Topical fluorometholone treatment and desiccating stress change inflammatory protein expression in tears

The aim of the present study was to investigate the protective effect of crocin on gastric mucosal lesions caused by ischemia-reperfusion (I/R) injury in rats. Thirty-two male rats were randomly divided into sham, I/R, I/R + crocin pretreatment and crocin alone groups. To induce I/R lesions, the celiac artery was clamped for 30 min, and the clamp was then removed to allow reperfusion for 3 h. Crocin-pretreated rats received crocin (15 mg/kg, i.p.) 30 min prior to the induction of I/R injury. Samples of gastric mucosa were collected to quantify the protein expression of caspase-3, an apoptotic factor, and inducible nitric oxide synthase (iNOS), a pro-inflammatory protein, by Western blot. Pretreatment with crocin decreased the total area of gastric lesions and decreased the protein expression levels of caspase-3 and iNOS induced by I/R injury. Our findings showed a protective effect of crocin in gastric mucosa against I/R injury. This effect of crocin was mainly mediated by reducing the protein expression of iNOS and caspase-3.

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Abstract 2346: Curcumin suppresses PhIP induced inflammatory protein expression in breast epithelial cells

10.1158/1538-7445.sabcs18-2346 ◽

2019 ◽

Author(s):

Ashok Jain

Keyword(s):

Epithelial Cells ◽

Protein Expression ◽

Breast Epithelial Cells ◽

Inflammatory Protein ◽

Breast Epithelial

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P0979BENEFICIAL EFFECT OF CHLOROQUINE AND AMODIAQUINE ON DIABETIC TUBULOPATHY BY ATTENUATING MITOCHONDRIAL NOX4 AND ENDOPLASMIC RETICULUM STRESS

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfaa142.p0979 ◽

2020 ◽

Vol 35 (Supplement_3) ◽

Author(s):

So-Young Lee ◽

Dong Ho Yang ◽

Yu Ho Lee ◽

Mi Jung Lee ◽

Hyung-Jong Kim ◽

...

Keyword(s):

Endoplasmic Reticulum ◽

Protein Expression ◽

Er Stress ◽

High Glucose ◽

Kidney Tissue ◽

Nicotinamide Adenine Dinucleotide Phosphate ◽

Diabetic Mice ◽

Chronic Hyperglycemia ◽

Inflammatory Protein ◽

Diabetic Tubulopathy

Abstract Background and Aims Oxidative stress induced by chronic hyperglycemia is recognized as a significant mechanistic contributor to the development of diabetic kidney disease (DKD). Nonphagocytic nicotinamide adenine dinucleotide phosphate oxidase 4 (Nox4) is a major source of reactive oxygen species (ROS) in many cell types and in the kidney tissue of diabetic animals. We designed this study to explore the therapeutic potential of chloroquine and amodiaquine for inhibiting mitochondrial Nox4 and diabetic tubular injury. Method Human renal proximal tubular epithelial cells (hRPTCs) were cultured in high-glucose media (30 mM D-glucose), and diabetes was induced with streptozotocin (STZ, 50 mg/kg i.p. for 5 days) in male C57/BL6J mice. Chloroquine and amodiaquine were administered to the mice via intraperitoneal injection for 14 weeks. Results Chloroquine and amodiaquine inhibited mitochondrial Nox4 and increased mitochondrial mass in hRPTCs under high-glucose conditions. Reduced mitochondrial ROS production after treatment with the drugs resulted in decreased endoplasmic reticulum (ER) stress, suppressed inflammatory protein expression and reduced cell apoptosis in hRPTCs under high-glucose conditions. Notably, chloroquine and amodiaquine treatment diminished Nox4 activation and ER stress in the kidneys of STZ-induced diabetic mice. In addition, we observed attenuated inflammatory protein expression and albuminuria in STZ-induced diabetic mice after chloroquine and amodiaquine treatment. Conclusion We substantiated the protective actions of chloroquine and amodiaquine in diabetic tubulopathy associated with reduced mitochondrial Nox4 activation and ER stress alleviation. Further studies exploring the roles of mitochondrial Nox4 in the pathogenesis of DKD could suggest new therapeutic targets for patients with DKD. Figure None

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Calpain inhibition decreases inflammatory protein expression in vessel walls in a model of chronic myocardial ischemia

Surgery ◽

10.1016/j.surg.2016.11.009 ◽

2017 ◽

Vol 161 (5) ◽

pp. 1394-1404 ◽

Cited By ~ 4

Author(s):

Brittany A. Potz ◽

Ashraf A. Sabe ◽

Nassrene Y. Elmadhun ◽

Sharif A. Sabe ◽

Benedikt J.V. Braun ◽

...

Keyword(s):

Myocardial Ischemia ◽

Protein Expression ◽

Inflammatory Protein ◽

Vessel Walls ◽

Calpain Inhibition ◽

Chronic Myocardial Ischemia

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Adiponectin, an Anti-Inflammatory Adipokine, Modulates Inflammatory Protein Expression and Human Saphenous Vein Endothelial Cell Phenotype: Implications for Bypass Graft Failure

Journal of Surgical Research ◽

10.1016/j.jss.2010.11.079 ◽

2011 ◽

Vol 165 (2) ◽

pp. 343

Author(s):

M.A. Aleshin ◽

H. Lancero ◽

E.M. Owens ◽

C. Nabzdyk ◽

K.P. Nguyen ◽

...

Keyword(s):

Endothelial Cell ◽

Protein Expression ◽

Saphenous Vein ◽

Graft Failure ◽

Bypass Graft ◽

Cell Phenotype ◽

Human Saphenous Vein ◽

Inflammatory Protein ◽

Anti Inflammatory

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Redox Signaling in an In Vivo Murine Model of Tailored Wall Shear Stress

ASME 2009 Summer Bioengineering Conference, Parts A and B ◽

10.1115/sbc2009-206511 ◽

2009 ◽

Author(s):

Nick J. Willett ◽

John Oshinski ◽

Don Giddens ◽

Robert Guldberg ◽

W. Robert Taylor

Keyword(s):

Shear Stress ◽

Wall Shear Stress ◽

Protein Expression ◽

Fluid Dynamic ◽

Inflammatory Marker ◽

Inflammatory Protein ◽

Wall Shear ◽

Acute Changes ◽

High Degree

Wall Shear Stress (WSS) has been identified as an important factor in the pathogenesis of atherosclerosis. We developed a novel murine aortic coarctation model to alter the hemodynamic environment in vivo. The model utilizes the shape memory response of nitinol clips to provide a high degree of control over aortic diameter and subsequently WSS. We employed this model to test the hypothesis that acute changes in WSS in vivo induce upregulation of inflammatory proteins mediated by Reactive Oxygen Species (ROS). WSS was mapped through a computational fluid dynamic model and correlated to inflammatory marker expression. C57B16 control mice were compared to tempol treated, apocynin treated, p47phox KO, and catalase overexpressor mice in this study. The results show that the coarctation produces low mean oscillatory WSS in the region downstream of the clip. The WSS in this region correlates to a large increase in VCAM-1 expression in wild-type mice. This WSS dependent increase in protein expression is unchanged in animal models of decreased ROS. This suggests that although the redox state is important to the overall pathogenesis of the disease, individual ROS or ROS sources may not be sufficient to inhibit a WSS dependent inflammatory response. Further analysis with this model utilizing other reagent treatments, transgenic mice, and markers will allow us to analyze the functional contribution of transcription factors, ROS, and ROS sources to WSS dependent inflammatory protein expression.

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