuals aged 30 to 65 years were examined. Plasma metabolomic profiling of HFO [visceral fat area (VFA) at L4 ≥ 100 cm2 ] and LFO (L4 VFA <100 cm2 ) individuals matched for age, gender, and BMI was performed. RESULTS: HFO subjects showed higher VFA at L1 and L4 than LFO subjects. The HFO group showed higher blood pressure, lipid profile, high-sensitivity C-reactive protein, malondialdehyde, oxidized low-density lipoprotein (LDL), and homeostasis model assessment-insulin resistance and lower high-density lipoprotein-cholesterol levels. In plasma metabolite identification, the HFO group showed significantly higher levels of long-chain (C14:1, C16:1, C16) acylcarnitines (ACs), medium-chain (C12:1, C12) ACs, urobilinogen, docosahexaenoic acid (C22:6ω3), lysoPE (22:6), lysoPC (22:6), lysoPC (22:5), methoxybenzenepropanoic acid, and isodesmosine. All five ACs correlated positively with VFA and oxidized LDL levels and negatively with high-density lipoprotein-cholesterol levels and LDL particle size. CONCLUSIONS: Twelve major metabolites, including three long-chain fatty acids and two medium-chain ACs, are important for distinguishing HFO and LFO. Chronic lipid surplus from visceral fat in HFO is likely associated with substantial increases in plasma medium-chain ACs and long-chain fatty acids, which are closely related to atherogenic traits.

Red Ginseng as an Ergogenic Aid: A Systematic Review of Clinical Trials.

Purpose: This systematic review was performed to summarize clinical trials assessing the effect of Red Ginseng (RG) supplementation on exercise performance and fatigue recovery. Methods: Two English databases (PUBMED, MEDLINE) and two Korean databases (KISS, RISS) were used as systematic searching engines. We included only articles written in the English and Korean languages. Clinical trials, which evaluated exercise performance and recovery variables with RG supplementation, were included in this review. The methodological quality of all studies was assessed using the Cochrane Risk of Bias tool. Analysis was conducted with Comprehensive Meta-Analysis Version 3. Results: In total, 135 potentially relevant studies were identified, and 14 studies were included. Overall, the aerobic capacity (VO2max, heart rate, time to exhaustion, shuttle run, and anaerobic threshold) exhibited no improvement with RG supplementation. In anaerobic capacity (peak power, mean power, and 30 m dash run), no significant improvements with RG supplementation was described in most of the studies. The antioxidant function predominantly measured by levels of superoxide dismutase (SOD) and malondialdehyde (MDA) showed mixed results. Red Ginseng's effects on fatigue recovery were evaluated using lactate as a main outcome. Two studies observed significant effects while other 5 studies showed no significant effects. Conclusion: The clinical effects of RG have been assessed in various conditions. Although the number of studies presented in this review is small and results of studies are mixed, it is hypothesized that this review article may provide useful guideline to design and conduct future studies investigating efficacy of RG supplementation on exercise performance and fatigue recovery in human trials.

Protective effects of TES trioleate, an inhibitor of phospholipase A2, on reactive oxygen species and UVA-induced cell damage.

2-[Tris(oleoyloxymethyl)methylamino]-1-ethane sulfonic acid (TES trioleate) is an inhibitor of phospholipase A2 (PLA2), which hydrolyzes cell membrane phospholipids to produce arachidonic acid (AA) and lysophospholipids (LysoPLs). Here, we investigated the protective effects of TES trioleate on cell damage caused by ultraviolet A (UVA) light and reactive oxygen species (ROS). Pre-incubation with 250-1000µM TES trioleate resulted in concentration-dependent protection from UVA-induced damage in HaCaT cells. Additionally, 25-1000µM TES trioleate provided protection against H2O2 in a concentration-dependent manner. In human erythrocytes treated with 1O2, 10-100µM TES trioleate showed concentration-dependent protective effects, similar to but stronger than the controls, 4-BPB and lipophilic antioxidant (+)-α-tocopherol at 100µM. TES trioleate did not have detectable radical scavenging activity. Moreover, compared with (+)-α-tocopherol and rutin, TES trioleate showed low ROS scavenging activity. Thus, although TES trioleate showed cell protective effects against UVA, H2O2, and 1O2-induced damages, these effects were not caused by the scavenging ability of the radical or ROS. Finally, pretreatment of HaCaT cells and human erythrocytes with l-α-lysophosphatidylcholine produced by PLA2 promoted increased cell damage at low concentrations. Thus, the protective effects of TES trioleate on cellular damage by UVA and ROS may be associated with inhibition of PLA2-dependent cell damage rather than ROS scavenging.

Effects of Cassia tora fiber supplement on serum lipids in Korean diabetic patients.

Cassia tora fiber supplement consisting of 2 g of soluble fiber extracted from Cassia semen (C. tora L.), 200 mg of alpha-tocopherol, 500 mg of ascorbic acid, and 300 mg of maltodextrin was formulated in a pack, and given to 15 type II diabetic subjects (seven men and eight women 57.1 +/- 2.9 years old) with instructions to take two packs per day for 2 months. Placebo contained maltodextrin only with a little brown caramel color. Lifestyle factors and dietary intakes of the subjects were not altered during the 2-month period. Serum total cholesterol was moderately (P < .1) decreased in the C. tora group compared with the age- and gender-matched placebo group, as was the ratio of apolipoprotein B to apolipoprotein A1 (P < .1). Levels of serum triglycerides and low-density lipoprotein-cholesterol tended to decrease more in the C. tora-supplemented group than in the placebo group. Serum alpha-tocopherol was increased (P < .01) but lipid peroxides were not significantly lower in the C. tora group. Fasting blood glucose, hemoglobin A1c, blood urea nitrogen, creatinine, and activities of serum aspartate aminotransferase and alanine aminotransferase were not changed by the fiber supplement. We concluded that C. tora supplements can help improve serum lipid status in type II diabetic subjects without serious adverse effects.

Propyl gallate inhibits adipogenesis by stimulating extracellular signal-related kinases in human adipose tissue-derived mesenchymal stem cells.

Propyl gallate (PG) used as an additive in various foods has antioxidant and anti-inflammatory effects. Although the functional roles of PG in various cell types are well characterized, it is unknown whether PG has effect on stem cell differentiation. In this study, we demonstrated that PG could inhibit adipogenic differentiation in human adipose tissue-derived mesenchymal stem cells (hAMSCs) by decreasing the accumulation of intracellular lipid droplets. In addition, PG significantly reduced the expression of adipocyte-specific markers including peroxisome proliferator-activated receptor-γ (PPAR-γ), CCAAT enhancer binding protein-α (C/EBP-α), lipoprotein lipase (LPL), and adipocyte fatty acid-binding protein 2 (aP2). PG inhibited adipogenesis in hAMSCs through extracellular regulated kinase (ERK) pathway. Decreased adipogenesis following PG treatment was recovered in response to ERK blocking. Taken together, these results suggest a novel effect of PG on adipocyte differentiation in hAMSCs, supporting a negative role of ERK1/2 pathway in adipogenic differentiation.