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ELISA Kit for Monocyte Chemotactic Protein 1 (MCP1) Organism: Rhesus monkey (Simian)

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[#E90087Si] ELISA Kit for Monocyte Chemotactic Protein 1 (MCP1) Organism: Rhesus monkey (Simian)


E90087Si | ELISA Kit for Monocyte Chemotactic Protein 1 (MCP1) Organism: Rhesus monkey (Simian), 96T
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(1) The role of NOX2-derived reactive oxygen species in collagenase-induced osteoarthritis.[TOP]

Pubmed ID :30195046
Publication Date : //
Synovitis in collagenase-induced osteoarthritis (CiOA) is driven by locally released S100A8/A9 proteins and enhances joint destruction. S100A8/A9 can induce reactive oxygen species (ROS) release by phagocytes in OA synovium via neutrophil cytosolic factor-1 (Ncf1)-regulated NOX2 activation. In the present study we investigated whether NOX2-derived ROS affect joint pathology during CiOA.

Authors : van Dalen S C M, Kruisbergen N N L, Walgreen B, Helsen M M A, Slöetjes A W, Cremers N A J, Koenders M I, van de Loo F A J, Roth J, Vogl T, Blom A B, van der Kraan P M, van Lent P L E M, van den Bosch M H J,

(2) Inhibition of C-X-C Motif Chemokine 10 (CXCL10) Protects Mice from Cigarette Smoke-Induced Chronic Obstructive Pulmonary Disease.[TOP]

Pubmed ID :30118441
Publication Date : //
BACKGROUND Chronic obstructive pulmonary disease (COPD) is a type of obstructive lung disease characterized by long-term breathing problems and poor airflow. COPD can progress to persistent decline of pulmonary function. This study explored the effect of CXCL10 on COPD induced by cigarette smoke (CS) and its underlying mechanism. MATERIAL AND METHODS Wild-type (WT) mice were randomly assigned into 3 groups: the control group, the CS group, and the intervention group. Mice in the CS group were exposed to CS and mice in the CXCL10 group were exposed to CS and CXCL10 neutralizing antibody. At 24 h after the last CS exposure, body weight and lung functions of each mouse were recorded. Mice were then anesthetized for collecting bronchoalveolar lavage fluid (BALF) and lung tissues. Levels of interleukin-6 (IL-6), keratinocyte chemotactic factor (KC), and monocyte chemoattractant protein-1 (MCP-1) in supernatant and lung homogenate were detected by ELISA and real-time PCR (RT-PCR), respectively. For in vitro experiments, human bronchial epithelial cells 16HBE were stimulated with different concentrations of cigarette smoke extract (CSE) and CXCL10. Cell viability and levels of inflammatory cytokines in the cell supernatant were detected by Cell Counting Kit-8 (CCK-8) and ELISA assay, respectively. RESULTS Our data showed significant weight loss and reduction of lung functions in mice in the CS group compared with those in the control group and intervention group. Increased levels of IL-6, KC, and MCP-1 in BALF and lung homogenate were observed in mice in the model group compared to those in the control group and intervention group. In vitro experiments also confirmed that CXCL10-neutralizing antibody can inhibit CSE-induced cell necrosis and activation of inflammatory cytokines. CONCLUSIONS Inhibited CXCL10 protects against COPD progression by decreasing secretion of inflammatory factors, which provides a new direction for the clinical prevention and treatment of COPD.

Authors : Jing Hongyu, Liu Lingyun, Zhou Junfeng, Yao Hanxin,

(3) Zedoarondiol Attenuates Endothelial Cells Injury Induced by Oxidized Low-Density Lipoprotein via Nrf2 Activation.[TOP]

Pubmed ID :30064139
Publication Date : //
Zedoarondiol, a sesquiterpene lactone compound, showed an anti-proliferative activity on vascular smooth muscle cells in our previous study. However, whether it has a beneficial effect on endothelial cells injury induced by oxidized low-density lipoprotein (ox-LDL) remains unclear. This study was designed to investigate the protective effect of zedoarondiol on ox-LDL-induced injury of endothelial cells and explored its underlying mechanism.

Authors : Mao Huimin, Tao Tianqi, Wang Xiaoren, Liu Mi, Song Dandan, Liu Xiuhua, Shi Dazhuo,

(4) Tumour necrosis factor-related apoptosis-inducing ligand expression in patients with diabetic nephropathy.[TOP]

Pubmed ID :29999450
Publication Date : //
The objective of this study was to evaluate the expression profile of tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) in patients with diabetic nephropathy (DN).

Authors : Chang Wei-Wei, Liang Wei, Yao Xin-Ming, Zhang Liu, Zhu Li-Jun, Yan Chen, Jin Yue-Long, Yao Ying-Shui,

(5) [Methyltransferase-like 3 Promotes the Proliferation of Acute Myeloid Leukemia Cells by Regulating N6-methyladenosine Levels of MYC].[TOP]

Pubmed ID :29978784
Publication Date : //
Objective To investigate the role of methyltransferase-like 3(METTL3) in the proliferation of acute myeloid leukemia (AML) cells and its mechanism. Methods METTL3 expression in AML patients was analyzed in Gene Expression Omnibus data files. METTL3 expression was inhibited by lentivirus-mediated gene transduction in MOLM13 cells,after which cell proliferation was analyzed by cell counting kit-8,N6-methyladenosine (m6A) levels of total mRNA was analyzed by ELISA,specific m6A on MYC was analyzed by gene-specific m6A RNA immunoprecipitation,and MYC expression was analyzed by RT-qPCR and Western blot analysis. Results METTL3 level was slightly increased in AML-M5 patients,and its expression was significantly higher in immature cells than in mature monocytes (t=4.504,P=0.0098). METTL3 knock-down significantly suppressed cell proliferation (P<0.001),reduced m6A level of total mRNA (t=3.606,P=0.042) and specific m6A level on MYC mRNA (P<0.01),and suppressed MYC expression (P<0.01). Conclusion METTL3 acts as an oncogene in MOLM13 cells by upregulating MYC expression.

Authors : Wang Xiao-Shuang, He Jin-Rong, Yu Shan, Yu Jia,

(6) Investigation of Immune-Regulatory Effects of Mageumsan Hot Spring via Protein Microarray .[TOP]

Pubmed ID :29853747
Publication Date : //
Empirical evidences for efficacy of hot spring (HS) water in inflammatory skin disorders have not been substantiated with sufficient, immunological "hard evidence". HS water, characterized by its weakly-alkaline properties and low total dissolved solids content, has been known to alleviate various immune-inflammatory skin diseases, including atopic dermatitis (AD).

Authors : Hahn Hyung Jin, Kim Jung Soo, Kim Yeong Ho, Lee Young Bok, Yu Dong Soo, Kim Jin-Wou,

(7) Lowering the n-6/n-3 PUFAs ratio inhibits the formation of THP-1 macrophage-derived foam cell.[TOP]

Pubmed ID :29801502
Publication Date : //
The balance between n-6 and n-3 PUFAs is an important determinant in the risk for cardiovascular disease. The study was to investigate the influence of the n-6 and n-3 PUFAs ratio on the formation of THP-1 monocyte-derived foam cells and explore the probable mechanism of anti-atherosclerosis.

Authors : Song Zhixiu, Xia Hui, Yang Ligang, Wang Shaokang, Sun Guiju,

(8) Modulation the crosstalk between tumor-associated macrophages and non-small cell lung cancer to inhibit tumor migration and invasion by ginsenoside Rh2.[TOP]

Pubmed ID :29783929
Publication Date : //
Tumor-associated macrophages (TAMs) play a critical role in modulating the tumor microenvironment and promote tumor metastases. Our studies have demonstrated that ginsenoside Rh2 (G-Rh2), a monomeric compound extracted from ginseng, is a promising anti-tumor agent in lung cancer cells. However, it remains unclear whetherG-Rh2 can modulate the differentiation of TAMs and its interaction with tumor microenvironment. In this study, we investigated how G-Rh2 regulates the phenotype of macrophages and affects the migration of non-small cell lung cancer (NSCLC) cells.

Authors : Li Honglin, Huang Nan, Zhu Weikang, Wu Jianchun, Yang Xiaohui, Teng Wenjing, Tian Jianhui, Fang Zhihong, Luo Yingbin, Chen Min, Li Yan,

(9) Puerarin prevents vascular endothelial injury through suppression of NF-κB activation in LPS-challenged human umbilical vein endothelial cells.[TOP]

Pubmed ID :29775893
Publication Date : //
In the present study, we aimed to explore the effects of puerarin on vascular endothelial cell injury induced by lipopolysaccharide (LPS) and its underlying mechanisms.

Authors : Deng Hua-Fei, Wang Sha, Li Lian, Zhou Qin, Guo Wan-Bei, Wang Xiao-Li, Liu Mei-Dong, Liu Ke, Xiao Xian-Zhong,

(10) Hydrogen sulfide exposure induces NLRP3 inflammasome-dependent IL-1β and IL-18 secretion in human mononuclear leukocytes .[TOP]

Pubmed ID :29744188
Publication Date : //
The aim was to investigate if hydrogen sulfide (HS) induces the formation of the NLRP3 inflammasome and subsequent IL-1β and IL-18 secretion in human peripheral blood mononuclear cells (PBMCs) and in the human monocyte cell line THP1. Bacterial production of HS has been suggested to participate in the inflammatory host response in periodontitis pathogenesis. HS is a toxic gas with pro-inflammatory properties. It is produced by bacterial degradation of sulfur-containing amino acids, for example, cysteine. We hypothesize that HS affects the inflammatory host response by inducing formation of the NLRP3 inflammasome and thereby causes the secretion of IL-1ß and IL-18. PBMCs from eight healthy blood donors, the human monocyte cell line THP1 Null, and two variants of the THP1 cell line unable to form the NLRP3 inflammasome were cultured in the presence or absence of 1 mM sodium hydrosulfide (NaHS) in 24-well plates at 37°C for 24 hr. Supernatants were collected and the IL-1β and IL-18 concentrations were measured with DuoSet ELISA Development kit. PBMCs exposed to NaHS produced more IL-1ß and IL-18 than unexposed control cells ( = .023 and  = .008, respectively). An increase of extracellular potassium ions (K) inhibited the secretion of IL-1ß and IL-18 ( = .008). Further, NaHS triggered the secretion of IL-1ß and IL-18 in human THP1-Null monocytes ( = .0006 and  = .002, respectively), while the NaHS-dependent secretion was reduced in the monocyte cell lines unable to form the NLRP3 inflammasome. Hence, the results suggest that NaHS induces the formation of the NLRP3 inflammasome and thus the secretion of IL-1ß and IL-18. Enhanced NLRP3 inflammasome-dependent secretion of IL-1β and IL-18 in human mononuclear leukocytes exposed to NaHS is reported. This may be a mode for HS to contribute to the inflammatory host response and pathogenesis of periodontal disease.

Authors : Basic Amina, Alizadehgharib Sara, Dahlén Gunnar, Dahlgren Ulf,