Methanol Extracts from Cirsium japonicum DC. var. australe Kitam. and Their Active Components Reduce Intracellular Oxidative Stress in Caenorhabditis elegans.

Cirsium japonicum DC. var. australe Kitam. has been used as an herbal remedy and often involves using the whole plant or roots. However, the bioactivities of different parts of the plant have been far less explored. This study aimed to evaluate the antioxidative ability of methanol extracts from the flowers, leaves, stems, and roots of the Cirsium plant and their possible active components against juglone-induced oxidative stress in the nematode Caenorhabditis elegans. The results showed that the highest dry weight (12.3 g per plant) was observed in leaves, which was followed by stems (8.0 g). The methanol extract yields from the flowers, leaves, and roots were all similar (13.0-13.8%), while the yield from stems was the lowest (8.6%). The analysis of the silymarin contents in the extracts indicated that the flowers, leaves, stems, and roots contained silychristin and taxifolin; however, silydianin was only found in the leaves, stems, and roots. The flower, leaf, and stem extracts, at a concentration of 10 mg/L, significantly reduced juglone-induced oxidative stress in C. elegans, which was potentially due to the presence of silychristin and taxifolin. Overall, C. japonicum DC. var. australe Kitam. contains a significant amount of silymarin and exhibits in vivo antioxidative activity, suggesting that the prospects for the plant in terms of health supplements or as a source of silymarin are promising.

Glucosamine Interferes With Myelopoiesis and Enhances the Immunosuppressive Activity of Myeloid-Derived Suppressor Cells.

Glucosamine (GlcN) is the most widely consumed dietary supplement and exhibits anti-inflammatory effects. However, the influence of GlcN on immune cell generation and function is largely unclear. In this study, GlcN was delivered into mice to examine its biological function in hematopoiesis. We found that GlcN promoted the production of immature myeloid cells, known as myeloid-derived suppressor cells (MDSCs), both in vivo and in vitro. Additionally, GlcN upregulated the expression of glucose transporter 1 in hematopoietic stem and progenitor cells (HSPCs), influenced HSPC functions, and downregulated key genes involved in myelopoiesis. Furthermore, GlcN increased the expression of arginase 1 and inducible nitric oxide synthase to produce high levels of reactive oxygen species, which was regulated by the STAT3 and ERK1/2 pathways, to increase the immunosuppressive ability of MDSCs. We revealed a novel role for GlcN in myelopoiesis and MDSC activity involving a potential link between GlcN and immune system, as well as the new therapeutic benefit.

Red Quinoa Bran Extract Prevented Alcoholic Fatty Liver Disease via Increasing Antioxidative System and Repressing Fatty Acid Synthesis Factors in Mice Fed Alcohol Liquid Diet.

Alcohol is metabolized in liver. Chronic alcohol abuse results in alcohol-induced fatty liver and liver injury. Red quinoa (Chenopodium formosanum) was a traditional staple food for Taiwanese aborigines. Red quinoa bran (RQB) included strong anti-oxidative and anti-inflammatory polyphenolic compounds, but it was usually regarded as the agricultural waste. Therefore, this study is to investigate the effect of water and ethanol extraction products of RQB on the prevention of liquid alcoholic diet-induced acute liver injury in mice. The mice were given whole grain powder of red quinoa (RQ-P), RQB ethanol extract (RQB-E), RQB water extract (RQB-W), and rutin orally for 6 weeks, respectively. The results indicated that RQB-E, RQB-W, and rutin decreased alcoholic diet-induced activities of aspartate aminotransferase and alanine aminotransferase, and the levels of serum triglyceride, total cholesterol, and hepatic triglyceride. Hematoxylin and eosin staining of liver tissues showed that RQB-E and RQB-W reduced lipid droplet accumulation and liver injury. However, ethanol extraction process can gain high rutin and antioxidative agents contents from red quinoa, that showed strong effects in preventing alcoholic fatty liver disease and liver injury via increasing superoxide dismutase/catalase antioxidative system and repressing the expressions of fatty acid synthesis enzyme acetyl-CoA carboxylase.

Plasma Homocysteine Concentration is Associated with the Expression Level of Folate Receptor 3.

Folic acid and folate receptors (FOLRs) play an important role in the downregulation of homocysteine (Hcy), a risk factor of Alzheimer's disease, thrombosis, neuropsychiatric illness and fractures. While several studies have reported that FOLR1 and FOLR2 import folic acid into cells, the role of FOLR3 remains unknown. In this study, we evaluated the impact of FOLR3 on the metabolism of Hcy alongside its protective effect against homocysteine-induced neurotoxicity. To reveal the role of FOLR3, we constructed FOLR3-overexpressed HEK293 cells (FOLR3+ cells) and evaluated cell growth, folic acid intake and Hcy-induced neurotoxicity. Subjects with a high expression of FOLR3 exhibited low levels of plasma homocysteine. The ectopic expression of FOLR3 enhanced cell growth, and the enhanced effect was neutralised by folic acid-deficient media. The Western blot analysis revealed that FOLR3 is secreted into cell supernatant. The folic acid intake of FOLR3+ cells was higher than that of wild-type cells. Supernatant from FOLR3+ cells showed a protective effect on Hcy-induced cytotoxicity. FOLR3 expression in plasma is negatively correlated with plasma homocysteine. Our study emphasizes the role of FOLR3 in the intake of folic acid into cells on the one hand and its protective role in Hcy-induced cytotoxicity on the other.

Development of calcium phosphate/calcium sulfate biphasic biomedical material with hyaluronic acid containing collagenase and simvastatin for vital pulp therapy.

OBJECTIVE: In vital pulp therapy (VPT), a barrier is created with appropriate capping to protect the remaining pulp and thus maintain pulp vitality. Here, we evaluated the feasibility of a biphasic calcium phosphate cement (CPC)-calcium sulfate hemihydrate (CSH) biomaterial containing simvastatin (Sim) and collagenase (Col) for VPT. METHODS: Combinations of varying CPC and CSH concentrations were analyzed for their handling properties and setting times, with their structures observed through scanning electron microscopy-energy dispersive X-ray spectrometry (SEM-EDS). Drug release patterns of simvastatin and collagenase combined with CPC-CSH (CPC-CSH-Sim-Col) were also analyzed, followed by biocompatibility and bioactivity tests on human dental pulp stem cells (hDPSCs) and in vivo animal study in canine models; the in vivo results were obtained through microcomputed tomography and histological analysis. RESULTS: The results revealed that 70 wt% CPC (CPC7) with 30 wt% CSH (CSH3) exhibited optimal setting time and porous structure for clinical use. The cell viability and cytotoxicity analysis demonstrated that CPC7-CSH3 with or without simvastatin or collagenase did not injure hDPSCs. In vivo, the CPC7-CSH3-Sim-Col induced dentin bridge formation. SIGNIFICANCE: CPC7-CSH3-Sim-Col in this study has great potential as a VPT biomaterial to enhance the dentin bridge formation.

Red Quinoa Bran Extracts Protects against Carbon Tetrachloride-Induced Liver Injury and Fibrosis in Mice via Activation of Antioxidative Enzyme Systems and Blocking TGF-ß1 Pathway.

The late stages of liver fibrosis are considered to be irreversible. Red quinoa (Chenopodium formosanum Koidz), a traditional food for Taiwanese aborigines, was gradually developed as a novel supplemental food due to high dietary fibre and polyphenolic compounds. Its bran was usually regarded as the agricultural waste, but it contained a high concentration of rutin known as an antioxidant and anti-inflammatory agent. This study is to explore the effect of red quinoa bran extracts on the prevention of carbon tetrachloride (CCl4)-induced liver fibrosis. BALB/c mice were intraperitoneally injected CCl4 to induce liver fibrosis and treated with red quinoa whole seed powder, bran ethanol extracts, bran water extracts, and rutin. In the results, red quinoa powder provided more protection than rutin against CCl4-induced oxidative stress, pro-inflammatory factor expression and fibrosis development. However, the bran ethanol extract with high rutin content provided the most liver protection and anti-fibrosis effect via blocking the tumor necrosis factor alpha (TNF-α)/interleukin 6 (IL-6) pathway and transforming growth factor beta 1 (TGF-ß1) pathway.

Molecular Mechanisms Responsible for Neuron-Derived Conditioned Medium (NCM)-Mediated Protection of Ischemic Brain.

The protective value of neuron-derived conditioned medium (NCM) in cerebral ischemia and the underlying mechanism(s) responsible for NCM-mediated brain protection against cerebral ischemia were investigated in the study. NCM was first collected from the neuronal culture growing under the in vitro ischemic condition (glucose-, oxygen- and serum-deprivation or GOSD) for 2, 4 or 6 h. Through the focal cerebral ischemia (bilateral CCAO/unilateral MCAO) animal model, we discovered that ischemia/reperfusion (I/R)-induced brain infarction was significantly reduced by NCM, given directly into the cistern magna at the end of 90 min of CCAO/MCAO. Immunoblocking and chemical blocking strategies were applied in the in vitro ischemic studies to show that NCM supplement could protect microglia, astrocytes and neurons from GOSD-induced cell death, in a growth factor (TGFß1, NT-3 and GDNF) and p-ERK dependent manner. Brain injection with TGFß1, NT3, GDNF and ERK agonist (DADS) alone or in combination, therefore also significantly decreased the infarct volume of ischemic brain. Moreover, NCM could inhibit ROS but stimulate IL-1ß release from GOSD-treated microglia and limit the infiltration of IL-ß-positive microglia into the core area of ischemic brain, revealing the anti-oxidant and anti-inflammatory activities of NCM. In overall, NCM-mediated brain protection against cerebral ischemia has been demonstrated for the first time in S.D. rats, due to its anti-apoptotic, anti-oxidant and potentially anti-glutamate activities (NCM-induced IL-1ß can inhibit the glutamate-mediated neurotoxicity) and restriction upon the infiltration of inflammatory microglia into the core area of ischemic brain. The therapeutic potentials of NCM, TGFß1, GDNF, NT-3 and DADS in the control of cerebral ischemia in human therefore have been suggested and require further investigation.