PMID: 

Biomed Pharmacother. 2018 Jul ;103:362-372. Epub 2018 Apr 24. PMID: 29669302

Abstract Title: 

Cytotoxic and partial hepatoprotective activity of sodium ascorbate against hepatocellular carcinoma through inhibition of sulfatase-2 in vivo and in vitro.

Abstract: 

Hepatocellular carcinoma (HCC) is characterized by elevation in the activity of sulfatase-2, an extracellular enzyme that catalyzes removal of 6-O-sulfate groups from heparan sulfate. Therefore, we conducted this study to investigate the cytotoxic activity of the strong water-soluble antioxidant, sodium ascorbate, against HCC both in vivo and in vitro. Sodium ascorbate enhanced animal survival in vivo and reduced HepG2 cells survival. The protein levels of heparan sulfate proteoglycans (HSPGs), insulin like growth factor (IGF)-2, sulfatase-2 and glypican-3 were assessed. Inflammation was evaluated by measuring the gene and protein expression of NFκB, TNF-α, IL-1β, IL-4, IL-6 and IL-10. We found that sodium ascorbate blocked HCC-induced activation of sulfatase-2 leading to restoration of HSPGs receptors associated with reduction in IGF-2 and glypican-3. Sodium ascorbate exerts anti-inflammatory activity by reducing the expression of NFκB,CRP, TNF-α, IL-1β and IL-6 associated with enhanced expression of the anti-inflammatory cytokines, IL-4 and IL-10. In conclusion, cytotoxic effects of sodium ascorbate against HCC can be partially explained by inhibition of sulfatase-2, restoration of HSPGs receptors and deactivation of the inflammatory pathway.

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PMID: 

Mol Cell Biochem. 2020 Feb 21. Epub 2020 Feb 21. PMID: 32080778

Abstract Title: 

Resveratrol potentiates intracellular ascorbic acid enrichment through dehydroascorbic acid transport and/or its intracellular reduction in HaCaT cells.

Abstract: 

L-Ascorbic acid (AsA), a reduced vitamin C (VC), is an important antioxidant, and the internal accumulation and maintenance of AsA are thought to play a significant role in various physiological activities in humans. We focused on resveratrol (RSV), a natural polyphenolic compound, as a candidate for an AsA transport modulator and investigated whether RSV can affect the intracellular VC accumulation after either AsA or dehydroascorbic acid (DHA) addition in HaCaT keratinocytes. Our results demonstrate that RSV treatment could significantly enhance intracellular VC levels after either AsA or DHA supplementation, and intracellular VC accumulated mainly as AsA. Our results also indicate that most of the intracellular transported DHA was reduced to AsA and accumulated after uptake into cells. In addition, RSV could induce several AsA or DHA transport-related and intracellular DHA reduction-related genes including SVCT2, GLUT3, TXNRD2, and TXNRD3, necessary for AsA transport, DHA transport, and DHA reduction/regeneration, respectively. On the other hand, the both protein expression levels and the localizations of sodium-dependent vitamin C transporters 2 (SVCT2) and glucose transporter 3(GLUT3) were scarcely affected by RSV treatment. Furthermore, RSV-induced enrichment of intracellular AsA levels was completely suppressed by a GLUT inhibitor cytochalasin B. These results suggest that RSV can potentiate intracellular AsA accumulation via activation of the DHA transport and subsequent intracellular reduction from DHA to AsA. Thus, RSV might be useful for maintaining substantial AsA accumulation in the skin keratinocytes.

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PMID: 

J Cell Physiol. 2005 Jul ;204(1):192-7. PMID: 15672419

Abstract Title: 

Sodium ascorbate (vitamin C) induces apoptosis in melanoma cells via the down-regulation of transferrin receptor dependent iron uptake.

Abstract: 

Sodium ascorbate (vitamin C) has a reputation for inconsistent effects upon malignant tumor cells, which vary from growth stimulation to apoptosis induction. Melanoma cells were found to be more susceptible to vitamin C toxicity than any other tumor cells. The present study has shown that sodium ascorbate decreases cellular iron uptake by melanoma cells in a dose- and time-dependent fashion, indicating that intracellular iron levels may be a critical factor in sodium ascorbate-induced apoptosis. Indeed, sodium ascorbate-induced apoptosis is enhanced by the iron chelator, desferrioxamine (DFO) while it is inhibited by the iron donor, ferric ammonium citrate (FAC). Moreover, the inhibitory effects of sodium ascorbate on intracellular iron levels are blocked by addition of transferrin, suggesting that transferrin receptor (TfR) dependent pathway of iron uptake may be regulated by sodium ascorbate. Cells exposed to sodium ascorbate demonstrated down-regulation of TfR expression and this precedes sodium ascorbate-induced apoptosis. Taken together, sodium ascorbate-mediated apoptosis appears to be initiated by a reduction of TfR expression, resulting in a down-regulation of iron uptake followed by an induction of apoptosis. This study demonstrates the specific mechanism of sodium ascorbate-induced apoptosis and these findings support future clinical trial of sodium ascorbate in the prevention of human melanoma relapse.

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With the boom in CBD I am sure you have asked yourself, is this safe to put in your body?

Not only is CBD becoming more popular in medicine, it is also showing up on menu items in bars and restaurants. It is even sold in pet products. In the US, CBD is legal in all 50 states with different degrees of restriction, according to the Drug Enforcement Agency. Forbes predicts that the CBD industry is worth billions. More and more people are using it to treat a wide array of health conditions. But is CBD a safe and effective medical treatment?

It has been know to treat many conditions such as…

• Chronic Pain
• Epilepsy
• Parkinson’s disease
• Huntington’s disease
• sleep disorders
• glaucoma

So as you see it has been used to treat some serious conditions that before CBD didn’t have any real way to offer the patient relief. Now just because it does offer help for most doesn’t mean that it can’t be harmful to others but up until now there have been no known cases of any serious harmful effects.

Despite a lack of research, it is clear that many individuals are seeking treatment for a variety of conditions with CBD, as this industry continues to boom we will see much more evidence and breakthroughs on this wonderful herb.

PMID: 

Cardiol Res Pract. 2019 ;2019:8723076. Epub 2019 May 2. PMID: 31192006

Abstract Title: 

Primary Mechanism Study ofFlower (Herb) on Myocardial Infarction in Rats.

Abstract: 

Background: (Burk.) F. H. Chen is one of the most common herbs in China. Because of its good efficacy and little adverse reaction,has been used widely to treat cardiovascular diseases (CVDs).Objective: To investigate effects offlower (PN-F) on rats with myocardial infarction (MI).Methods: The proximal left anterior descending coronary artery in rats was ligated to induce acute myocardial infarction. Then, animals were randomly assigned to four experimental groups: MI control group, Betaloc control group (with Betaloc 10 mg/kg/d), FD500 (low-dose) group (flower decoction 500 mg/kg,=10), and FD1000 (high-dose) group (flower decoction 1000 mg/kg,=10).flower decoction or Betaloc was orally administrated for two to four weeks before and after operation. Sham-operated group was used as a normal untreated group, in which animals were treated with double distilled water, once daily. HE (hematoxylin and eosin) staining, immunofluorescent assay, TUNEL assay, quantitative real-time PCR, and western blot analysis were, respectively, performed to observe morphology, count mean minimal vessels, investigate apoptotic cells, and record gene (HIF-1, VEGFA, and KDR) and protein (Bcl-2 and Bax) expressions.Results: Two weeks after MI, PN-F significantly enhanced capillary density in the border area of MI, decreased infarct size, improved minimal vessels, suppressed cell apoptosis, and enhanced expressions of genes (HIF-1, VEGFA, and KDR) and proteins (Bcl-2 and Bax).Conclusions: PN-F demonstrated a potential herb to treat rats with myocardial infarction through promoting angiogenesis and inhibition of apoptosis in the infarct area.

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PMID: 

Evid Based Complement Alternat Med. 2019 ;2019:2971604. Epub 2019 Dec 31. PMID: 31975996

Abstract Title: 

Astragalus Membranaceus Treatment Protects Raw264.7 Cells from Influenza Virus by Regulating G1 Phase and the TLR3-Mediated Signaling Pathway.

Abstract: 

Influenza is an acute respiratory infection disease caused by the influenza virus. At present, due to the high mutation rate of influenza virus, it is difficult for the existing antiviral drugs to play an effective antiviral effect continually, so it is urgent to develop a new anti-influenza drug. Recently, more and more studies have been conducted on the antiviral activity of, but the specific antiviral mechanism of this traditional Chinese medicine is not clear. In this study, the results proved that theinjection showed obvious anti-influenza virus activity. It could improve the survival rate of Raw264.7 cells which were infected with influenza virus, while it improved the blocking effect of influenza virus on cell cycle after infection, increased the SOD activity, and reduced the MDA content. At the same time, the innate immunity was affected by regulating the expression of TLR3, TAK1, TBK1, IRF3, and IFN-in the TLR3-mediated signaling pathway, thus exerting its antiviral effect in vitro.

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PMID: 

J Cosmet Dermatol. 2020 Feb ;19(2):529-534. Epub 2019 Jul 2. PMID: 31267657

Abstract Title: 

Panax notoginseng saponins promotes cutaneous wound healing and suppresses scar formation in mice.

Abstract: 

BACKGROUND & AIM: Panax notoginseng saponins are believed to promote wound healing due to its anti-proliferative effect on fibroblasts. The present work was therefore aimed to examine the beneficial effect of PNS on wound healing in vitro and in a murine model of cutaneous wound.METHODS: The in vitro effects of Panax notoginseng saponins on the proliferation of and nitric oxide (NO) synthesis in human fibroblast 3T3 cells were studied. The in vivo effects of Panax notoginseng saponins were examined in C57 mice with dorsal cutaneous wound. The healing rate and scar formation were followed after treatment with Panax notoginseng saponins. The histology and fibroblast accumulation in the wounds were studied using hematoxylin and eosin (H&E) staining. Expression ofα-smooth muscle actin (α-SMA) was examined by immunohistochemistry.RESULTS: Panax notoginseng saponins inhibited the proliferation of human fibroblast 3T3 with an ECof 1.825 mM Panax notoginseng saponins (0.1 mM) significantly promoted NO production (P 

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PMID: 

Mar Drugs. 2020 Feb 8 ;18(2). Epub 2020 Feb 8. PMID: 32046368

Abstract Title: 

Fucoidan Inhibition of Osteosarcoma Cells Is Species and Molecular Weight Dependent.

Abstract: 

Fucoidan is a brown algae-derived polysaccharide having several biomedical applications. This study simultaneously compares the anti-cancer activities of crude fucoidans fromand, and effects of low (LMW, 10-50 kDa), medium (MMW, 50-100 kDa) and high (HMW,>100 kDa) molecular weight fractions offucoidan against osteosarcoma cells. Glucose, fucose and acid levels were lower and sulphation was higher incrude fucoidan compared tocrude fucoidan. MMW had the highest levels of sugars, acids and sulphation among molecular weight fractions. There was a dose-dependent drop in focal adhesion formation and proliferation of cells for all fucoidan-types, butfucoidan and HMW had the strongest effects. G1-phase arrest was induced byfucoidan, MMW and HMW, howeverfucoidan treatment also caused accumulation in the sub-G1-phase. Mitochondrial damage occurred for all fucoidan-types, howeverfucoidan led to mitochondrial fragmentation. Annexin V/PI, TUNEL and cytochrome c staining confirmed stress-induced apoptosis-like cell death forfucoidan and features of stress-induced necrosis-like cell death forfucoidans. There was also variation in penetrability of different fucoidans inside the cell. These differences in anti-cancer activity of fucoidans are applicable for osteosarcoma treatment.

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PMID: 

Biomolecules. 2020 Feb 9 ;10(2). Epub 2020 Feb 9. PMID: 32050429

Abstract Title: 

Oral Administration of Fucoidan Can Exert Anti-Allergic Activity after Allergen Sensitization by Enhancement of Galectin-9 Secretion in Blood.

Abstract: 

A previous study revealed that fucoidan inhibited mast cell degranulation through the upregulation of galectin-9 in blood. The purpose of this study is to elucidate its mechanism using ovalbumin (OVA) induced anaphylaxis model mice (BALB/c, Female, 5-week-old) and mast cell line (RBL-2H3 cells). Oral administration of fucoidan after sensitization with OVA/Al(OH)inhibited reduction of rectal temperature induced by activation of mast cells. Fucoidan increased galectin-9 mRNA expression only in colonic epithelial cells. These results suggested that fucoidan could suppress the allergic symptoms in sensitized mice by inducing galectin-9 production from colonic epithelial cells. In addition, to check the influence of galectin 9 on the degranulation of mast cells, RBL-2H3 cell lines were treated directly with recombinant galectin-9. As expected, galectin-9 inhibited degranulation of RBL-2H3 cells pre-bound with IgE. Moreover, the residual amounts of IgE on RBL-2H3 cells were decreased by an addition of galectin-9. It was demonstrated that galectin-9 could remove IgE even if IgE was already bound to mast cells and suppress the mast cells degranulation induced by antigen. This study shows that fucoidan might become an effective therapeutic agent for patients already developed type I allergic diseases.

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PMID: 

Int J Biol Macromol. 2020 Feb 11 ;150:304-314. Epub 2020 Feb 11. PMID: 32057847

Abstract Title: 

Low molecular weight fucoidan alleviates diabetic nephropathy by binding fibronectin and inhibiting ECM-receptor interaction in human renal mesangial cells.

Abstract: 

Diabetic nephropathy (DN) is the most common cause of end-stage renal disease (ESRD). Currently, approximately 20-40% of individuals with diabetes are diagnosed with DN. Mesangial cells (MCs) are critical for maintaining and regulating glomerular filtration, and the abnormal proliferation of MCs causes the accumulation of mesangial extracellular matrix (ECM), further promoting glomerular dysfunction and renal diseases. Low molecular weight fucoidan (LMWF) extracted from Saccharina japonica could alleviate DN, but the mechanism was not analysed. Based on the ability of LMWF to ameliorate the human renal mesangial cell (HRMC) injury caused by advanced glycation end products (AGEs), we identified fibronectin (FN) as the most obviously impacted protein in the ECM-receptor interaction by proteomic analysis. The co-localization of LMWF and FN indicated direct interaction between them, and surface plasmon resonance (SPR) analysis confirmed the specific binding with a Kof 453.7 μmol L. Positively charged protamine sulfate (PS) promoted the combination of LMWF and HRMCs and further enhanced the effect of LMWF on HRMC injury. Our results indicated that LMWF alleviates the HRMC injury caused by AGEs via binding FN and inhibiting the ECM-receptor interaction pathway. These results provide a foundation for the in-depth analysis of the mechanism of polysaccharide functions.

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