scholarly journals Tumor-associated macrophages favor C26 murine colon carcinoma cell proliferation in an oxidative stress-dependent manner

2017 ◽  
Vol 37 (4) ◽  
pp. 2472-2480 ◽  
Author(s):  
Lavinia Luput ◽  
Emilia Licarete ◽  
Alina Sesarman ◽  
Laura Patras ◽  
Marius Costel Alupei ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Proliferation ◽  
Colon Carcinoma ◽  
Carcinoma Cell ◽  
Dependent Manner ◽  
Tumor Associated Macrophages ◽  
Murine Colon Carcinoma ◽  
Stress Dependent ◽  
Murine Colon

Alcoholic extracts of Epilobium, Urtica dioica and Evernia prunastri with 5-fluorouracil in controlling murine colon carcinoma cell growth in vitro

2017 ◽  
Vol 17 (4) ◽  
pp. 325-336 ◽  
Author(s):  
Valentina Zunino ◽  
Giorgia Meineri ◽  
Graziella Bellone ◽  
Barbara Vizio ◽  
Adriana Prati ◽  
...  
Keyword(s):  
Cell Growth ◽  
Colon Carcinoma ◽  
Carcinoma Cell ◽  
Urtica Dioica ◽  
Evernia Prunastri ◽  
Murine Colon Carcinoma ◽  
Murine Colon

scholarly journals Oxidative stress increases megalin expression in the renal proximal tubules during the normoalbuminuric stage of diabetes mellitus

2018 ◽  
Vol 314 (3) ◽  
pp. F462-F470 ◽  
Author(s):  
Yoshifumi Kurosaki ◽  
Akemi Imoto ◽  
Fumitaka Kawakami ◽  
Masanori Yokoba ◽  
Tsuneo Takenaka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Hydrogen Peroxide ◽  
High Glucose ◽  
Renal Cortex ◽  
Dependent Manner ◽  
Phosphatidylinositol 3 Kinase ◽  
Phosphorylated Akt ◽  
Stress Dependent ◽  
Phosphatidylinositol 3

Megalin, an endocytic receptor expressed in proximal tubule cells, plays a critical role in renal tubular protein reabsorption and is associated with the albuminuria observed in diabetic nephropathy. We have previously reported increased oxidant production in the renal cortex during the normoalbuminuric stage of diabetes mellitus (DM); however, the relationship between oxidative stress and renal megalin expression during the normoalbuminuric stage of DM remains unclear. In the present study, we evaluated whether oxidative stress affects megalin expression in the normoalbuminuric stage of DM in a streptozotocin-induced diabetic rat model and in immortalized human proximal tubular cells (HK-2). We demonstrated that increased expression of renal megalin accompanies oxidative stress during the early stage of DM, before albuminuria development. Telmisartan treatment prevented the diabetes-induced elevation in megalin level, possibly through an oxidative stress-dependent mechanism. In HK-2 cells, hydrogen peroxide significantly increased megalin levels in a dose- and time-dependent manner; however, the elevation in megalin expression was decreased following prolonged exposure to severe oxidative stress induced by 0.4 mmol/l hydrogen peroxide. High-glucose treatment also significantly increased megalin expression in HK-2 cells. Concurrent administration of the antioxidant N-acetyl-cysteine blocked the effects of high glucose on megalin expression. Furthermore, the hydrogen peroxide-induced increase in megalin expression was blocked by treatment with phosphatidylinositol 3-kinase and Akt inhibitors. Increase of phosphorylated Akt expression was also seen in the renal cortex of diabetic rats. Taken together, our results indicate that mild oxidative stress increases renal megalin expression through the phosphatidylinositol 3-kinase-Akt pathway in the normoalbuminuric stage of DM.

scholarly journals Empagliflozin improves endothelial and cardiomyocyte function in human heart failure with preserved ejection fraction via reduced pro-inflammatory-oxidative pathways and protein kinase Gα oxidation

2020 ◽  
Author(s):  
Detmar Kolijn ◽  
Steffen Pabel ◽  
Yanna Tian ◽  
Mária Lódi ◽  
Melissa Herwig ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Ejection Fraction ◽  
Linear Regression Analysis ◽  
Lipid Peroxide ◽  
Dependent Manner ◽  
Preserved Ejection Fraction ◽  
Human Heart Failure ◽  
Stress Dependent

Abstract Aims Sodium-glucose-cotransporter-2 inhibitors showed favourable cardiovascular outcomes, but the underlying mechanisms are still elusive. This study investigated the mechanisms of empagliflozin in human and murine heart failure with preserved ejection fraction (HFpEF). Methods and results The acute mechanisms of empagliflozin were investigated in human myocardium from patients with HFpEF and murine ZDF obese rats, which were treated in vivo. As shown with immunoblots and ELISA, empagliflozin significantly suppressed increased levels of ICAM-1, VCAM-1, TNF-α, and IL-6 in human and murine HFpEF myocardium and attenuated pathological oxidative parameters (H2O2, 3-nitrotyrosine, GSH, lipid peroxide) in both cardiomyocyte cytosol and mitochondria in addition to improved endothelial vasorelaxation. In HFpEF, we found higher oxidative stress-dependent activation of eNOS leading to PKGIα oxidation. Interestingly, immunofluorescence imaging and electron microscopy revealed that oxidized PKG1α in HFpEF appeared as dimers/polymers localized to the outer-membrane of the cardiomyocyte. Empagliflozin reduced oxidative stress/eNOS-dependent PKGIα oxidation and polymerization resulting in a higher fraction of PKGIα monomers, which translocated back to the cytosol. Consequently, diminished NO levels, sGC activity, cGMP concentration, and PKGIα activity in HFpEF increased upon empagliflozin leading to improved phosphorylation of myofilament proteins. In skinned HFpEF cardiomyocytes, empagliflozin improved cardiomyocyte stiffness in an anti-oxidative/PKGIα-dependent manner. Monovariate linear regression analysis confirmed the correlation of oxidative stress and PKGIα polymerization with increased cardiomyocyte stiffness and diastolic dysfunction of the HFpEF patients. Conclusion Empagliflozin reduces inflammatory and oxidative stress in HFpEF and thereby improves the NO–sGC–cGMP–cascade and PKGIα activity via reduced PKGIα oxidation and polymerization leading to less pathological cardiomyocyte stiffness.

scholarly journals Dihydroartemisinin Inhibits Proliferation and Induces Apoptosis of Human Hepatocellular Carcinoma Cell by Upregulating Tumor Necrosis Factor via JNK/NF-κB Pathways

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Long Wu ◽  
Yanlei Cheng ◽  
Junjian Deng ◽  
Weiping Tao ◽  
Junjie Ye
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Differentially Expressed Genes ◽  
Carcinoma Cell ◽  
Expression Profiles ◽  
Human Hepatocellular Carcinoma ◽  
Differentially Expressed ◽  
Venn Diagram ◽  
Dependent Manner ◽  
Hepatocellular Carcinoma Cell

Background. Dihydroartemisinin (DHA) is a predominant compound in Artemisia annua L., and it has been shown to inhibit tumorigenesis. Methods. In this study, the antitumor potential of DHA was investigated in the MHCC97-L hepatocellular carcinoma cell line. Cells were treated at various concentrations of DHA, and then the cell cycle, viability, and DNA synthesis were measured to evaluate cell proliferation. Furthermore, the expression of genes and proteins related to proliferation and apoptosis was measured to determine the effects of DHA. Finally, the mechanism was investigated using RNA-sequencing to identify differentially expressed genes and signaling pathways, and JNK/NF-κB pathways were evaluated with Western blotting. Results. Cells were treated with a concentration range of DHA from 1 to 100 μM, and cell proliferation was suppressed in a dose-dependent manner. In addition, the genes and proteins involved in typical cellular functions of MHCC97-L cells were significantly inhibited. DHA treatment downregulated the angiogenic gene ANGPTL2 and the cell proliferation genes CCND1, E2F1, PCNA, and BCL2. DHA treatment significantly upregulated the apoptotic genes CASP3, CASP8, CASP9, and TNF. Global gene expression profiles identified 2064 differentially expressed genes (DEGs). Among them, 744 were upregulated and 1320 were downregulated. Furthermore, MAPK, NF-kappa B, and TNF pathways were enriched based on the DEGs, and the consensus DEG was identified as TNF using a Venn diagram of those pathways. DHA promoted phosphorylation of JNK, inhibited nuclear p65, and then significantly induced TNF-α synthesis. Conclusion. DHA inhibited cell proliferation and induced apoptosis in human hepatocellular carcinoma cells by upregulating TNF expression via JNK/NF-κB pathways.

Induction of systemic immunity by expression of interleukin-23 in murine colon carcinoma cells

2003 ◽  
Vol 105 (6) ◽  
pp. 820-824 ◽  
Author(s):  
Yan-Qing Wang ◽  
Shin-ichi Ugai ◽  
Osamu Shimozato ◽  
Ling Yu ◽  
Kiyoko Kawamura ◽  
...  
Keyword(s):  
Colon Carcinoma ◽  
Carcinoma Cells ◽  
Systemic Immunity ◽  
Colon Carcinoma Cells ◽  
Murine Colon Carcinoma ◽  
Interleukin 23 ◽  
Murine Colon

scholarly journals Expression of the interleukin-21 gene in murine colon carcinoma cells generates systemic immunity in the inoculated hosts

2003 ◽  
Vol 10 (3) ◽  
pp. 187-192 ◽  
Author(s):  
Shin-ichi Ugai ◽  
Osamu Shimozato ◽  
Kiyoko Kawamura ◽  
Yan-Qing Wang ◽  
Taketo Yamaguchi ◽  
...  
Keyword(s):  
Colon Carcinoma ◽  
Carcinoma Cells ◽  
Systemic Immunity ◽  
Colon Carcinoma Cells ◽  
Murine Colon Carcinoma ◽  
Interleukin 21 ◽  
Murine Colon

Abstract 2619: Combination of ECP1014 and anti-PD-L1 reduces tumor growth in the CT26 murine colon carcinoma model of a cold tumor

2017 ◽  
Author(s):  
Bobby W. Sandage ◽  
John J. Talley ◽  
Eduardo J. Martinez ◽  
Maryland R. Franklin ◽  
Mary Anne Meade ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Colon Carcinoma ◽  
Murine Colon Carcinoma ◽  
Murine Colon

scholarly journals Effective Photoimmunotherapy of Murine Colon Carcinoma Induced by the Combination of Photodynamic Therapy and Dendritic Cells

2004 ◽  
Vol 10 (13) ◽  
pp. 4498-4508 ◽  
Author(s):  
Ahmad Jalili ◽  
Marcin Makowski ◽  
Tomasz Świtaj ◽  
Dominika Nowis ◽  
Grzegorz M. Wilczyński ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Photodynamic Therapy ◽  
Colon Carcinoma ◽  
Murine Colon Carcinoma ◽  
Murine Colon
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