Search results for: EnzyLight™ Cytotoxicity Assay Kit
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Effects of Salvia miltiorrhiza Polysaccharides on Lipopolysaccharide-Induced Inflammatory Factor Release in RAW264.7 Cells.This study investigated the anti-inflammatory effects and possible underlying mechanisms of Salvia miltiorrhiza polysaccharides (SMP) in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. The cytotoxicity of SMP was detected by the MTT method. The morphological change of RAW264.7 was observed by Diff-Quik staining. Enzyme-linked immunosorbent assay was used to evaluate the production of cytokines in LPS-induced RAW264.7 cells. The nitric oxide (NO) kit assay detected the NO release from LPS-induced RAW264.7 cells. Real-time polymerase chain reaction was used to detect the transcriptions of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), inducible NO synthase (iNOS), and cyclooxygenase (COX)-2 in LPS-induced RAW264.7 cells. The protein expression of nuclear NF-κB was measured by Western blot. The results showed that the safe medication range of SMP was less than 3 mg/mL. Compared with the LPS model group, SMP (2, 1, and 0.5 mg/mL) improved the degree of cell deformation and reduced the amount of pseudopodia, and statistically reduced the secretions of cytokines in cells induced by LPS (P < 0.01) at different time points. SMP significantly inhibited the mRNA transcriptions of TNF-α, IL-6, iNOS, and COX-2 and the protein expressions of NF-κB, p-p65, and p-IκBa. In conclusion, this study preliminarily proved the protective effect of SMP on LPS-induced RAW264.7 macrophage. Its mechanism might be related to inhibition of NF-κB signal pathway and the gene expressions and secretion of cytokines.
2878 related Products with: Effects of Salvia miltiorrhiza Polysaccharides on Lipopolysaccharide-Induced Inflammatory Factor Release in RAW264.7 Cells.Macrophage Colony Stimula Macrophage Colony Stimula TGF beta induced factor 2 Goat Anti-Human Factor XI Human, Allograft Inflamma Insulin promoter factor 1 Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m
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Tormentic acid inhibits IL-1β-induced chondrocyte apoptosis by activating the PI3K/Akt signaling pathway.Interleukin-1β (IL-1β) accelerates degradation of the cartilage matrix and induces apoptosis of chondrocytes. Tormentic acid (TA) is a triterpene isolated from the stem bark of the Vochysia divergens plant, which has been demonstrated to exert in vitro inhibitory activity against hepatocyte apoptosis. However, the effects of TA on IL‑1β‑induced apoptosis of human chondrocytes remain unclear. Therefore, the present study investigated the in vitro effects of TA on human osteoarthritic chondrocyte apoptosis cultivated in the presence of IL‑1β. Human chondrocytes were pretreated with or without various concentrations of TA and then co‑incubated in the absence or presence of IL‑1β for 24 h. Cell viability was determined using the MTT assay, and cell apoptosis was detected using a Nucleosome ELISA kit. Caspase‑3 activity was detected using a caspase‑3 colorimetric assay kit. The levels of B‑cell lymphoma 2 (Bcl‑2)‑associated X protein (Bax), Bcl‑2, phosphorylated (p)‑phosphoinositide 3‑kinase (PI3K), PI3K, p‑protein kinase B (Akt) and Akt were measured by western blotting. The results revealed that pretreatment with TA inhibited IL‑1β‑induced cytotoxicity and apoptosis in chondrocytes. In addition, TA pretreatment increased B‑cell lymphoma (Bcl)‑2 expression, and decreased caspase‑3 activity and Bax expressionin human chondrocytes. In addition, pretreatment with TA markedly increased the expression of p‑PI3K and p‑Akt in IL‑1β‑induced chondrocytes. Collectively, these results indicate that TA inhibits IL‑1β‑induced chondrocyte apoptosis by activating the PI3K/Akt signaling pathway. Therefore, TA may be considered a potential therapeutic target for the treatment of osteoarthritis.
1417 related Products with: Tormentic acid inhibits IL-1β-induced chondrocyte apoptosis by activating the PI3K/Akt signaling pathway.AKT PKB Signaling Phospho Human Epstein-Barr Virus Hh Signaling Pathway Anta Mouse Epstein-Barr Virus AP-1 Reporter – HEK293 Wnt Signaling Pathway TCF BYL-719 Mechanisms: PI3K- Apoptosis antibody array AKT Phospho-Specific Arra AMPK Signaling Phospho-Sp Cancer Apoptosis Phospho- ErbB Her Signaling Phosph
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APRIL promotes non-small cell lung cancer growth and metastasis by targeting ERK1/2 signaling.Non-small-cell lung cancer (NSCLC) is the major subtype of lung cancer, which is the most common cause of cancer-related mortality in the world. It is a complex disease involving multiple genetic alterations. As a cytokine belonging to the Tumor Necrosis Factor-α (TNF- α) family, the - a proliferation-inducing ligand (APRIL) expression and its signaling have been studied in many human solid tumor types, but the data on APRIL signaling in NSCLC are lacking. The aim of this study was to evaluate the APRIL expression and investigate its signaling in NSCLC. The expression of APRIL and its receptors, B cell maturation antigen (BCMA) and transmembrane activator and calcium-modulatorand cyclophilin ligand interactor (TACI), was analyzed by using immunohistochemistry in NSCLC samples. Quantitative RT-PCR was performed to evaluate mRNA expression of APRIL, BCMA and TACI in human lung adenocarcinoma cell lines A549, H1299, and H1650. Cell proliferation was measured by using the cell proliferation and cytotoxicity assay kit 8 (CCK8) assay, cell migration by using wound healing assay, and cell invasion by using transwall assay. The protein level of APRIL, BCMA and TAC, and the activation of extracellular regulated protein kinases 1/2 (ERK1/2) signaling, were determined by western blot. Our results indicated, APRIL and its receptors BCMA and TACI, were overexpressed in most of human NSCLC samples and cell lines; APRIL promoted tumor proliferation, migration and metastasis in A549 and H1299 cells via BCMA and TACI. Furthermore, ERK1/2 activation was involved in APRIL signaling through TACI but not BCMA in A549 and H1299 cells. APRIL might serve as a potential prognostic biomarker for NSCLC, and APRIL related signaling pathway could be a therapeutic target for NSCLC.
2113 related Products with: APRIL promotes non-small cell lung cancer growth and metastasis by targeting ERK1/2 signaling.Non-small cell lung cance Lung non small cell cance Non small cell lung carci Lung small cell carcinoma Multiple lung carcinoma ( Non small cell lung carci Non small cell lung carci Non small cell lung carci Non small cell lung carci Non small cell lung carci IGF-1R Signaling Phospho- Lung cancer tissue array,
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Combination of novel DR5 targeting agonistic scFv antibody TR2-3 with cisplatin shows enhanced synergistic antitumor activity in vitro and in vivo.To investigate the antitumor activity of a novel agonistic single chain fragment variable (scFv) antibody TR2-3 targeting death receptor 5 (DR5) combined with cisplatin in vitro and in vivo.
1391 related Products with: Combination of novel DR5 targeting agonistic scFv antibody TR2-3 with cisplatin shows enhanced synergistic antitumor activity in vitro and in vivo.Interleukin-34 IL34 (N-t Interleukin-34 IL34 anti Proteinase Inhibitor 6 (P Cytokine (Mouse) Antibody Cytokine (Mouse) Antibody Cytokine (Rat) Antibody A Th1 Th2 Th17 (Human) Anti Chemokine (Human) Antibod Cytokine (Human) Antibody Cytokine (Mouse) Antibody Cytokine (Mouse) Antibody Cytokine (Rat) Antibody A
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Deficiency of IL-18 Aggravates Esophageal Carcinoma Through Inhibiting IFN-γ Production by CD8+T Cells and NK Cells.To investigate the potential role of interleukin-18 (IL-18) in immunomodulation during tumorigenesis of esophageal carcinoma and elucidate the underlying molecular mechanism, we employed IL-18 knockout mice for this purpose. Carcinogen 4-nitroquinoline 1-oxide (4NQO) was administrated in drinking water to induce occurrence of esophageal squamous cell carcinoma (ESCC). T cell activation as indicated by the surface CD molecules was analyzed with flow cytometry. The serous content of interferon-γ (IFN-γ) along with other cytokines was determined by inflammatory human cytokine cytometric bead array. The cytotoxicity assay was performed by co-culture of tumor cells with immune cells and relative cell viability was determined by lactate dehydrogenase (LDH) assay. Apoptotic cells were stained with Annexin-V/propidium iodide (PI) and analyzed by flow cytometry. Cell proliferation was measured with Cell Counting Kit-8 (CCK-8) assay. Our data demonstrated that deficiency of IL-18 promoted the progression and development of 4NQO-induced ESCC. Loss of IL-18 suppressed the activation of T cells in the esophagus. Deficiency of IL-18 inhibited the IFN-γ production by CD8+ T cells and natural killer (NK) cells. Absence of IL-18 inhibited the cytotoxicity of CD8+ T cells and NK cell in vitro. Moreover, deficiency of IL-18 promoted the apoptosis of CD8+ T cells and inhibited the proliferation of CD8+ T cells in vitro. Our data elucidated the immunomodulatory role of IL-18 during tumorigenesis of ESCC, whose deficiency compromised antitumor immunity and contributed to immune escape of esophageal carcinoma. Our results also indicated the therapeutic potential of exogenous IL-18 against ESCC, which warrants further investigations.
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Anti-adipogenic effects of the traditional herbal formula Dohongsamul-tang in 3T3-L1 adipocytes.Blood stasis syndrome (BSS) is a general pattern identification and refers to pathological stagnation of blood circulation, dysfunction of endothelial cells or metabolic disorder in traditional Korean medicine (TKM). Dohongsamul-Tang (DHSMT) is a well-known traditional herbal formula which used for treatment and prevention of BSS by promoting blood circulation in TKM.
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Extracts of Cordyceps sinensis inhibit breast cancer cell metastasis via down-regulation of metastasis-related cytokines expression.Cordyceps sinensis is a traditional Chinese medicine and has been used as adjuvant treatments for cancer and it has been also demonstrated to be effective in cancer patients.
1725 related Products with: Extracts of Cordyceps sinensis inhibit breast cancer cell metastasis via down-regulation of metastasis-related cytokines expression.Breast cancer tissue arra Middle advanced stage bre Middle advanced stage bre Mid advanced stage bladde Tissue array of breast ca Breast fibroadenoma tissu Tissue array of breast ca Colon cancer tissue array Colorectal (colon and rec Colorectal (colon and rec Mid advanced stage uterin Middle advanced stage eso
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Diethyl citrate and sodium citrate reduce the cytotoxic effects of nanosized hydroxyapatite crystals on mouse vascular smooth muscle cells.This study aimed to investigate the damage mechanism of nanosized hydroxyapatite (nano-HAp) on mouse aortic smooth muscle cells (MOVASs) and the injury-inhibiting effects of diethyl citrate (Et2Cit) and sodium citrate (Na3Cit) to develop new drugs that can simultaneously induce anticoagulation and inhibit vascular calcification.
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Mechanisms of P-Glycoprotein Modulation by Semen Strychni Combined with Radix Paeoniae Alba.Semen Strychni has been extensively used as a Chinese herb, but its therapeutic window is narrowed by the strong toxicity of the compound, which limits its effectiveness. Radix Paeoniae Alba has been reported to reduce the toxic effects and increase the therapeutic effects of Semen Strychni, but the underlying mechanism remains unknown. This research aimed to explore the mechanism through which P-glycoprotein (P-gp) is modulated by Semen Strychni combined with Radix Paeoniae Alba in vitro. An MTT assay was used to study cytotoxicity in an MDCK-MDR1 cell model. Rh123 efflux and accumulation were measured to assess P-gp function. The expression levels of MDR1 mRNA and P-gp protein in MDCK-MDR1 cells were investigated. A P-gp ATPase activity assay kit was applied to detect the effect on P-gp ATPase activity. Semen Strychni combined with Radix Paeoniae Alba could induce P-gp-mediated drug transport by inhibiting brucine and strychnine transport in MDCK-MDR1 cells, enhancing the P-gp efflux function, upregulating the P-gp expression and MDR1 mRNA levels, and stimulating P-gp ATPase activity.
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Human CD26high T cells elicit tumor immunity against multiple malignancies via enhanced migration and persistence.CD8+ T lymphocytes mediate potent immune responses against tumor, but the role of human CD4+ T cell subsets in cancer immunotherapy remains ill-defined. Herein, we exhibit that CD26 identifies three T helper subsets with distinct immunological properties in both healthy individuals and cancer patients. Although CD26neg T cells possess a regulatory phenotype, CD26int T cells are mainly naive and CD26high T cells appear terminally differentiated and exhausted. Paradoxically, CD26high T cells persist in and regress multiple solid tumors following adoptive cell transfer. Further analysis revealed that CD26high cells have a rich chemokine receptor profile (including CCR2 and CCR5), profound cytotoxicity (Granzyme B and CD107A), resistance to apoptosis (c-KIT and Bcl2), and enhanced stemness (β-catenin and Lef1). These properties license CD26high T cells with a natural capacity to traffic to, regress and survive in solid tumors. Collectively, these findings identify CD4+ T cell subsets with properties critical for improving cancer immunotherapy.
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