Anti-inflammatory effect of allylpyrocatechol in LPS-induced macrophages is mediated by suppression of iNOS and COX-2 via the NF-κB pathway

Sarkar, Debabrata; Saha, Piu; Gamre, Sunita; Bhattacharjee, Surajit; Hariharan, Chellaram; Ganguly, Sudipto; Sen, Rupashree; Mandal, Gautam; Chattopadhyay, Subrata; Majumdar, Subrata; Chatterjee, Mitali

doi:10.1016/j.intimp.2008.05.003

Cited by 98 publications

(60 citation statements)

References 32 publications

(34 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…NF-κB is widely responsible for the regulation of PTGS2 gene expression in various cells in response to numerous stimuli. 26,27 It has been demonstrated that NF-κB acts as a positive regulator of PTGS2 transcription in inflammation-associated cancer. 28 Huang et al 29 demonstrated that the expression and activity of NF-κB/p65 were significantly correlated with COX-2 protein levels, providing indirect proof of the NF-κB regulation of PTGS2.…”

Section: Y-s LI L-p Wu K-h Li Et Al Genistein Regulation Of Cox-2 mentioning

confidence: 99%

Involvement of Nuclear Factor κB (NF-κB) in the Downregulation of Cyclo-Oxygenase-2 (COX-2) by Genistein in Gastric Cancer Cells

Ли

et al. 2011

J Int Med Res

View full text Add to dashboard Cite

Genistein induces growth inhibition in various human cancer cell lines but its mechanism of action remains unknown. This study determined whether the effect of genistein is mediated via suppression of cyclo-oxygenase (COX)-2 protein, and elucidated the mechanism of action of this effect in the human gastric cancer cell line BGC-823. Genistein treatment inhibited cell proliferation and induced apoptosis in a dose-and time-dependent manner; Western blotting analysis indicated a significant dose-dependent decrease in COX-2 protein levels. Genistein treatment exerted a significant inhibitory effect on activation of the transcription factor nuclear factor kB (NF-kB). Additionally, the NF-kB inhibitor pyrrolidine dithiocarbamate caused a reduction in COX-2 protein levels and NF-kB activation, similar to the effect of genistein. Suppression of COX-2 protein may be important for the antiproliferative and proapoptotic effects of genistein in BGC-823 cells, and these effects may be partly mediated through the NF-kB pathway.

show abstract

Section: Y-s LI L-p Wu K-h Li Et Al Genistein Regulation Of Cox-2 mentioning

confidence: 99%

Involvement of Nuclear Factor κB (NF-κB) in the Downregulation of Cyclo-Oxygenase-2 (COX-2) by Genistein in Gastric Cancer Cells

Ли

et al. 2011

J Int Med Res

View full text Add to dashboard Cite

show abstract

“…COX-2 derived bioactive lipids, including prostaglandin E2, are potent inflammatory mediators. PGE 2 increases vascular permeability along with other vasoactive components such as histamine, bradykinin or nitric oxide thereby causing oedema, pain and hyperalgesia at the local inflammatory 33 . Although cellular repair system corrects most of these damages, the free radicals induced DNA lesions that accumulated with age, can be an important aetiology of inflammatory autoimmune diseases like rheumatoid arthritis 41 .…”

mentioning

confidence: 99%

Free radical biology in cellular inflammation related to rheumatoid arthritis

Bala¹,

Haldar²

2013

OA Arthritis

View full text Add to dashboard Cite

“…ROS stimulate this process through the activation of cyclooxygenases. Prostaglandins, also, activate NADPH oxidase, which produces superoxide anion radical [153]. Therefore, this system becomes cyclic, ROS activate cyclooxygenases and so the prostaglandins biosynthesis, further prostaglandins trigger NAPH oxidases, increasing ROS.…”

Section: Some Ros Such As Omentioning

confidence: 99%

Oxidative Stress: Noxious but Also Vital

Bagatini¹,

Jaques²,

Oliveira³

et al. 2018

Novel Prospects in Oxidative and Nitrosative Stress

View full text Add to dashboard Cite

The imbalance between reactive oxygen species (ROS) production and antioxidant defenses determines the condition called oxidative stress. When there is an increase in ROS production or a decrease in the antioxidant defenses, this systemic antioxidant/pro-oxidant imbalance may lead to the accumulation of oxidative damage, which, in turn, may lead to a modification of biomolecules. These consist of reactions resulting in protein adducts, DNA oxidation, and formation of lipid peroxides, which, in turn, reduce the cellular functional capacity and increase the risk of disease development. The body has natural scavenging systems against free radicals and other reactive species. However, sometimes the endogenous antioxidant capacity is exceeded by the production of ROS. When this occurs, exogenous antioxidants exert important function for the human health. These bioactive compounds act preventing and neutralizing the formation of new reactive species and free radical s .I ns o m ec a s e s ,a n increase of ROS can help the host to resolve an infection or even to control the tumor growth. Finally, the levels of ROS can be perceived by signal transduction pathways involving known targets(i.e.,p53,Ras,andNF-κB) and regulate physiopathological events such as the cellular cycle, apoptosis, and inflammation.Keywords: reactive species, cellular oxidation, antioxidant system, health, disease © 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Cellular respiration and generation of reactive species in the mitochondria: implications in cell viability and agingOxidative phosphorylation is the center of energy metabolism in plants, animals and several microbial life forms [1]. In eukaryotes, this process occurs in mitochondria. The mitochondria is a cytoplasmic organelle surrounded by two membranes, outer and inner membrane, which main function is the production of most of the phosphate compounds necessary for the energetic balance of the cell. In addition, other functions such as the regulation of the body'sheatgeneration [2][3][4] programmed cell death [5][6][7], reactive oxygen species (ROS) generation and cell signaling [8] is also associated with mitochondria. Cellular vitality is directly related to mitochondria, and mitochondrial dysfunctions are frequent causes of accidental cell death [5,[9][10][11], cancer [12, 13], diabetes [14][15][16] and neurodegenerative diseases [17][18][19], among others.The characterization of the respiratory electron chain could be performed in studies using the fractionation of its components by certain detergents that at low concentrations break the interactions between proteins and lipids in the membranes, leaving associations between proteins intact [20]. In electron transport chain, through this process, four protein complexes were found....

show abstract

Anti-inflammatory effect of allylpyrocatechol in LPS-induced macrophages is mediated by suppression of iNOS and COX-2 via the NF-κB pathway

Cited by 98 publications

References 32 publications

Involvement of Nuclear Factor κB (NF-κB) in the Downregulation of Cyclo-Oxygenase-2 (COX-2) by Genistein in Gastric Cancer Cells

Involvement of Nuclear Factor κB (NF-κB) in the Downregulation of Cyclo-Oxygenase-2 (COX-2) by Genistein in Gastric Cancer Cells

Free radical biology in cellular inflammation related to rheumatoid arthritis

Oxidative Stress: Noxious but Also Vital

Contact Info

Product

Resources

About