Response of normal human keratinocytes to sulfur mustard (HD): cytokine release using a non-enzymatic detachment procedure

1999 ◽  
Vol 18 (1) ◽  
pp. 1-11 ◽  
Author(s):  
C M Arroyo ◽  
R J Schafer ◽  
E M Kurt ◽  
C A Broomfield ◽  
A J Carmichael
Keyword(s):  
Sulfur Mustard ◽  
Cell Suspensions ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Cytokine Release ◽  
Cell Control ◽  
Variable Effect ◽  
Average Cell ◽  
Tnf Α ◽  
Normal Human

Cytokines play a major role in both acute and chronic inflammatory processes, including those produced by sulfur mustard (HD). This study describes responses of normal human epidermal keratinocyte (NHEK) cells to 2,2′-dichlorodiethyl sulfide, sulfur mustard (HD), defined by interleukin-1 beta (IL-1β), interleukin-6 (IL-6), inter-leukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-α) release. A new method for detaching cell to cell adhesion between keratinocytes has been applied. This method permits the characterization of endogenous fluid from cellular content that could be applied for the development of therapeutic intervention. NHEK (typical average cell density 4.4×106 cells/mL) were exposed to HD (100 and 300 μM) in keratinocyte growth medium (KGM) for 24 h at 37°C in humidified air. Commercially available enzyme-linked immunosorbent assay (ELISA) kits were used to measure the cytokine release in NHEK during exposure to 100 and 300 μM of HD. Exposure to 100 μM HD increased release of cytokines. IL-1β (exposed: 1.41×10-5 pg/ cell±1.60×10-6 pg/cell: control 7.10×10-6 pg/ cell±1.20× 10-6 pg/cell), TNF-α (exposed: 1.06× 10-5 pg/cell±7.3× 10-7 pg/cell; control: 4.04×10-6±2.80×10-7 pg/cell) and IL-8 (exposed: 3.71×10-5 pg/ cell±3.26×10-6 pg/cell; control: 2.99×10-6 pg/cell±8.80×10-7 pg/cell) were significantly enhanced when NHEK cells were detached from culture flasks by non-enzymatic procedures. Cell suspensions of NHEK released low amounts of IL-6 when exposed to 100 μM for 24 h (exposed: 1.47×10-6±1.60×10-7 pg/cell; control: 1.28×10-6± 8.40×10-8 pg/cell). However, cell suspensions of NHEK increased levels of IL-6 after exposure to 300 μM HD (4.67×10-5 pg/cell±3.90×10-6 pg/cell; control: 3.99× 10-6 pg/cell±5.50×10-7 pg/cell). The amount of IL-8 and TNF-α present in cell suspensions increased up to 59-fold and fourfold, respectively, above control levels when NHEK cells were exposed to 300 μM HD. Exposure of NHEK to 300 μM HD had a highly variable effect on the release of IL-1β, where sometimes the secretion of IL-1β increased above baseline level and other times decreased in cell suspensions. Supernatants were collected from cell culture flasks 24 h after exposure of 100 and 300 μM and significantly increased levels of IL-6 were observed. IL-6 was released in a concentration-dependent manner, 3.6- fold up to 8.4-fold, respectively, in supernatant. These proinflammatory mediators IL-1β, IL-8, TNF-α and IL-6 may play an important role in HD injury. The present findings suggest that cytokine changes detected could be used as potential biomarkers of cutaneous vesicant injury.

scholarly journals Anti-inflammatory and Matrix Metallopeptidase-1-Inhibitory Effects of the Cassia obtusifolia L. Seed Extract on Particulate Matter-induced Skin

2021 ◽  
Vol 19 (3) ◽  
pp. 355-363
Author(s):  
Jung-Wook Kang ◽  
In-Chul Lee
Keyword(s):  
Particulate Matter ◽  
Seed Extract ◽  
Enzyme Linked Immunosorbent Assay ◽  
No Production ◽  
Dependent Manner ◽  
Inhibitory Effects ◽  
Cassia Obtusifolia ◽  
Tnf Α ◽  
Matrix Metallopeptidase ◽  
Anti Inflammatory

Purpose: This study aimed to investigate the effects of the Cassia obtusifolia L. seed extract (CSE) on particulate matter (PM)-induced skin.Methods: The effects of CSE on cell viability were evaluated using a skin cell line. To determine the anti-inflammatory effects and matrix metallopeptidase-1 (MMP-1)-inhibitory effects of CSE on PM-induced skin, NO and MMP-1 expressions were measured using an enzyme-linked immunosorbent assay (ELISA) kit. Also, the effects of CSE was investigated the induction of IL-8 and TNF-α treated PM on reconstructed human full thickness skin models.Results: It was observed that CSE decreased NO production in PM-induced RAW 264.7 cells without cytotoxicity. In addition, CSE decreased the expression of MMP-1 in PM-induced cells in a dose-dependent manner. CSE decreased IL-8 and TNF-α production in a PM-reconstructed human skin model.Conclusion: These results indicate that CSE could be used as a cosmetic material to induce anti-inflammation and inhibition of MMP-1 in PM-induced skin.

Angiography significantly decreased serum levels of IL-8 independent of artery stenosis

2020 ◽  
Author(s):  
Lida Zare ◽  
Akram Eidi ◽  
Mohammad Safarian ◽  
Mohammad Kazemi Arababadi
Keyword(s):  
Protective Factor ◽  
Serum Levels ◽  
Artery Stenosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Before And After ◽  
Elisa Technique ◽  
Factor Alpha

Abstract Background Angiography is a safe cardiovascular technique for the diagnosis and treatment of the cardiovascular disorders. The potential effects of angiography on the cytokines are yet to be clarified completely. Interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-α) are the important pro-inflammatory cytokines that participate in the pathogenesis of artery stenosis. The aim of his project was to study the angiography effects on the serum levels of IL-8 and TNF-α. Methods Fifty-five participants in three groups, without, with one and with more than one artery stenosis, were explored in this project. Serum levels of IL-8 and TNF-α were measured in the participants before and after angiography using enzyme linked immunosorbent assay (ELISA) technique. Results Serum levels of IL-8, but not TNF-α, were significantly decreased following angiography. X-ray doses had moderate positive correlation with serum levels of TNF-α in the patients with more than one artery stenosis. Serum levels of IL-8 and TNF-α were not different among male and female participants in all groups. Discussion Angiography may be a protective factor for inflammation in IL-8 dependent manner. Using angiography in the patients with more than one artery stenosis needs to be executed cautiously.

scholarly journals Expression of Cytokine and Chemokine Genes by Human Middle Ear Epithelial Cells Induced by Influenza A Virus and Streptococcus pneumoniae Opacity Variants

2003 ◽  
Vol 71 (8) ◽  
pp. 4289-4296 ◽  
Author(s):  
H. H. Tong ◽  
J. P. Long ◽  
P. A. Shannon ◽  
T. F. DeMaria
Keyword(s):  
Streptococcus Pneumoniae ◽  
Mrna Expression ◽  
Influenza A Virus ◽  
Middle Ear ◽  
Influenza A ◽  
Primary Cultures ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Tnf Α ◽  
Human Middle Ear

ABSTRACT Real-time PCR and enzyme-linked immunosorbent assay were used to evaluate the ability of influenza A virus and Streptococcus pneumoniae opacity variants, either alone or in combination, to induce cytokine and chemokine genes in primary cultures of human middle ear epithelial (HMEE) cells. Following treatment with influenza A virus, the induction of gene expression, which occurred in a dose- and time-dependent manner, was strong for macrophage inflammatory protein 1α (MIP-1α) and MIP-1β; moderate for tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), and IL-8; and weak for IL-1β and monocyte chemotactic peptide 1 (MCP-1). Except for TNF-α, all the gene products were detected in the cell culture supernatants. In contrast, infection of HMEE cells with S. pneumoniae alone induced low levels of mRNA expression of MIP-1α and MIP-1β and did not significantly induce the transcription of the other cytokines and chemokines examined. However, both S. pneumoniae opacity variants increased mRNA expression of MIP-1α, MIP-1β, IL-6, and MCP-1 in HMEE cells activated by a prior influenza A virus infection compared to levels in cells treated with either agent alone. Up-regulation of IL-6, IL-8, and MCP-1 mRNA expression and production by the virus in combination with opaque S. pneumoniae was two- to threefold higher than that induced by the virus combined with the transparent S. pneumoniae variant. These data indicate that the activation of HMEE cells by influenza A virus enhances the induction of cytokine and chemokine gene transcripts by S. pneumoniae and that this effect appears to be most pronounced when S. pneumoniae is in the opaque phase.

scholarly journals Organ Injury and Cytokine Release Caused by Peptidoglycan Are Dependent on the Structural Integrity of the Glycan Chain

2004 ◽  
Vol 72 (3) ◽  
pp. 1311-1317 ◽  
Author(s):  
Anders E. Myhre ◽  
Jon Fredrik Stuestøl ◽  
Maria K. Dahle ◽  
Gunhild Øverland ◽  
Christoph Thiemermann ◽  
...  
Keyword(s):  
Structural Integrity ◽  
Inflammatory Responses ◽  
Ex Vivo ◽  
Organ Injury ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cytokine Release ◽  
Ex Vivo Model ◽  
Glycan Chain ◽  
Tnf Α ◽  
Glutamyl Transferase

ABSTRACT Several studies have implicated a role of peptidoglycan (PepG) as a pathogenicity factor in sepsis and organ injury, in part by initiating the release of inflammatory mediators. We wanted to elucidate the structural requirements of PepG to trigger inflammatory responses and organ injury. Injection of native PepG into anesthetized rats caused moderate but significant increases in the levels of alanine aminotransferase, aspartate aminotransferase, γ-glutamyl transferase, and bilirubin (markers of hepatic injury and/or dysfunction) and creatinine and urea (markers of renal dysfunction) in serum, whereas PepG pretreated with muramidase to digest the glycan backbone failed to do this. In an ex vivo model of human blood, PepG containing different amino acids induced similar levels of the cytokines tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), IL-8, and IL-10, as determined by plasma analyses (enzyme-linked immunosorbent assay). Hydrolysis of the Staphylococcus aureus cross-bridge with lysostaphin resulted in moderately reduced release of TNF-α, IL-6, IL-8, and IL-10, whereas muramidase digestion nearly abolished the ability to induce cytokine release and IL-6 mRNA accumulation in CD14+ monocytes compared to intact PepG. However, additional experiments showed that muramidase-treated PepG synergized with lipopolysaccharide to induce TNF-α and IL-10 release in whole blood, despite its lack of inflammatory activity when administered alone. Based on these studies, we hypothesize that the structural integrity of the glycan chain of the PepG molecule is very important for the pathogenic effects of PepG. The amino acid composition of PepG, however, does not seem to be essential for the inflammatory properties of the molecule.

Effects of Sulfur Mustard on Cytokines Released from Cultured Human Epidermal Keratinocytes

1998 ◽  
Vol 17 (3) ◽  
pp. 223-229 ◽  
Author(s):  
Elien M. Kurt ◽  
Robert J. Schafer ◽  
Carmen M. Arroyo
Keyword(s):  
Sulfur Mustard ◽  
Cell Types ◽  
Epidermal Keratinocytes ◽  
Cytokine Release ◽  
Experimental Conditions ◽  
Human Epidermal Keratinocytes ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Cytokine Levels ◽  
Factor Alpha

The release of the cytokines interleukin (IL)-1α, IL-1β, IL-6, IL-8, and tumor necrosis factor alpha (TNF-α was measured from epiderm alkeratinocytes in an attempt to characterize the immunologic response in keratinocytes following exposure to bis (2-chloroethyl)sulfide (sulfur mustard, HD). Enzyme-linked immunosorbentassay (ELISA) was used to measure cytokine levels in adult and neonatal culture human epidermal keratinocytes (HEK) 3 h after exposure to 0.50 and 1.0 m M HD. A two-way analysis of variance was carried out for cell type and HD concentration. That analysis showed significant differences between cell types for IL-1α and IL-1β(p =.001 and p =.015, respectively). In both of these cytokines, release in neonatal HEK decreased less than in adult HEK. A significant effectof HD concentration was shown only for IL-1β (P <.001), with cytokine release decreasing with increasing HD dose. In addition, a significant cell donor type by HD concentration interaction effect was found for IL-1β under the experimental conditions described in materials and methods. With increasing HD concentration, the relative decrease in cytokine release was much greater for adult than for neonatal HEK.

Protective effects of diosmetin extracted from Galium verum L. on the thymus of U14-bearing mice

2011 ◽  
Vol 89 (9) ◽  
pp. 665-673 ◽  
Author(s):  
Rui Zhao ◽  
Zhibao Chen ◽  
Guiyan Jia ◽  
Jian Li ◽  
Yaping Cai ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Growth ◽  
Serum Levels ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Proliferation Assay ◽  
Cell Proliferation Assay ◽  
Tnf Α ◽  
Thymus Tissue ◽  
Tgf Β1

Diosmetin (DGVL) extracted from the traditional Chinese herb Galium verum L. has been found to have anticancer activity. In this study, the effects of DGVL on the thymus of U14-bearing mice were investigated. Using flow cytometry, peripheral blood lymphocytes were characterized based on the expression of surface markers for T helper cells (CD4+) and T suppressor cells (CD8+). Serum levels of tumor necrosis factor α (TNF-α), interleukin-2 (IL-2), IL-10, and transforming growth factor β1 (TGF-β1) and a cell proliferation assay were determined with an enzyme-linked immunosorbent assay. The expression of Fas and Fas ligand (FasL) on the thymus was determined by Western blotting. Our results showed that DGVL inhibited tumor growth and significantly increased the thymus weight compared with the control. Also, DGVL elevated serum levels of IL-2 and significantly reduced levels of TNF-α, TGF-β1, and IL-10 in a dose-dependent manner. Histological study and terminal dUTP nick end labeling staining results showed that DGVL protected thymus tissue against the onslaught of tumor growth by inhibiting thymus lymphocyte apoptosis. The cell proliferation assay revealed that DGVL might promote more thymus lymphocytes towards proliferation. Furthermore, the ratio of CD4+/CD8+ T lymphocytes was significantly increased from 0.69 to 2.29 by treatment with DGVL. Immunoblotting analyses revealed that the expression of Fas and FasL on the thymus was lower in mice in the DGVL treatment group than in the control mice. In conclusion, DGVL can inhibit tumor growth and protect tumor-induced apoptosis of the thymus, and the mechanism is closely associated with reduced cell death in the thymus and a Fas–FasL-dependent pathway.

scholarly journals Eleutheroside K Isolated from Acanthopanax henryi (Oliv.) Harms Inhibits the Expression of Virulence-Related Exoproteins in Methicillin-Resistant Staphylococcus aureus

2021 ◽  
Author(s):  
Qian-Qian Li ◽  
Jiao Luo ◽  
Xiang-Qian Liu ◽  
Ok-Hwa Kang ◽  
Dong-Yeul Kwon
Keyword(s):  
Virulence Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Methicillin Resistant ◽  
Innovative Strategy ◽  
Expression Of Genes ◽  
Tnf Α ◽  
Single Compound ◽  
Mrsa Infection ◽  
Dose Dependent

AbstractMethicillin-resistant Staphylococcus (S.) aureus (MRSA) is a representative pathogen that produces numerous virulence factors involving manifold cytotoxins and exotoxins. The present study was designed to investigate the influence of Eleutheroside K (ETSK), a single compound isolated from the leaves of Acanthopanax (A.) henryi (Oliv.) Harms, on the exotoxins secreted by MRSA. The transcription and translation of the exotoxins (α-hemolysin and staphylococcal enterotoxins) related to virulence in S. aureus were determined via quantitative RT-PCR and western blot analysis. The effect of ETSK on the production of tumor necrosis factor (TNF)-α was evaluated using enzyme-linked immunosorbent assay. As a result, ETSK at sub-MIC concentrations could reduce the protein expression of α-hemolysin and enterotoxin, and the expression of genes that regulate virulence factors was also inhibited. In addition, the TNF-inducing activity of S. aureus was attenuated by ETSK in a dose-dependent manner. These results revealed that ETSK not only reduced the protein and gene expression levels of related exotoxins but also suppressed the ability of S. aureus to induce macrophages to release cytokines. This study indicated that the inhibition of MRSA infection by ETSK may be achieved by reducing the virulence of S. aureus and highlighted the potential of ETSK as an innovative strategy for the prevention and treatment of MRSA infections.

scholarly journals Ruscogenin alleviates palmitic acid-induced endothelial cell inflammation by suppressing TXNIP/NLRP3 pathway

2020 ◽  
Vol 19 (8) ◽  
pp. 1605-1610
Author(s):  
Hongtao Liu ◽  
Simin Zheng ◽  
Hongfei Xiong ◽  
Xiaoli Niu
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cardiovascular Diseases ◽  
Palmitic Acid ◽  
Umbilical Vein ◽  
Intercellular Adhesion Molecule ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Intercellular Adhesion Molecule 1 ◽  
Tnf Α

Purpose: To investigate the involvement of ruscogenin in palmitic acid (PA)-induced endothelial cell inflammation. Method: Cultured human umbilical vein endothelial cells (HUVECs) were divided into five groups: control (normal untreated cells), PA (cell treated with palmitic acid), and PA + ruscogenin (1, 10, or 30 μM). Cell viability and apoptosis rate were determined using MTT (3-(4,5)-dimethylthiahiazo(-z-y1)-3,5- di-phenytetrazolium bromide) and flow cytometry assays, respectively. The levels of cytokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), intercellular adhesion molecule-1 (ICAM-1), and monocyte chemo-attractant protein-1 (MCP-1) were determined by an enzyme-linked immunosorbent assay. Western blotting and real-time polymerase chain reaction (RT-PCR) were used to evaluate the underlying mechanisms of action. Results: PA treatment decreased the viability of HUVECs and induced apoptosis (p < 0.05). Ruscogenin attenuated PA-induced cell death in a dose-dependent manner (p < 0.05). On the other hand, PA induced an increase in IL-1β, TNF-α, ICAM-1, MCP-1, TXNIP (thioredoxin-interacting protein),as well as NLRP3 (nucleotide oligomerization domain-, leucine-rich repeat- and pyrin domain-containing protein 3), all of which were attenuated by ruscogenin (p < 0.05). Conclusion: Ruscogenin alleviates PA-induced endothelial cell inflammation via TXNIP/NLRP3 pathway, thereby providing an insight into new therapeutic strategies to treat cardiovascular diseases. Keywords: Ruscogenin, Palmitic acid, Endothelial cells, Inflammation, TXNIP, NLRP3, Cardiovascular diseases

scholarly journals Saussurea lappa Clarke extract exhibits potent antioxidant effect and attenuates neuroinflammatory responses in lipopolysaccharide-stimulated microglial cells

2020 ◽  
Vol 19 (9) ◽  
pp. 1911-1917
Author(s):  
Sung-Gyu Lee ◽  
Hyun Kang
Keyword(s):  
Nitric Oxide ◽  
Radical Scavenging Activity ◽  
Antioxidant Properties ◽  
Radical Scavenging ◽  
Enzyme Linked Immunosorbent Assay ◽  
No Production ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Saussurea Lappa ◽  
Tnf Α

Purpose: To investigate the antioxidant and anti-neuroinflammatory potential of Saussurea lappa Clarke (SLC-EA) extract in LPS-stimulated BV-2 microglial cells.Methods: Cell viability was measured by using the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay while antioxidant activity was evaluated by using the DPPH (1,1-diphenyl-2-picrylhydrazyl) radical scavenging activity. Lipopolysaccharide (LPS) was used to stimulate BV-2 microglia. Griess assay was employed to assess nitric oxide (NO) production. iNOS (inducible NO synthase) expression and TNF-α (tumor necrosis factor-alpha) cytokine production were measured by ELISA (enzyme-linked immunosorbent assay) and immuno blot analysis, respectively.Results: Pretreatment of 100 mg/ml of SLC-EA (p < 0.001) was inhibited Nitric Oxide (NO) by 1 ug/ml of LPS-treated murine BV-2 cells. The expression of iNOS and TNF-α were reduced by SLC-EA concentration dependent manner (p < 0.001 at 100 mg/ml). SLC-EA were scavenged 1, 1-diphenyl-2-picrylhydrazyl (DPPH) radicals in a dose-dependent manner with an IC50 value of approximately 51.4 μg/ml.Conclusion: The results indicate that SLC-EA extract exhibits strong antioxidant properties and inhibits excessive pro-inflammatory cytokine due probably to the antioxidant phenolic compounds present in SLC-EA extract. Further work in exploring the in-depth mechanisms of SLC-EA extract in regulating inflammatory signaling pathways in treating neuroinflammatory diseases is necessary. Keywords: Saussurea lappa, Antioxidant, Neuroinflammation, Microglia, TNF-α, iNOS

scholarly journals The Acidic Fraction of Isatidis Radix Regulates Inflammatory Response in LPS-Stimulated RAW264.7 Macrophages through MAPKs and NF-κB Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Zhenyu Fan ◽  
Liangliang Cai ◽  
Yage Wang ◽  
Qiuyan Zhu ◽  
Shengnan Wang ◽  
...  
Keyword(s):  
Sore Throat ◽  
Mechanism Of Action ◽  
Inflammatory Activity ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Raw264.7 Macrophages ◽  
Tnf Α ◽  
Acidic Fraction ◽  
Cox 2 ◽  
Anti Inflammatory

Isatidis Radix, the dried root of Isatidis indigotica Fort, is a traditional heat-clearing and detoxicating herb, which has the antiviral and anti-inflammatory activity and immune regulation. It has been widely used to treat cold, fever, sore throat, mumps, and tonsillitis in clinics. A previous study demonstrated that the acidic fraction of Isatidis Radix (RIAF) had strong anti-inflammatory activity, but the mechanism of action was not well elucidated. Lipopolysaccharide- (LPS-) induced RAW264.7 cells were employed to observe the anti-inflammatory activity of RIAF. The level of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), nitric oxide (NO), prostaglandin E2 (PGE2), and interleukin-6 (IL-6) was determined by enzyme-linked immunosorbent assay kits. Western blot was performed to quantify the expression of extracellular signal-regulated kinase (ERK) 1/2, c-jun NH2-termianl kinase (JNK), p38, inducible NO synthetase (iNOS), cyclooxygenase (COX)-2, andnuclear factor-κB (NF-κB). Immunofluorescence assay and electrophoretic mobility shift assay (EMSA) were used to quantify the translocation and the binding-DNA activity of NF-κB. RIAF could inhibit the secretion of inflammatory cytokines (PGE2, IL-6, IL-1β, and NO, other than TNF-α) in a dose-dependent manner. Further investigation showed that the expression of iNOS and COX-2 induced by LPS were downregulated by treatment with RIAF. Meanwhile, data from the signal pathway exhibited that RIAF significantly suppressed the phosphorylation of ERK1/2, JNK, and p38 and reduced the translocation of NF-κB from the cytoplasm to nucleus, as well as the binding-DNA activity. The anti-inflammatory mechanism of action of RIAF was to reduce inflammation-associated gene expression (iNOS, COX-2, IL-1β, IL-6) by regulating the phosphorylation of the mitogen-activated protein kinases (MAPK) pathway and interventing the activation of the NF-κB pathway, which partly illustrated the basis of treatment of Isatidis Radix on cold, fever, sore throat, mumps, and tonsillitis in clinics.

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