2016

Osteoarthritis (OA) is one of the major joint diseases, and the synovial inflammation is involved in the pathogenesis and progression of OA. Glucosamine (GlcN) is widely used as a dietary supplement for OA, and is expected to exert the antiinflammatory action in OA. However, the detailed mechanism for the antiinflammatory action of GlcN remains poorly understood. In this study, to elucidate the molecular mechanism involved in the GlcN-medicated regulation of synovial cell activation, we comprehensively analyzed the effect of GlcN on the gene expression using a human synovial cell line MH7A by DNA microarray. The results indicated that GlcN significantly downregulates the expression of 187 genes (≤1/1.5-fold) and upregulates the expression of 194 genes (≥1.5-fold) in IL-1β-stimulated MH7A cells. Interestingly, pathway analysis indicated that among the 10 pathways into which the GlcN-regulated genes are categorized, the 4 pathways are immune-related. Furthermore, GlcN suppressed the expression of proinflammatory cytokine genes (such as IL-6, IL-8, IL-24 and TNF-α genes). In addition, GlcN-mediated O-GlcNAc modification was involved in the downregulation of TNF-α and IL-8 genes but not IL-6 and IL-24 genes, based on the effects of alloxan, an O-GlcNAc transferase inhibitor. Thus, GlcN likely exerts an antiinflammatroy action in OA by suppressing the expression of proinflammatory cytokine genes in synovial MH7A cells by O-GlcNAc modification-dependent and -independent mechanisms.

Osteoarthritis is a degenerative disease that causes substantial changes in joint tissues, such as cartilage degeneration and subchondral bone sclerosis. Chondroitin sulfate and glucosamine are commonly used products for the symptomatic treatment of osteoarthritis. The aim of the present study was to investigate the effects of these products when used as structure-modifying drugs on the progression of osteoarthritis in the rabbit temporomandibular joint. Thirty-six New Zealand rabbits were divided into 3 groups (n = 12/group): control (no disease); osteoarthritis (disease induction); and treatment (disease induction and administration of chondroitin sulfate and glucosamine). Osteoarthritis was induced by intra-articular injection of monosodium iodoacetate. Animals were killed at 30 and 90 days after initiation of therapy. The treatment was effective in reducing disease severity, with late effects and changes in the concentration of glycosaminoglycans in the articular disc. The results indicate that chondroitin sulfate and glucosamine may have a structure-modifying effect on the tissues of rabbit temporomandibular joints altered by osteoarthritis.

Background Fucoidan extract (FE), an enzymatically digested compound with a low molecular weight, is extracted from brown seaweed. As a natural compound with various actions, FE is attractive, especially in Asian countries, for improving the therapeutic efficacy and safety of cancer treatment. The present study was carried out to investigate the anti-tumor properties of FE in human carcinoma cells and further examine the underlying mechanisms of its activities. Methodology/Principal Finding FE inhibits the growth of MCF-7, MDA-MB-231, HeLa, and HT1080 cells. FE-mediated apoptosis in MCF-7 cancer cells is accompanied by DNA fragmentation, nuclear condensation, and phosphatidylserine exposure. FE induces mitochondrial membrane permeabilization (MMP) through loss of mitochondrial membrane potential (ΔΨm) and regulation of the expression of Bcl-2 family members. Release of apoptosis-inducing factor (AIF) and cytochrome c precedes MMP. AIF release causes DNA fragmentation, the final stage of apoptosis, via a caspase-independent mitochondrial pathway. Additionally, FE was found to induce phosphorylation of c-Jun N-terminal kinase (JNK), p38, and extracellular signal-regulated kinase (ERK) 1/2, and apoptosis was found to be attenuated by inhibition of JNK. Furthermore, FE-mediated apoptosis was found to involve the generation of reactive oxygen species (ROS), which are responsible for the decrease of ΔΨm and phosphorylation of JNK, p38, and ERK1/2 kinases. Conclusions/Significance These data suggest that FE activates a caspase-independent apoptotic pathway in MCF-7 cancer cells through activation of ROS-mediated MAP kinases and regulation of the Bcl-2 family protein-mediated mitochondrial pathway. They also provide evidence that FE deserves further investigation as a natural anticancer and cancer preventive agent.

Cardiovascular diseases, including heart attacks and strokes, continue to be the leading causes of deaths resulting in more than 17 million deaths each year worldwide. Cardiovascular disease (CVD) man...

Background Cancer metastasis is the main cause leading to disease recurrence and high mortality in cancer patients. Therefore, inhibiting metastasis process or killing metastatic cancer cells by inducing apoptosis is of clinical importance in improving cancer patient survival. Previous studies revealed that fucoidan, a fucose-rich polysaccharide isolated from marine brown alga, is a promising natural product with significant anti-cancer activity. However, little is known about the role of endoplasmic reticulum (ER) stress in fucoidan-induced cell apoptosis. Principal Findings We reported that fucoidan treatment inhibits cell growth and induces apoptosis in cancer cells. Fucoidan treatments resulted in down-regulation of the glucose regulated protein 78 (GRP78) in the metastatic MDA-MB-231 breast cancer cells, and of the ER protein 29 (ERp29) in the metastatic HCT116 colon cancer cells. However, fucoidan treatment promoted ER Ca2+-dependent calmodulin-dependent kinase II (CaMKII) phosphorylation, Bcl-associated X protein (Bax) and caspase 12 expression in MDA-MB-231 cells, but not in HCT116 cells. In both types of cancer cells, fucoidan activated the phosphorylation of eukaryotic initiation factor 2 alpha (p-eIF2α)\CCAAT/enhancer binding protein homologous protein (CHOP) pro-apoptotic cascade and inhibited the phosphorylation of inositol-requiring kinase 1 (p-IRE-1)\X-box binding proteins 1 splicing (XBP-1s) pro-survival cascade. Furthermore, CHOP knockdown prevented DNA damage and cell death induced by fucoidan. Conclusion/Significance Fucoidan exerts its anti-tumor function by modulating ER stress cascades. Contribution of ER stress to the fucoidan-induced cell apoptosis augments our understanding of the molecular mechanisms underlying its anti-tumour activity and provides evidence for the therapeutic application of fucoidan in cancer.

The gut-microbiota-targeted prebiotic intervention has been a hot topic in the study of health modulation. To examine the effect of fucoidan supplementation on the health of long-cared elderly subjects (88years ± 3.41) with malnutrition (MNA-SF score ≤ 7), an eight-week randomized, single-blind clinical trial was carried out in a community hospital. The subjects were divided into a test group (TG, n = 45), which received the fucoidan supplementation (1g/d) and a control group (CG, n = 20). Preliminary data on metagenomes, plasma metabolomes, prealbumin, twelve cytokines, and clinical records from six people were analyzed. The results showed that with prebiotic intervention, prealbumin, a sensitive nutrition marker slightly increased. Furthermore, in the test group, there were 42 significantly enriched gut microbial species (t-test, p < 0.05), including multiple beneficial bacteria (Bifidobacterium breve, Roseburia hominis, and Lactobacillus acidipiscis), which positively correlated with Medium-Chain Fatty Acid (MCFA)-associated carnitines (octanoylcarnitine and decanoylcarnitine), and chenodeoxycholic acid. The defecation and neuropsychological activities of the participants in the test group also improved slightly. The preliminary data suggests that fucoidan has the potential to improve metabolism, gut function, and nutrition in elderly people by changing the gut microbiota and enriching beneficial bacteria. A larger sample size analysis is needed for a deeper understanding of the effects and mechanism.

Kim SH, et al. Food Suppl Biomater Health. 2023 Jun;3(2):e8. https://doi.org/10.52361/fsbh.2023.3.e8

There are many plants with interesting pharmaceutical activities but Aloe vera is probably the most applied medicinal plant worldwide. Since biblical …

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D-Allulose is a rare sugar that exists in nature. It is a food ingredient with nearly zero calories (

In this exciting episode, join us as we unravel the benefits of MCT oil! Ever wondered what MCT oil is? Well, we're taking a step back to explore the fascinating world of fats and how each type can supercharge your health. ———————————————————————— Order Dr. Gundry’s latest book “Gut Check” here: https://www.amazon.com/Gut-Check-Microbiome-Transform-Emotional/dp/0062911775?&tag=dgpodcast.-20 MCT, short for medium-chain triglycerides, is a potent source comprised entirely of ketones – the energy heroes typically produced from fat cells when your sugar levels dip. These ketones play a vital role in fueling your body, especially during those nights when you're not snacking. Embark on this journey with us to comprehend how MCT oil can revolutionize your health. We'll simplify the types of MCT oil and provide guidance on selecting the best one for a healthier, more vibrant you. Get ready to explore the science and benefits of MCT oil – your body will thank you! If you liked this, you may enjoy: Stop Wasting Your Money on These 7 USELESS Supplements! https://youtu.be/4r7mrHPYhoU Fish Oil Benefits: The Game-Changing Reason Why Fish Oil is a Must! https://youtu.be/JY0JVl3pB20

Dr. Steven Gundry is a pioneer in nutrition research and one of the world's top cardiothoracic surgeons, He has spent the past 25 years helping people restore their health by optimizing diet and lifestyle choices alone. Based on his many years of research, Dr. Gundry founded the wellness brand Gundry MD where he personally tests the efficacy of every formula he collaborates on. Dr. Gundry is also the author of four New York Times best-selling books including The Plant Paradox™ which details his famous lectin-free diet, Plant Paradox: Quick & Easy, Longevity Paradox, Energy Paradox, and two lectin-light cookbooks. Dr. Gundry’s latest book, Unlocking the Keto Code, reveals the key to longevity is optimizing mitochondrial uncoupling and shares simple dietary tips to do this. For more information, sign up for his free newsletter at drgundry.com, subscribe to the Gundry MD Youtube channel, follow @drstevengundry and @drgundrypodcast on Instagram, and @drgundrypodcast on TikTok.

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