Molecular mechanisms of apoptosis induction by 2-dodecylcyclobutanone, a radiolytic product of palmitic acid, in human lymphoma U937 cells

APOPTOSIS ◽  
2012 ◽  
Vol 17 (6) ◽  
pp. 636-645 ◽  
Author(s):  
Da-Yong Yu ◽  
Qing-Li Zhao ◽  
Masakazu Furuta ◽  
Setsuko Todoriki ◽  
Keisuke Izumi ◽  
...  
2011 ◽  
Vol 25 (8) ◽  
pp. 1687-1693 ◽  
Author(s):  
Zheng-Guo Cui ◽  
Ryohei Ogawa ◽  
Jin-Lan Piao ◽  
Kei Hamazaki ◽  
Loreto B. Feril ◽  
...  

2002 ◽  
Vol 283 (1) ◽  
pp. C93-C102 ◽  
Author(s):  
C. K. Domingos Ng ◽  
Shailesh S. Deshpande ◽  
Kaikobad Irani ◽  
B. Rita Alevriadou

Production of reactive oxygen species (ROS) by ischemic tissue after ischemia-reperfusion (I/RP) is an important factor that contributes to tissue injury. The small GTPase Rac1 mediates the oxidative burst, and ROS act on signaling pathways involved in expression of inflammatory genes. Because there is evidence implicating monocytes in the pathogenesis of I/RP injury, our objective was to determine the molecular mechanisms that regulate adhesive interactions between monocytes and hypoxia-reoxygenation (H/RO)-exposed cultured endothelial cells (ECs). When U937 cells were perfused over human umbilical vein ECs at 1 dyn/cm2, H (1 h at 1% O2)/RO (13 h) significantly increased the fluxes of rolling and stably adherent U937 cells. Either EC treatment with the antioxidant pyrrolidine dithiocarbamate (PDTC) or infection with AdRac1N17, which results in expression of the dominant-negative form of Rac1, abolished H/RO-induced ROS production, attenuated rolling, and abolished stable adhesion of U937 cells to H/RO-exposed ECs. Infection with AdRac1N17 also abolished H/RO-induced upregulation of vascular cell adhesion molecule (VCAM)-1. In turn, blocking VCAM-1 abolished U937 cell stable adhesion and slightly increased rolling. We concluded that the Rac1-dependent ROS partially regulate rolling and exclusively regulate stable adhesion of monocytic cells to ECs after H/RO and that stable adhesion, but not rolling, is mediated by ROS-induced expression of VCAM-1.


Biomolecules ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 795 ◽  
Author(s):  
Qing Zhang ◽  
Jia Liu ◽  
Mengmeng Zhang ◽  
Shujun Wei ◽  
Ruolan Li ◽  
...  

Rheumatoid arthritis (RA) is a known chronic autoimmune disease can cause joint deformity and even loss of joint function. Fibroblast-like synoviocytes (FLS), one of the main cell types in synovial tissues of RA patients, are key effector cells in the development of RA and are considered as promising therapeutic targets for treating RA. Herbal medicines are precious resources for finding novel agents for treating various diseases including RA. It is reported that induction of apoptosis in FLS is an important mechanism for the herbal medicines to treat RA. Consequently, this paper reviewed the current available references on pro-apoptotic effects of herbal medicines on FLS and summarized the related possible signal pathways. Taken together, the main related signal pathways are concluded as death receptors mediated apoptotic pathway, mitochondrial dependent apoptotic pathway, NF-κB mediated apoptotic pathways, mitogen-activated protein kinase (MAPK) mediated apoptotic pathway, endoplasmic reticulum stress (ERS) mediated apoptotic pathway, PI3K-Akt mediated apoptotic pathway, and other reported pathways such as janus kinase/signal transducers and activators of transcription (JAK-STAT) signal pathway. Understanding the apoptosis induction pathways in FLS of these herbal medicines will not only help clear molecular mechanisms of herbal medicines for treating RA but also be beneficial for finding novel candidate therapeutic drugs from natural herbal medicines. Thus, we expect the present review will highlight the importance of herbal medicines and its components for treating RA via induction of apoptosis in FLS, and provide some directions for the future development of these mentioned herbal medicines as anti-RA drugs in clinical.


2009 ◽  
Vol 25 (5) ◽  
pp. 364-373 ◽  
Author(s):  
Da-Yong Yu ◽  
Qing-Li Zhao ◽  
Zheng-Li Wei ◽  
Mohammad Shehata ◽  
Takashi Kondo

2013 ◽  
Vol 205 (2) ◽  
pp. 119-127 ◽  
Author(s):  
Jin-Lan Piao ◽  
Zheng-Guo Cui ◽  
Yukihiro Furusawa ◽  
Kanwal Ahmed ◽  
Mati Ur Rehman ◽  
...  

2008 ◽  
Vol 270 (2) ◽  
pp. 286-294 ◽  
Author(s):  
Yoshiaki Tabuchi ◽  
Ichiro Takasaki ◽  
Qing-Li Zhao ◽  
Shigehito Wada ◽  
Takeshi Hori ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Eunji Kim ◽  
Woo Seok Yang ◽  
Ji Hye Kim ◽  
Jae Gwang Park ◽  
Han Gyung Kim ◽  
...  

In this study, we aimed to examine the cellular and molecular mechanisms of lancemaside A fromCodonopsis lanceolata(Campanulaceae) in the inflammatory responses of monocytes (U937 cells) and macrophages (RAW264.7 cells). Lancemaside A significantly suppressed the inflammatory functions of lipopolysaccharide- (LPS-) treated RAW264.7 cells by suppressing the production of nitric oxide (NO), the expression of the NO-producing enzyme inducible NO synthase (iNOS), the upregulation of the costimulatory molecule CD80, and the morphological changes induced by LPS exposure. In addition, lancemaside A diminished the phagocytic activity of RAW264.7 cells and boosted the neutralizing capacity of these cells when treated with the radical generator sodium nitroprusside (SNP). Interestingly, lancemaside A strongly blocked the adhesion activity of RAW264.7 cells to plastic culture plates, inhibited the cell-cell and cell-fibronectin (FN) adhesion of U937 cells that was triggered by treatment with an anti-β1-integrin (CD29) antibody and immobilized FN, respectively. By evaluating the activation of various intracellular signaling pathways and the levels of related nuclear transcription factors, lancemaside A was found to block the activation of inhibitor ofκB kinase (IKK) and p65/nuclear factor- (NF-)κB. Taken together, our findings strongly suggest that the anti-inflammatory function of lancemaside A is the result of its strong antioxidative and IKK/NF-κB inhibitory activities.


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