Free Shipping on orders over 50$

British Pound Sterling - GBP Euro - EUR US Dollar - USD (EUR)

Welcom to Gentaur Biotech Products!

ELISA Kit for Tumor Necrosis Factor Alpha (TNFa) Organism: Rhesus monkey (Simian)

Be the first to review this product

Availability: In stock


Quick Overview

[#E90133Si] ELISA Kit for Tumor Necrosis Factor Alpha (TNFa) Organism: Rhesus monkey (Simian)


E90133Si | ELISA Kit for Tumor Necrosis Factor Alpha (TNFa) Organism: Rhesus monkey (Simian), 96T
More informations about ELISA Kit for Tumor Necrosis Factor Alpha (TNFa) Organism: Rhesus monkey (Simian) in

Product Tags

Use spaces to separate tags. Use single quotes (') for phrases.

(1) Inhibition of PLA2G4A Reduces the Expression of Lung Cancer-Related Cytokines.[TOP]

Pubmed ID :30328712
Publication Date : //
Phospholipase A2-IVA (PLA2G4A) is the most abundant subtype of cytoplasmic phospholipase A2 (cPLA2) and is an important enzyme in tumor development. Our study aimed to explore the role of PLA2G4A in the regulation of lung cancer. The contents of cell-related cytokines (microsomal prostaglandin E synthase-1 [mPGES], PGE2, and prostacyclin [PGI2]) in A549 cells were analyzed by ELISA kits. Cell counting kit-8 (CCK8) was used to detect the effects of inhibitor of cPLA2 (arachidonyl trifluoromethyl ketone [AACOCF3]) on the proliferation of A549 cells. The migration and invasion of A549 cells were tested by cell scratch wound healing assay and transwell assay, respectively. Real-time quantitative PCR and Western blotting were used to detect the effect of inhibitor AACOCF3 on the expression of related mRNA and protein in A549 cells. ELISA result showed that the levels of mPGES, PGE2, and PGI2 in control group were significantly higher than those in the AACOCF3 group. Cell inhibition rate in the control group was significantly lower than that in the AACOCF3 group. The percentage of wound healing in the control group was significantly higher than that in the AACOCF3 group. Meanwhile, the relative invasive number of cells in the control group was significantly higher than those in the AACOCF3 group. The expression levels of related mRNA of PLA2G4A and cyclooxygenase-2 (COX-2) and the expression levels of mPGES, COX-1, and COX-2 protein in the control group were significantly higher than those in the AACOCF3 group. Our research showed that PLA2G4A was involved in migration and invasion of lung cancer cells.

Authors : Zhang Weiwei, Wang Xiumei, Zhang Liangming, Geng Dongmei, Wang Yanchun, Sun Dengjun, Sui Ping, Zhao Xuan, Xin Chunxia, Jiang Jing, Sui Minghua,

(2) MiR-218 produces anti-tumor effects on cervical cancer cells in vitro.[TOP]

Pubmed ID :30314496
Publication Date : //
As indoleamine-2,3-dioxygenase 1 (IDO1) is critical in tumor immune escape, we determined to study the regulatory mechanism of miR-218 on IDO1 in cervical cancer.

Authors : Zhu Li, Tu Huaidong, Liang Yanmei, Tang Dihong,

(3) CYLD suppression enhances the pro-inflammatory effects and hyperproliferation of rheumatoid arthritis fibroblast-like synoviocytes by enhancing NF-κB activation.[TOP]

Pubmed ID :30285829
Publication Date : //
Rheumatoid arthritis fibroblast-like synoviocytes (RA-FLSs) actively drive joint inflammation and degradation by producing inflammatory cytokines and matrix-degrading molecules, making them key factors in the pathogenesis of RA. Cylindromatosis (CYLD) is a tumor suppressor that downregulates nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation by deubiquitinating NF-κB essential modulator and tumor necrosis factor receptor-associated factors 2 and 6. In this study, we aimed to determine CYLD expression in the synovium of patients with RA, analyze its correlation with NF-κB activation and clinical disease activity, further investigate CYLD expression in RA-FLSs, and explore CYLD's roles and mechanisms in the pro-inflammatory effects, proliferation, apoptosis, and cell cycles of RA-FLSs.

Authors : Zhang Le-Meng, Zhou Jing-Jing, Luo Chun-Lei,

(4) Hydrogen peroxide-induced mitophagy contributes to laryngeal cancer cells survival via the upregulation of FUNDC1.[TOP]

Pubmed ID :30284230
Publication Date : //
The purpose of our study was to investigate an underlying mechanism that hydrogen peroxide-induced mitophagy contributed to laryngeal cancer cells survivals under oxidative stress condition.

Authors : Hui L, Wu H, Wang T-W, Yang N, Guo X, Jang X-J,

(5) HIF-1α promotes inflammatory response of chronic obstructive pulmonary disease by activating EGFR/PI3K/AKT pathway.[TOP]

Pubmed ID :30280794
Publication Date : //
Chronic obstructive pulmonary disease (COPD) is an incomplete, reversible disease with progressive inflammation obstruction in airways. This study aims to explore the regulatory mechanism of hypoxia-inducible factor-1α (HIF-1α) in inflammatory response and progression of COPD.

Authors : Zhang H-X, Yang J-J, Zhang S-A, Zhang S-M, Wang J-X, Xu Z-Y, Lin R-Y,

(6) Intestinal dysbacteriosis activates tumor-associated macrophages to promote epithelial-mesenchymal transition of colorectal cancer.[TOP]

Pubmed ID :30246585
Publication Date : //
In this study we investigated the association between intestinal dysbacteriosis with colorectal cancer progress and the underlying molecular mechanisms. Tumor progression was evaluated using xenograft mice model. The epithelial-mesenchymal transition (EMT) markers were quantified by both real-time PCR and immunoblotting. The serum content of IL-6 and TNF-α were measured with ELISA kits. Cell proliferation was determined by the Cell Counting Kit-8. Intestinal dysbacteriosis was successfully simulated by the administration of a large dose of antibiotics and was demonstrated to promote xenograft tumor growth and induce EMT. Accordingly, the serum concentrations of cytokines IL-6 and TNF-α were significantly increased. Furthermore, the production and secretion of IL-6 and TNF-α were remarkably elevated in macrophages isolated from intestinal dysbiotic mice in comparison with the normal counterparts, and conditioned medium from these was shown to significantly stimulate EMT process in HT29 cells in vitro. Macrophage depletion completely abrogated the pro-tumor effect of intestinal dysbacteriosis. Our results suggest that intestinal dysbacteriosis stimulates macrophage activation and subsequently induces EMT process via secreted pro-inflammatory cytokines IL-6 and TNF-α.

Authors : Wan Guangsheng, Xie Manli, Yu Hongjie, Chen Hongyu,

(7) Sinomenine Regulates Inflammatory Response and Oxidative Stress via Nuclear Factor kappa B (NF-κB) and NF-E2-Related Factor 2 (Nrf2) Signaling Pathways in Ankle Fractures in Children.[TOP]

Pubmed ID :30237391
Publication Date : //
BACKGROUND This study aimed to investigate the effects of SIN on ankle fracture and the underlying mechanisms in MG-63 cells. MATERIAL AND METHODS qRT-PCR and ELISA assay were used to detect the mRNA and protein levels of cytokines in peripheral blood of children with or without ankle fracture. The expression and activity of antioxidant and detoxifying enzymes were detected by ELISA assay. Pretreated MG-63 cells with/without SIN were stimulated with 1 μg/ml bradykinin (BK). A CCK-8 kit was used to detect the cell viability. The cytokines produced from MG-63 cells were detected by Western blotting and qRT-PCR. Moreover, Western blotting was used to detect the levels of p-p38 and p-NF-κB (p65), and the activation level of the Nrf2 signaling pathway was examined by qRT-PCR and Western blotting. RESULTS In this study, we found that compared with the healthy children, the mRNA and protein levels of interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α) were significantly upregulated in children with ankle fracture. In addition, the expression and activity of antioxidant and detoxifying enzymes were imbalanced in children with ankle fracture. SIN treatment did not have a cytotoxic effect on MG-63 cells. SIN dose-dependently suppressed BK-induced upregulation of IL-1β, IL-6, TNF-α, p-p38, and p-NF-κB (p65). Furthermore, SIN dramatically inhibited oxidative stress induced by BK via balancing the expression and activity of antioxidant and detoxifying enzymes and inhibited the activation of Nrf2 signaling. CONCLUSIONS SIN might be a potential agent for the treatment of ankle fracture through reducing inflammatory response and oxidative stress.

Authors : Shen Jie, Yao Rong, Jing Mei, Zhou Zhiyu,

(8) HSCs-derived COMP drives hepatocellular carcinoma progression by activating MEK/ERK and PI3K/AKT signaling pathways.[TOP]

Pubmed ID :30231922
Publication Date : //
Cartilage oligomeric matrix protein (COMP) is known to promote fibrosis in skin, lung and liver. Emerging evidence shows that COMP plays critical roles in tumor development, including breast cancer, colon cancer and hepatocellular carcinoma (HCC). Nevertheless, the role of COMP in HCC proliferation and metastasis and its underlying mechanisms remain fully unclear.

Authors : Li Qing, Wang Cong, Wang Yufeng, Sun Liankang, Liu Zhikui, Wang Liang, Song Tao, Yao Yingmin, Liu Qingguang, Tu Kangsheng,

(9) IL-10 targets Th1/Th2 balance in vascular dementia.[TOP]

Pubmed ID :30229836
Publication Date : //
The pathogenesis of vascular dementia (VD) is not fully elucidated. Th1/Th2 balance may change in VD, leading to numerous inflammatory cytokines secretion. Interleukin-10 (IL-10) is an immune suppressor, while its function in VD and correlation with Th1/Th2 balance are still unclear.

Authors : Liu Q-Q, Zhong D, Zhang X, Li G-Z,

(10) Strontium ion attenuates lipopolysaccharide-stimulated proinflammatory cytokine expression and lipopolysaccharide-inhibited early osteogenic differentiation of human periodontal ligament cells.[TOP]

Pubmed ID :30221352
Publication Date : //
Periodontitis is a chronic inflammatory disease characterized by the destruction of the periodontium. The strontium ion (Sr ) can prevent the bone loss associated with periodontitis and promote the regeneration of the bone. The mechanisms by which the Sr works remain poorly understood. We aim to investigate the effects of the Sr ion on cell proliferation, inflammatory regulation and osteogenic differentiation of human periodontal ligament cells (hPDLCs) in pathological conditions.

Authors : Wei Lingfei, Jiang Yuxi, Zhou Wenjuan, Liu Shutai, Liu Yuelian, Rausch-Fan Xiaohui, Liu Zhonghao,