scholarly journals Crocetin Downregulates the Proinflammatory Cytokines in Methylcholanthrene-Induced Rodent Tumor Model and Inhibits COX-2 Expression in Cervical Cancer Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Bing Chen ◽  
Zhao-Hui Hou ◽  
Zhe Dong ◽  
Chun-Dong Li
Keyword(s):  
Cervical Cancer ◽  
Interleukin 1 ◽  
Mrna Level ◽  
Tumor Model ◽  
Uterine Cervical Cancer ◽  
Polymorphonuclear Cells ◽  
Cervical Cancer Cells ◽  
Cox 2 ◽  
Oxide Synthase ◽  
Necrosis Factor

The effect of crocetin (C20H24O4) on methylcholanthrene- (MCA-) induced uterine cervical cancer in mice was studied in this paper. After the mice were treated orally with crocetin, maleic dialdehyde (MDA), polymorphonuclear cells (PMN), interleukin-1β(IL-1β), and tumor necrosis factor-α(TNF-α) were examined by ELISA or immunohistochemistry. The inducible nitric oxide synthase (iNOS) activation inHeLacells was analyzed using fluorescence microscopy for light microscopic examination. The MCA mice showed a significant increase in plasma MDA, PMN, IL-1β, TNF-α, and nitrates levels. At the same time, the mRNA level of COX-2 inHeLacells was also significantly increased. These changes were attenuated by crocetin supplementation in the MCA mice. Crocetin supplementation in the MCA mice also showed protection against cervical cancer. These results suggest that crocetin may act as a chemopreventive and an anti-inflammatory agent.

scholarly journals Granulocyte Macrophage-Colony Stimulating Factor (GM-CSF) Downregulates the Expression of Protumor Factors Cyclooxygenase-2 and Inducible Nitric Oxide Synthase in a GM-CSF Receptor-Independent Manner in Cervical Cancer Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Nanyan Jiang ◽  
Zhiqiang Tian ◽  
Jun Tang ◽  
Rongying Ou ◽  
Yunsheng Xu
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Inos Expression ◽  
Independent Manner ◽  
Gm Csf ◽  
Cervical Cancer Cells ◽  
Cox 2 ◽  
Macrophage Colony ◽  
Cancer Tissues ◽  
Oxide Synthase

Enhanced expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) is associated with the pathogenic processes of various tumor types. COX-2 and iNOS expression in the immunomodulatory dendritic cells is mediated by the granulocyte macrophage-colony stimulating factor (GM-CSF), which is also expressed by cervical cancer cells; however, whether and how GM-CSF regulates COX-2 and iNOS expression in clinical cervical cancer cells remain unknown. In this study, we found that the COX-2 and iNOS expression was upregulated in the cervical cancer tissues and positively correlated with cancer metastasis and stage. About one-half of the cervical cancer tissues showed strong/moderate GM-CSF expression, while the normal cervical tissues showed >80% positive rate; no GM-CSFR protein was detectable on the cervical cancer cells. The GM-CSF expression was negatively correlated with the COX-2 and iNOS expression in the cervical cancer tissues and the functional negative regulatory effect of GM-CSF on COX-2/iNOS expression was demonstrated in various cervical cancer cell lines. Therefore, in cervical cancer cells, GM-CSF might contribute an antitumor response by inhibiting iNOS and COX-2 expression in a GM-CSFR independent manner.

scholarly journals Diethylcarbamazine Attenuates the Development of Carrageenan-Induced Lung Injury in Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Edlene Lima Ribeiro ◽  
Karla Patricia de Souza Barbosa ◽  
Ingrid Tavares Fragoso ◽  
Mariana Aragão Matos Donato ◽  
Fabiana Oliveira dos Santos Gomes ◽  
...  
Keyword(s):  
Acute Inflammation ◽  
Pleural Cavity ◽  
Interleukin 1 ◽  
Polymorphonuclear Cells ◽  
Inflammation Markers ◽  
Acute Lung Inflammation ◽  
Anti Inflammatory ◽  
Oxide Synthase ◽  
Necrosis Factor ◽  
Inducible Nitric Oxide

Diethylcarbamazine (DEC) is an antifilarial drug with potent anti-inflammatory properties as a result of its interference with the metabolism of arachidonic acid. The aim of the present study was to evaluate the anti-inflammatory activity of DEC in a mouse model of acute inflammation (carrageenan-induced pleurisy). The injection of carrageenan into the pleural cavity induced the accumulation of fluid containing a large number of polymorphonuclear cells (PMNs) as well as infiltration of PMNs in lung tissues and increased production of nitrite and tumor necrosis factor-αand increased expression of interleukin-1β, cyclooxygenase (COX-2), and inducible nitric oxide synthase. Carrageenan also induced the expression of nuclear factor-κB. The oral administration of DEC (50 mg/Kg) three days prior to the carrageenan challenge led to a significant reduction in all inflammation markers. The present findings demonstrate that DEC is a potential drug for the treatment of acute lung inflammation.

scholarly journals Natural Compound Modulates the Cervical Cancer Microenvironment—A Pharmacophore Guided Molecular Modelling Approaches

2018 ◽  
Vol 7 (12) ◽  
pp. 551 ◽  
Author(s):  
Shailima Rampogu ◽  
Doneti Ravinder ◽  
Smita Pawar ◽  
Keun Lee
Keyword(s):  
Cervical Cancer ◽  
Md Simulations ◽  
Data Bank ◽  
Docking Studies ◽  
New Drugs ◽  
Binding Modes ◽  
Cervical Cancer Cells ◽  
Causative Agents ◽  
Nitric Oxide Synthase 2 ◽  
Oxide Synthase

Cervical cancer is regarded as one of the major burdens noticed in women next to breast cancer. Although, human papilloma viruses (HPVs) are regarded as the principal causative agents, they require certain other factors such as oestrogen hormone to induce cervical cancer. Aromatase is an enzyme that converts androgens into oestrogens and hindering this enzyme could subsequently hamper the formation of oestrogen thereby alleviating the disease. Accordingly, in the current investigation, a structure based pharmacophore was generated considering two proteins bearing the Protein Data Bank (PDB) codes 3EQM (pharm 1) and 3S7S (pharm 2), respectively. The two models were employed as the 3D query to screen the in-house built natural compounds database. The obtained 51 compounds were escalated to molecular docking studies to decipher on the binding affinities and to predict the quintessential binding modes which were affirmed by molecular dynamics (MD) simulations. The compound has induced dose-dependent down regulation of PP2B, Nitric oxide synthase-2 (NOS2), and Interleukin 6 (IL-6) genes in the HeLa cells and has modulated the expression of apoptotic genes such as Bax, Bcl2, and caspases-3 at different concentrations. These results guide us to comprehend that the identified aromatase inhibitor was effective against the cervical cancer cells and additionally could server as scaffolds in designing new drugs.

scholarly journals RANK-RANKL Signaling in Cancer of the Uterine Cervix: A Review

2019 ◽  
Vol 20 (9) ◽  
pp. 2183 ◽  
Author(s):  
Peter A. van Dam ◽  
Yannick Verhoeven ◽  
Julie Jacobs ◽  
An Wouters ◽  
Wiebren Tjalma ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Tumor Necrosis Factor ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Uterine Cervix ◽  
Tumor Necrosis ◽  
Immune Therapy ◽  
Mrna Levels ◽  
Cervical Cancer Cells ◽  
Necrosis Factor

RANK ligand (RANKL) is a member of the tumor necrosis factor alpha superfamily of cytokines. It is the only known ligand binding to a membrane receptor named receptor activator of nuclear factor-kappa B (RANK), thereby triggering recruitment of tumor necrosis factor (TNF) receptor associated factor (TRAF) adaptor proteins and activation of downstream pathways. RANK/RANKL signaling is controlled by a decoy receptor called osteoprotegerin (OPG), but also has additional more complex levels of regulation. The existing literature on RANK/RANKL signaling in cervical cancer was reviewed, particularly focusing on the effects on the microenvironment. RANKL and RANK are frequently co-expressed in cervical cancer cells lines and in carcinoma of the uterine cervix. RANKL and OPG expression strongly increases during cervical cancer progression. RANKL is directly secreted by cervical cancer cells, which may be a mechanism they use to create an immune suppressive environment. RANKL induces expression of multiple activating cytokines by dendritic cells. High RANK mRNA levels and high immunohistochemical OPG expression are significantly correlated with high clinical stage, tumor grade, presence of lymph node metastases, and poor overall survival. Inhibition of RANKL signaling has a direct effect on tumor cell proliferation and behavior, but also alters the microenvironment. Abundant circumstantial evidence suggests that RANKL inhibition may (partially) reverse an immunosuppressive status. The use of denosumab, a monoclonal antibody directed to RANKL, as an immunomodulatory strategy is an attractive concept which should be further explored in combination with immune therapy in patients with cervical cancer.

scholarly journals Maslinic Acid Ameliorates Inflammation via the Downregulation of NF-κB and STAT-1

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 106 ◽  
Author(s):  
Wonhwa Lee ◽  
Jaehong Kim ◽  
Eui Kyun Park ◽  
Jong-Sup Bae
Keyword(s):  
Nuclear Translocation ◽  
Inflammatory Diseases ◽  
Umbilical Vein ◽  
Lavage Fluid ◽  
Maslinic Acid ◽  
Tnf Α ◽  
Cox 2 ◽  
Umbilical Vein Endothelial Cells ◽  
Oxide Synthase ◽  
Necrosis Factor

Maslinic acid (MA), a natural compound of the triterpenoid group derived from olive, prevents the generation of pro-inflammatory cytokines and oxidative stress. In human umbilical vein endothelial cells (HUVECs) treated with lipopolysaccharide (LPS), we characterized the effects of MA on the regulation of heme oxygenase (HO)-1, cyclooxygenase (COX-)2, and inducible nitric oxide synthase (iNOS). MA was tested in the lung tissues of LPS-treated mice, to determine its effect on levels of iNOS expression and representative inflammatory mediators such as interleukin (IL)-1α and tumor necrosis factor (TNF)-α. We show that MA induced the expression of HO-1, reduced LPS-induced NF-κB-luciferase activity, and inhibited iNOS/NO and COX-2/PGE2, resulting in the downregulation of STAT-1 phosphorylation. Furthermore, our data show that MA induced the nuclear translocation of Nrf2, increased the binding of Nrf2 to ARE, and decreased IL-1α production in LPS-treated HUVECs. The MA-induced reduction in iNOS/NO expression was reversed by RNAi suppression of HO-1. In mice treated with LPS, MA significantly downregulated levels of iNOS in lung tissue and TNF-α in the bronchoalveolar lavage fluid. Taken together, our findings indicate that MA exerts a critical anti-inflammatory effect by modulating iNOS via the downregulation of NF-κB and p-STAT-1. Thus, we propose that MA may be an ideal substance to treat inflammatory diseases.

scholarly journals The Application of Arsenic Trioxide in Ameliorating ABT-737 Target Therapy on Uterine Cervical Cancer Cells through Unique Pathways in Cell Death

Cancers ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 108 ◽  
Author(s):  
I-Lun Hsin ◽  
Ying-Hsiang Chou ◽  
Wei-Li Hung ◽  
Jiunn-Liang Ko ◽  
Po-Hui Wang
Keyword(s):  
Cervical Cancer ◽  
Synergistic Effect ◽  
Cancer Cells ◽  
Arsenic Trioxide ◽  
Combination Treatment ◽  
Combined Treatment ◽  
B Cell Lymphoma ◽  
Uterine Cervical Cancer ◽  
Cervical Cancer Cells ◽  
Mediated Reduction

ABT-737, a B cell lymphoma-2 (Bcl-2) family inhibitor, activates apoptosis in cancer cells. Arsenic trioxide is an apoptosis activator that impairs cancer cell survival. The aim of this study was to evaluate the effect of a combination treatment with ABT-737 and arsenic trioxide on uterine cervical cancer cells. MTT (3-(4,5-dimethylthiazol-2-yl)-25-diphenyltetrazolium bromide) assay revealed that ABT-737 and arsenic trioxide induced a synergistic effect on uterine cervical cancer cells. Arsenic trioxide enhanced ABT-737-induced apoptosis and caspase-7 activation and the ABT-737-mediated reduction of anti-apoptotic protein Mcl-1 in Caski cells. Western blot assay revealed that arsenic trioxide promoted the ABT-737-mediated reduction of CDK6 and thymidylate synthetase in Caski cells. Arsenic trioxide promoted ABT-737-inhibited mitochondrial membrane potential and ABT-737-inhibited ANT expression in Caski cells. However, ABT-737-elicited reactive oxygen species were not enhanced by arsenic trioxide. The combined treatment induced an anti-apoptosis autophagy in SiHa cells. This study is the first to demonstrate that a combination treatment with ABT-737 and arsenic trioxide induces a synergistic effect on uterine cervical cancer cells through apoptosis. Our findings provide new insights into uterine cervical cancer treatment.

Sign in / Sign up

Export Citation Format

Share Document