Effects of idoxifene and estradiol on NF‐κB activation in cultured rat hepatocytes undergoing oxidative stress

Omoya, Toshihiro; Shimizu, Ichiro; Zhou, Yajun; Okamura, Yoshihiro; Inoue, Hiroshi; Lu, Guangming; Itonaga, Mina; Honda, Hirohito; Nomura, Masahiro; Ito, Susumu

doi:10.1034/j.1600-0676.2001.021003183.x

Cited by 57 publications

(55 citation statements)

References 35 publications

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“…In general, estrogen attenuates cytokine-induced NF-B activation, whereas selective estrogen receptor modifiers (SERM), including raloxifene and tamoxifen, have varied effects on NF-B activation. [32][33][34] However, NF-B activation was assessed several hours after estrogen exposure. We have described the effect of estrogen and 2 SERMs on rapid changes in NF-B activation status.…”

Section: Discussionmentioning

confidence: 99%

Estrogen, Heat Shock Proteins, and NFκB in Human Vascular Endothelium

Hamilton

Mbai

Gupta

et al. 2004

ATVB

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Background-We hypothesized that estrogen would increase HSP72 in human coronary artery endothelial cells (HCAEC), and that these would be more sensitive to estrogen than our previous observations in myocytes. Methods and Results-HCAEC were treated with 17␤-estradiol or tamoxifen, ranging from physiological to pharmacological(1 nM to 10 mol/L) for either 24 hours (early) or 7 days (chronic). HSP expression was assessed by Western blots. Both early and chronic 17␤-estradiol and tamoxifen increased HSP72. Electromobility shift assays (EMSA) showed activation of HSF-1 with early, but not chronic, 17␤-estradiol. 17␤-Estradiol activated NF B within 10 minutes, and the ER-␣ selective inhibitor, ICI 182 780, abolished this effect. Transcription factor decoys containing the heat shock element blocked HSP72 induction. Estrogen pretreatment decreased lactate dehydrogenase release with hypoxia. This protective effect persisted despite blockade of HSF-1 by decoys. However, an NF-B decoy prevented the increase in HSP72 and abolished the estrogen-associated protection during hypoxia. Conclusions-17␤-Estradiol upregulates HSP72 early and chronically via different mechanisms in HCAEC, and provides cytoprotection during hypoxia, independent of HSP72 induction. NF-B mediates the early increase in HSP72, suggesting that estrogen activates NF-B via a nongenomic, receptor-dependent mechanism, and this leads to activation of HSF-1. Activation of NF-B was critical for estrogen-associated protection. Further studies are needed to elucidate the involved signaling pathways.

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Section: Discussionmentioning

confidence: 99%

Estrogen, Heat Shock Proteins, and NFκB in Human Vascular Endothelium

Hamilton

Mbai

Gupta

et al. 2004

ATVB

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“…In silent cells, NF-κB inactively exists in cytoplasm, and can be activated by stimulation with nuclear translocation. It can bond the kb site of target gene initiator or enhanser to start or enhance genetic transcription (Lakshminarayanan et al, 2001;Moine et al, 2000;Valen et al, 2001;Omoya et al, 2001), and further participate in the injury process of tissue (Shames et al, 2002;Wang et al, 2002;Theuer et al, 2002). During occurrence of AP hepatic injury, the activation of hepatic NF-κB also plays an important role.…”

Section: Role Of Nf-κb and Its Regulation Of Icam-1 Expression In Sapmentioning

confidence: 99%

Study progress on mechanism of severe acute pancreatitis complicated with hepatic injury

Zhang

Wang

Zhang

2007

J. Zhejiang Univ. - Sci. B

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Study on the action mechanism of inflammatory mediators generated by the severe acute pancreatitis (SAP) in multiple organ injury is a hotspot in the surgical field. In clinical practice, the main complicated organ dysfunctions are shock, respiratory failure, renal failure, encephalopathy, with the rate of hepatic diseases being closely next to them. The hepatic injury caused by SAP cannot only aggravate the state of pancreatitis, but also develop into hepatic failure and cause patient death. Its complicated pathogenic mechanism is an obstacle in clinical treatment. Among many pathogenic factors, the changes of vasoactive substances, participation of inflammatory mediators as well as OFR (oxygen free radical), endotoxin, etc. may play important roles in its progression.

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“…After activation, nucleus translocation of NF-κB will occur. NF-κB will bind the κB site on promoter or enhancer of target genes to promote or enhance the expressions of corresponding cytokines in cell nucleus, adhesion molecules and chemotactic factors (Izumi et al, 2001;Antonelli et al, 2001;Ginis et al, 2002;Wright et al, 2002;Lakshminarayanan et al, 2001;Moine et al, 2000;Valen et al, 2001;Omoya et al, 2001), and to regulate inflammation and immunological reactions (Neurath et al, 1998). Although the massive production of inflammatory mediators in local intestinal tract is a defense reaction to the invasion of intestinal bacteria and toxin, it will cause injury of intestinal mucosa (Wang et al, 2002;Theuer et al, 2002).…”

Section: Influence Of Excessive Release Of Inflammatory Mediators On mentioning

confidence: 99%

Mechanism of acute pancreatitis complicated with injury of intestinal mucosa barrier

Zhang

Song

et al. 2007

J. Zhejiang Univ. - Sci. B

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Acute pancreatitis (AP) is a common acute abdomen in clinic with a rapid onset and dangerous pathogenetic condition.AP can cause an injury of intestinal mucosa barrier, leading to translocation of bacteria or endotoxin through multiple routes, bacterial translocation (BT), gutorigin endotoxaemia, and secondary infection of pancreatic tissue, and then cause systemic inflammatory response syndrome (SIRS) or multiple organ dysfunction syndrome (MODS), which are important factors influencing AP's severity and mortality. Meanwhile, the injury of intestinal mucosa barrier plays a key role in AP's process. Therefore, it is clinically important to study the relationship between the injury of intestinal mucosa barrier and AP. In addition, many factors such as microcirculation disturbance, ischemical reperfusion injury, excessive release of inflammatory mediators and apoptosis may also play important roles in the damage of intestinal mucosa barrier. In this review, we summarize studies on mechanisms of AP.

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Effects of idoxifene and estradiol on NF‐κB activation in cultured rat hepatocytes undergoing oxidative stress

Abstract: These findings suggest that idoxifene and estradiol function as antioxidants and protect hepatocytes from inflammatory cell injury.

Cited by 57 publications

References 35 publications

Estrogen, Heat Shock Proteins, and NFκB in Human Vascular Endothelium

Estrogen, Heat Shock Proteins, and NFκB in Human Vascular Endothelium

Study progress on mechanism of severe acute pancreatitis complicated with hepatic injury

Mechanism of acute pancreatitis complicated with injury of intestinal mucosa barrier

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