BACKGROUND: In this study, we have investigated whether human fetal cartilage progenitor cells (hFCPCs) have antiinflammatory activity and can alleviate osteoarthritis (OA) phenotypes in vitro. METHODS: hFCPCs were stimulated with various cytokines and their combinations and expression of paracrine factors was examined to find an optimal priming factor. Human chondrocytes or SW982 synoviocytes were treated with interleukin-1β (IL-1β) to produce OA phenotype, and co-cultured with polyinosinic-polycytidylic acid (poly(I-C))-primed hFCPCs to address their anti-inflammatory effect by measuring the expression of OA-related genes. The effect of poly(I-C) on the surface marker expression and differentiation of hFCPCs into 3 mesodermal lineages was also examined. RESULTS: Among the priming factors tested, poly(I-C) (1 μg/mL) most significantly induced the expression of paracrine factors such as indoleamine 2,3-dioxygenase, histocompatibility antigen, class I, G, tumor necrosis factor- stimulated gene-6, leukemia inhibitory factor, transforming growth factor-β1 and hepatocyte growth factor from hFCPCs. In the OA model in vitro, co-treatment of poly(I-C)-primed hFCPCs significantly alleviated IL-1b-induced expression of inflammatory factors such as IL-6, monocyte chemoattractant protein-1 and IL-1β, and matrix metalloproteinases in SW982, while it increased the expression of cartilage extracellular matrix such as aggrecan and collagen type II in human chondrocytes. We also found that treatment of poly(I-C) did not cause significant changes in the surface marker profile of hFCPCs, while showed some changes in the 3 lineages differentiation. CONCLUSION These results suggest that poly(I-C)-primed hFCPCs have an ability to modulate inflammatory response and OA phenotypes in vitro and encourage further studies to apply them in animal models of OA in the future.

As authorities braced for the arrival of the Omicron variant of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), infrastructure investments and government directives prompted action in central Viet Nam to establish capacity for genomic surveillance sequencing. From 17 November 2021 to 7 January 2022, the Pasteur Institute in Nha Trang sequenced 162 specimens from 98 150 confirmed SARS-CoV-2 cases in the region collected from 8 November to 31 December 2021. Of these, all 127 domestic cases were identified as the B.1.617.2 (Delta) variant, whereas 92% (32/35) of imported cases were identified as the B.1.1.529 (Omicron) variant, all among international flight passengers. Patients were successfully isolated, enabling health-care workers to prepare for additional cases. Most (78%) of the 32 Omicron cases were fully vaccinated, suggesting continued importance of public health and social measures to control the spread of new variants.

BACKGROUND: Respiratory mucosa defects result in airway obstruction and infection, requiring subsequent functionalrecovery of the respiratory epithelium. Because site-specific extracellular matrix (ECM) facilitates restoration of organfunction by promoting cellular migration and engraftment, previous studies considered decellularized trachea an idealECM; however, incomplete cell removal from cartilage and mucosal-architecture destruction are frequently reported. Here,we developed a decellularization protocol and applied it to the respiratory mucosa of separated porcine tracheas. METHODS: The trachea was divided into groups according to decellularization protocol: native mucosa, freezing–thawing (FT), FT followed by the use of Perasafe-based chemical agents before mucosal separation (wFTP), after mucosalseparation (mFTP), and followed by DNase decellularization (mFTD). Decellularization efficacy was evaluated by DNAquantification and hematoxylin and eosin staining, and ECM content of the scaffold was evaluated by histologic analysisand glycosaminoglycan and collagen assays. Biocompatibility was assessed by cell-viability assay and in vivotransplantation. RESULTS: The mFTP mucosa showed low antigenicity and maintained the ECM to form a proper microstructure.Additionally, tonsil-derived stem cells remained viable when cultured with or seeded onto mFTP mucosa, and the in vivohost response showed a constructive pattern following implantation of the mFTP scaffolds. CONCLUSION These results demonstrated that xenogenic acellular respiratory mucosa matrix displayed suitable biocompatibilityas a scaffold material for respiratory mucosa engineering.

BACKGROUND: Respiratory mucosa defects result in airway obstruction and infection, requiring subsequent functionalrecovery of the respiratory epithelium. Because site-specific extracellular matrix (ECM) facilitates restoration of organfunction by promoting cellular migration and engraftment, previous studies considered decellularized trachea an idealECM; however, incomplete cell removal from cartilage and mucosal-architecture destruction are frequently reported. Here,we developed a decellularization protocol and applied it to the respiratory mucosa of separated porcine tracheas. METHODS: The trachea was divided into groups according to decellularization protocol: native mucosa, freezing–thawing (FT), FT followed by the use of Perasafe-based chemical agents before mucosal separation (wFTP), after mucosalseparation (mFTP), and followed by DNase decellularization (mFTD). Decellularization efficacy was evaluated by DNAquantification and hematoxylin and eosin staining, and ECM content of the scaffold was evaluated by histologic analysisand glycosaminoglycan and collagen assays. Biocompatibility was assessed by cell-viability assay and in vivotransplantation. RESULTS: The mFTP mucosa showed low antigenicity and maintained the ECM to form a proper microstructure.Additionally, tonsil-derived stem cells remained viable when cultured with or seeded onto mFTP mucosa, and the in vivohost response showed a constructive pattern following implantation of the mFTP scaffolds. CONCLUSION These results demonstrated that xenogenic acellular respiratory mucosa matrix displayed suitable biocompatibilityas a scaffold material for respiratory mucosa engineering.

Inflammation is a biological response caused by overactivation of the immune system and is controlled by immune cells via a variety of cytokines. The overproduction of pro-inflammatory cytokines enhances abnormal host immunity, resulting in diseases such as rheumatoid arthritis, cardiovascular disease, Alzheimer's disease, and cancer. Inhibiting the production of pro-inflammatory cytokines such as interleukin (IL)-12p40, IL-6, and tumor necrosis factor (TNF)-α might be one way to treat these conditions. Here, we investigated the anti-inflammatory activity of compounds isolated from Cimicifuga dahurica (Turcz.) Maxim., which is traditionally used as an antipyretic and analgesic in Korea. In primary cell culture assays, 12 compounds were found to inhibit the production of pro-inflammatory cytokines (IL-12p40, IL-6, and TNF-α) in vitro in bone marrow-derived dendritic cells stimulated with LPS.
Alzheimer Disease ; Arthritis, Rheumatoid ; Cardiovascular Diseases ; Cimicifuga ; Cytokines ; Dendritic Cells ; Immune System ; In Vitro Techniques ; Inflammation ; Interleukin-6 ; Interleukins ; Korea ; Primary Cell Culture ; Ranunculaceae ; Tumor Necrosis Factor-alpha

Hangover is characterized by a number of unpleasant physical and mental symptoms that occur after heavy alcohol drinking. In addition, consistently excessive alcohol intake is considered as a major reason causes liver disease. The present study investigated the in vivo effects of DA-5513 (Morning care® Kang Hwang) on biological parameters relevant to hangover relief and alcoholic fatty liver. Blood alcohol and acetaldehyde concentrations were determined in rats administered a single dose of alcohol and treated with DA-5513 or commercially available hangover relief beverages (Yeomyung® and Ukon®). The effects of DA-5513 on alcoholic fatty liver were also determined in rats fed alcohol-containing Lieber-DeCarli diets for 4 weeks. Serum liver function markers (aspartate and alanine aminotransferase activities) and serum/liver lipid levels were assessed. Blood alcohol and acetaldehyde concentrations were lower in the groups treated with DA-5513 or Yeomyung®, as compared with control rats. However, Ukon® did not produce any significant effects on these parameters. Treatment with DA-5513 significantly reduced serum aspartate and alanine aminotransferase activities and markedly reduced serum cholesterol and triglyceride levels, as compared with control rats. Histological observations using Oil Red O staining found that DA-5513 delayed the development of alcoholic fatty liver by reversing hepatic fat accumulation. These findings suggest that DA-5513 could have a beneficial effect on alcohol-induced hangovers and has the potential to ameliorate alcoholic fatty liver.
Acetaldehyde ; Alanine Transaminase ; Alcohol Drinking ; Alcoholics* ; Animals ; Aspartic Acid ; Beverages ; Cholesterol ; Diet ; Fatty Liver, Alcoholic* ; Humans ; Liver ; Liver Diseases ; Metabolism* ; Rats* ; Triglycerides

In this report, we investigated the antioxidant (peroxyl radical-scavenging and reducing capacities) and anti-osteoporotic activities of extracts and isolated constituents (1 - 16) from the rhizomes of Kaempferia parviflora Wall. ex Baker on pre-osteoclastic RAW 264.7 cells. Compound 5 exhibited significant peroxyl radical-scavenging capacity, with TE value of 8.47 ± 0.52 µM, while compound 13 showed significant reducing capacity, with CUPRAC value of 5.66 ± 0.26 µM, at 10.0 µM. In addition, flavonoid compounds 2, 4, 6, 8, 10, 12, and terpene compound 15 showed significant inhibition of tartrate-resistant acid phosphatase (TRAP) in NF-κB ligand-induced osteoclastic RAW 264.7 cells, with values ranging from 16.97 ± 1.02 to 64.67 ± 2.76%. These results indicated that K. parviflora could be excellent sources for the antioxidant and anti-osteoporotic traditional medicinal plants.
Acid Phosphatase ; Osteoclasts ; Plants, Medicinal ; Rhizome* ; Zingiberaceae*

Inflammatory and fibrotic responses are accelerated during the reperfusion period, and excessive fibrosis and inflammation contribute to cardiac malfunction. NecroX compounds have been shown to protect the liver and heart from ischemia-reperfusion injury. The aim of this study was to further define the role and mechanism of action of NecroX-5 in regulating infl ammation and fi brosis responses in a model of hypoxia/reoxygenation (HR). We utilized HR-treated rat hearts and lipopolysaccharide (LPS)-treated H9C2 culture cells in the presence or absence of NecroX-5 (10 µmol/L) treatment as experimental models. Addition of NecroX-5 signifi cantly increased decorin (Dcn) expression levels in HR-treated hearts. In contrast, expression of transforming growth factor beta 1 (TGFβ1) and Smad2 phosphorylation (pSmad2) was strongly attenuated in NecroX-5-treated hearts. In addition, signifi cantly increased production of tumor necrosis factor alpha (TNFα), TGFβ1, and pSmad2, and markedly decreased Dcn expression levels, were observed in LPS-stimulated H9C2 cells. Interestingly, NecroX-5 supplementation effectively attenuated the increased expression levels of TNFα, TGFβ1, and pSmad2, as well as the decreased expression of Dcn. Thus, our data demonstrate potential antiinflammatory and anti-fibrotic effects of NecroX-5 against cardiac HR injuries via modulation of the TNFα/Dcn/TGFβ1/Smad2 pathway.
Animals ; Decorin ; Fibrosis ; Heart* ; Inflammation ; Liver ; Models, Theoretical ; Phosphorylation ; Rats* ; Reperfusion ; Reperfusion Injury ; Transforming Growth Factor beta ; Tumor Necrosis Factor-alpha

Although the antioxidant and cardioprotective effects of NecroX-5 on various in vitro and in vivo models have been demonstrated, the action of this compound on the mitochondrial oxidative phosphorylation system remains unclear. Here we verify the role of NecroX-5 in protecting mitochondrial oxidative phosphorylation capacity during hypoxia-reoxygenation (HR). Necrox-5 treatment (10 microM) and non-treatment were employed on isolated rat hearts during hypoxia/reoxygenation treatment using an ex vivo Langendorff system. Proteomic analysis was performed using liquid chromatography-mass spectrometry (LC-MS) and non-labeling peptide count protein quantification. Real-time PCR, western blot, citrate synthases and mitochondrial complex activity assays were then performed to assess heart function. Treatment with NecroX-5 during hypoxia significantly preserved electron transport chain proteins involved in oxidative phosphorylation and metabolic functions. NecroX-5 also improved mitochondrial complex I, II, and V function. Additionally, markedly higher peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC1alpha) expression levels were observed in NecroX-5-treated rat hearts. These novel results provide convincing evidence for the role of NecroX-5 in protecting mitochondrial oxidative phosphorylation capacity and in preserving PGC1alpha during cardiac HR injuries.
Animals ; Anoxia ; Blotting, Western ; Citric Acid ; Electron Transport ; Heart ; Mitochondria ; Oxidative Phosphorylation* ; Peroxisomes ; Rats ; Real-Time Polymerase Chain Reaction ; Spectrum Analysis