共查询到20条相似文献,搜索用时 15 毫秒
1.
Shu-Yan Li Wen-Ge Sun Yu-Hong Jia Guo-Sheng Wu Guo-Shun An Ju-Hua Ni Hong-Ti Jia 《Biochemistry. Biokhimii?a》2010,75(1):101-110
We demonstrate that activation of nuclear factor κB (NF-κB) in neurons is neuroprotective in response to kainic acid (KA)-induced
excitotoxicity. Combination of Western blotting, immunocytochemistry, and electrophoresis mobility shift assay showed that
KA exposure induced a fast but transient nuclear translocation of the NF-κB p65 subunit and increased DNA-binding activity
of NF-κB in primary cultured cortical neurons. The transient NF-κB activity was associated with upregulation of antiapoptotic
Bcl-xL and XIAP gene products revealed by real-time PCR. Knockdown of p65 decreased neuronal viability and antiapoptotic gene
expression. In addition, we showed that KA-stimulated DNA-binding activity of NF-κB was associated with reactive oxygen species
and calcium signals, using AMPA/KA receptor antagonist, calcium chelator, and antioxidant. These results suggest that the
fast and transient activation of NF-κB initiated by calcium signals is one of the important proximal events in response to
KA-induced excitotoxicity, which has neuroprotective effect against KA-induced apoptosis. 相似文献
2.
Sun CS Wu KT Lee HH Uen YH Tian YF Tzeng CC Wang AH Cheng CJ Tsai SL 《Journal of biomedical science》2008,15(5):633-643
The link of proto-oncogenic protein Wnt-1 production with NF-κB activation has been functionally demonstrated in PC12 cells, a rat pheochromocytoma cell line of neural
crest lineage, while it is not yet verified in human cells. The link can be indirectly supported in our previous report that
functional proteomics identifies enhanced expression of NF-κB-associated Wnt-1 production in human hepatocellular carcinoma tissues. This study aimed to further validate this link in human cells using
anti-sense strategy. The effects of sequence-specific anti-sense morpholino oligonucleotides (ONs) targeting against pre-mRNA
sequences of human p50 and p65 subunits of NF-κB as well as Wnt-1 genes were investigated. It revealed that all the three morpholino ONs inhibited NF-κB activation in human hepatoblastoma
cell line HepG2 cells along with decreased Wnt-1 production. Chromatin immunoprecipitation assay ascertained the direct binding of NF-κB-p50 to the Wnt-1 promoter. Additionally, anti-P50 and anti-P65 morpholino ONs also repressed the phosphorylation of Iκ Bα which temporarily
correlated with the inhibition of NF-κB activation accompanied by decreased Wnt-1 production by HepG2 cells. In summary, NF-κB activation is critically involved in the production of Wnt-1 by HepG2 cells. These results may have important oncology implications in treating patients with NF-κB-associated Wnt-1-producing cancers.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users. 相似文献
3.
Sammy Grimaldo Fang Tian Lu-Yuan Li 《Apoptosis : an international journal on programmed cell death》2009,14(6):788-795
Vascular endothelial growth inhibitor (VEGI) is an endogenous inhibitor of endothelial cell growth and a promising candidate
for cancer therapy. VEGI is able to inhibit tumor growth by specifically targeting the tumor neovasculature. Increasing the
anti-angiogenic potential of this cytokine is of great interest for its therapeutic potential. NF-κB is known to have an integral
role in TNF superfamily signaling, acting as a pro-survival factor. A role of VEGI-induced NF-κB activation in endothelial
cells has yet to be described. Here we show that suppression of the NF-κB pathway can increase the apoptotic potential of
VEGI. We used siRNA to deplete NF-κB or its activator IKK2 from adult bovine aortic endothelial cells. The siRNA treatments
diminished VEGI-induced NF-κB activation, evidenced from a reduced extent of NF-κB nuclear translocation and diminished expression
of NF-κB-target genes such as interleukins-6 and -1β. The siRNA-treated endothelial cells when exposed to VEGI exhibited a marked decrease in cell viability and a significant
increase in apoptosis. These results confirm that VEGI utilizes NF-κB as a pro-survival role factor in endothelial cells.
We then examined whether a combination of VEGI with NF-κB inhibitors would constitute a more potential therapeutic regiment.
We found that in the presence of the NF-κB inhibitors curcumin or BMS-345541 there was a marked increase in the apoptotic
potential of VEGI on endothelial cells. These findings indicate that a combination therapy using VEGI and NF-κB inhibitors
could be a potent approach for cancer treatment. 相似文献
4.
5.
Jia-He Wang Bo Yu Ping He Xue Bai 《World journal of microbiology & biotechnology》2011,27(8):1827-1838
We previously showed that infection of human monocytic U937 cells with nonpathogenic Escherichia coli (E. coli) induced rapid apoptosis in a dose- and time-dependent manner. We also found that E. coli increase p38 mitogen-activated protein Kinase (p38 MAPK) and c-Jun N-terminal kinase (JNK), and decrease extracellular-Regulated
Kinase1/2 (ERK1/2) phosphorylation and increase caspase-3 and -9 activity in U937 cells. The current study determines if Bcl-2,
Bax, the phosphatidylinositol 3-kinase (PI3K)/Akt and nuclear factor kappa B (NF-κB) regulates E. coli–induced U937 cell apoptosis. Studying the underlying mechanisms we found that the E. coli-induced apoptosis in U937 cells was associated with a more prominent reduction in expression of Bcl-2, levels of P-Akt and
NF-κB. Because levels of inhibition of apoptosis protein (cIAP), and X-chromosomelinked inhibitor of apoptosis protein (XIAP)
are regulated by NF-κB, E. coli decreased the levels of these proteins in U937 cells through inhibition of NF-κB. Moreover, E. coli markedly elevated Bax expression and cytochrome c redistribution. LY294002, PDTC and Embelin, specific inhibitors of PI3K, NF-κB and XIAP, induced U937 cell apoptosis and
the apoptosis is dependent on activity of caspase-3 and -9 in E. coli-treated U937 cells. Through using LY294002 and western blotting, we identified NF-κB was the downstream Akt target regulated
by E. coli. Taken together, these results clearly indicate reduced activation of NF-κB via impaired PI3K/Akt activation could result
in increased apoptosis of U937 cells infected by E. coli. Moreover, E. coli can induce apoptosis with an increased expression of Bax and a reduced expression of Bcl-2, which resulted in increased levels
of cytochrome c release and increase caspase-3 and -9 in U937 cells. 相似文献
6.
7.
Dedifferentiated hepatoma cells, in contrast to most other cell types including hepatoma cells, undergo apoptosis when treated
with lipopolysaccharide (LPS) plus the protein synthesis inhibitor cycloheximide (CHx). We recently reported that the dedifferentiated
hepatoma cells also exhibit a strong and prolonged NF-κB induction phenotype upon exposure to LPS, suggesting that NF-κB signaling
may play a pro-survival role, as reported in several other cell systems. To test the role of NF-κB in preventing LPS-mediated
apoptosis, we examined the dedifferentiated cell line M38. Results show that antioxidants strongly inhibited LPS + CHx-mediated
cell death in the M38 cells, yet only modestly inhibited NF-κB induction. In addition, inhibition of NF-κB translocation by
infection of the M38 cells with an adenoviral vector expressing an IκBα super-repressor did not result in LPS-mediated cell
death. These results suggest that unlike TNFα induction, the cell survival pathway activated in response to LPS is independent
of NF-κB translocation in the dedifferentiated cells. Addition of inhibitors of JNK, p38 and ERK pathways also failed to elicit
LPS-mediated apoptosis similar to that observed when protein synthesis is prevented. Thus, cell survival pathways other than
those involving NF-κB inducible gene expression or other well-known pathways appear to be involved in protecting the dedifferentiated
hepatoma variant cells from LPS-mediated apoptosis. Importantly, this pro-apoptotic function of LPS appears to be a function
of loss of hepatic gene expression, as the parental hepatoma cells resist LPS-mediated apoptosis in the presence of protein
synthesis inhibitors. 相似文献
8.
Lee TH Tai DI Cheng CJ Sun CS Lin CY Sheu MJ Lee WP Peng CY Wang AH Tsai SL 《Journal of biomedical science》2006,13(1):27-39
Summary Chronic infections with hepatitis B and C viruses (HBV and HCV) are etiologically linked to hepatitis, liver cirrhosis, and
hepatocellular carcinoma (HCC). Both viruses may induce activation of nuclear factor-kappa B (NF-κB) in hepatocytes that plays
a crucial role in the regulation of cell growth and apoptosis. Functional proteomics analysis of proteins associated with
NF-κB signaling complexes in both viruses-related HCC tumor and non-tumor tissues may disclose possible common mechanisms
in hepatocarcinogenesis. By functional proteomics, we analyzed proteins associated with NF-κB-signaling complexes in four-paired
human HCC tumor and non-tumor tissues from HBV- and HCV-infected patients, respectively, and in one-paired tissue with dual
viral infection. The quantity of NF-κB-associated proteins was semi-quantitatively measured by protein spot intensity on the
gels of two-dimensional polyacrylamide gel electrophoresis. The results showed that overexpression of NF-κB-associated Wnt-1 protein in tumor part was detected in the␣majority of HBV- and HCV-infected HCC samples. These data suggest that enhanced
expression of NF-κB-associated Wnt-1 protein might be a mechanism of hepatocarcinogenesis common to HBV- and HCV-infected patients. NF-κB signaling pathway and
Wnt-1 protein could be potential targets for designing highly effective therapeutic agents in treating HCC and for chemoprevention
of hepatocarcinogenesis. 相似文献
9.
10.
Tumor necrosis factor alpha (TNFα) activates the nuclear factor-kappaB (NF-κB) pathway in various cell types, leading to expression
of cell survival and inflammatory proteins. One mechanism of cell survival brought about by NF-κB is the inhibition of Activator
Protein-1 (AP-1), which when activated, could lead to cell death. However, TNFα can also induce the AP-1 pathway, and the
mechanisms by which these two pathways are regulated in response to TNFα are poorly understood. We proposed that Inhibitor
of κB Kinase gamma (IKKγ) (which is also known as NF-κB essential modulator, NEMO) plays a key role in integrating and coordinating
these two pathways. Our results showed that IKKγ activates the AP-1 pathway, via a mechanism that is dependent on the first
leucine zipper (LZ) domain of IKKγ, by interacting with two proteins of the AP-1 complex, c-Jun and c-Fos, and changing the
phosphorylation status of c-Jun. Even though IKKγ is required for the activation of NF-κB, we found that it reduced the activity
of NF-κB when it was overexpressed. In summary, we demonstrated that transfected IKKγ, while inhibiting the NF-κB pathway,
directly interacts with the AP-1 proteins and activates the AP-1 pathway independent of its effects on NF-κB. Our results
indicate that IKKγ regulates TNFα signaling by coordinating cell responses mediated by the AP-1 and NF-κB pathways.
A. S. Shifera and J. M. Friedman contributed equally to this article.
Marshall S. Horwitz—Deceased: This article is dedicated to his loving memory. 相似文献
11.
High levels of homocysteine promote cell damage mainly through induction of oxidative stress, endoplasmic reticulum (ER) stress,
and activation of pro-inflammatory factors. The effects of homocysteine were here examined in the continuously dividing neuroblastoma
cell line Neuro2a. Cell treatment with homocysteine (100–500 μM) for 4 h increased ROS production while reducing cell viability
in a dose-dependent manner. Cell exposure to 250 μM homocysteine was able to induce transglutaminase 2 up-regulation and increased
in situ transglutaminase activity. These effects were prevented by the incubation with the transglutaminase activity inhibitor
cystamine. Homocysteine also induced NF-κB activation that seemed associated with transglutaminase 2 up-regulation since the
specific NF-κB inhibition by SN50 was able to reduce transglutaminase expression and activity levels. In the light of these
observations, it may be postulated that TG2 up-regulation is involved in cell response to homocysteine-induced stress, in
which NF-κB activation plays also a pivotal role. 相似文献
12.
Petrova RD Mahajna J Reznick AZ Wasser SP Denchev CM Nevo E 《Molecular biology reports》2007,34(3):145-154
MCF7 breast cancer cell line, carrying a luciferase reporter gene under the control of nuclear factor kappa B (NF-κB)-responsive
promoter, was established and used for the screening of fungal organic extracts for their ability to interfere with the NF-κB
activation pathway. Twenty-eight crude fungal extracts, out of 242, were found to inhibit NF-κB reporter activity by more
than 40%. Furthermore, positive extracts were used to evaluate their antiproliferative activity as well as their ability to
influence the phosphorylation and degradation levels of IκBa. Fungal extracts prepared from Marasmius oreades and Cyathus striatus showed significant inhibitory effects on the NF-κB activation pathway. Taken together, our results support the notion of the presence of novel activities that might be utilized as cancer therapeutics. 相似文献
13.
Zhi-Jun Sun Gang Chen Xiang Hu Wei Zhang Yang Liu Ling-Xin Zhu Qian Zhou Yi-Fang Zhao 《Apoptosis : an international journal on programmed cell death》2010,15(7):850-863
Quercetin, one of the most common natural flavonoids, has been reported to possess significant anti-tumor activities both
in vitro and in vivo. The present study was to investigate the effects of quercetin on growth and apoptosis in human salivary
adenoid cystic carcinoma (ACC). The result from MTT assay showed that quercetin decreased cell viability of both low metastatic
cell line ACC-2 and high metastatic cell line ACC-M in a concentration- and time-dependent manner. Moreover, treatment with
quercetin resulted in significantly increased apoptosis in ACC cells. Our data also revealed that the apoptosis induced by
quercetin treatment was through a mitochondria-dependent pathway which showed close correlation with the down-regulation of
the PI3K/Akt/IKK-α/NF-κB pathway. Most importantly, quercetin significantly prevented in vivo growth of ACC xenografts in
nude mice, accompanied by induction of tumor cell apoptosis, suppression of NF-κB nuclear translocation, as well as down-regulation
of Akt and IKK-α activation. In addition, we explored the clinical significance of the PI3K/Akt/IKK-α/NF-κB signaling axis
in ACC by immunohistochemical analysis of tissue specimens followed by the clustering analyses. We determined that the PI3K/Akt/IKK-α/NF-κB
pathway is ubiquitously activated in ACC and plays an essential role in the evasion of apoptosis. Taken together, the results
from our study implicated that quercetin would be a promising chemotherapeutic agent against ACC through its function of down-regulating
the PI3K/Akt/IKK-α/NF-κB signaling pathway. 相似文献
14.
Valerie Leblanc Marie-Claude Dery Carl Shooner Eric Asselin 《Reproductive biology and endocrinology : RB&E》2003,1(1):59
During rat estrous cycle, the endometrium proliferates in response to sex steroids and specific endometrial epithelial cells
undergo apoptosis in absence of embryonic factors. The central executioner of apoptosis is a family of aspartic acid-specific
cysteine proteases known as caspases. Smac/DIABLO is released from the mitochondria during apoptosis and its stimulation promotes
caspases activation by neutralizing members of the inhibitor of apoptosis proteins (IAPs) family, such as X-linked inhibitor
of apoptosis protein (XIAP). The aim of this study was to investigate the involvement of Smac/DIABLO and XIAP in the control
of caspases activation in endometrium of cycling rats. Polyoestrus female rats were sacrificed at each stage of estrous cycle
(diestrus, proestrus, estrus, and metestrus). Endometrial protein extracts were collected to perform Western Blot analysis.
Alternatively, uterine horns were sectioned for immunohistochemistry (IHC). We and others showed previously the presence of
apoptosis at estrus in rat uterine epithelium. In the present study, cleaved caspase-3, -6, and -7 fragments were detected
at estrus. IHC confirmed that caspase-3 was present only in luminal and glandular epithelium at estrus. XIAP was highly expressed
at estrus in both epithelial and stromal cells. In contrast, expression of Smac/DIABLO was elevated at diestrus, proestrus
and metestrus but was minimal at estrus. Treatment of ovariectomized rats with 17β-estradiol induced XIAP expression and inhibited
Smac/DIABLO protein expression in the endometrium. Cleaved caspase-3, -6, and -7 fragments increased in endometrial protein
extracts following 17β-estradiol treatment. Expression of NF-κB and IκB proteins, and IκB phosphorylation status were detected
in the endometrium but were not influenced by the estrous cycle. These findings suggest that Smac/DIABLO and XIAP are regulated
differently and may play important roles in the regulation of endometrial cell fate. Moreover, this study confirms a key role
for executioner caspases in the control of apoptotic processes at estrus in the rat uterus. 相似文献
15.
Ranjan P Boss JM 《Apoptosis : an international journal on programmed cell death》2006,11(10):1837-1849
The CCAAT enhancer binding protein-β (C/EBPβ) is a critical regulator of many cellular processes. Exposure of C/EBPβ-deficient
fibroblasts to tumor necrosis factor-α (TNF) resulted in their death due to apoptosis. While, the expression of Bad, Bcl-2,
Bcl-x, CAS, and hILP/XIAP, as well as the nuclear translocation of NF-κB was normal in C/EBPβ-deficient cells, induction of
manganous superoxide dismutase (MnSOD) gene did not occur. Ectopic expression of C/EBPβ in C/EBPβ–deficient fibroblasts prevented
TNF-induced apoptosis. C/EBPβ complemented cells were able to induce MnSOD in response to TNF, ruling out the possibilities
that C/EBPβ could render protection by regulating early apoptotic gene expression and/or NF-κB p65 expression. Moreover, C/EBPβ-deficient
cells stably transfected with an MnSOD expression vector bypassed the requirement of C/EBPβ in protection against TNF-induced
cell death, suggesting that C/EBPβ protects TNF-induced apoptotic cell death through its role in activating MnSOD expression.
Mechanistically, C/EBPβ was required for induced NF-κB p65 binding to MnSOD’s intronic TNF response element and indispensable
for histone acetylation of the element in response to TNF. These results suggest a role for C/EBPβ in MnSOD regulation through
remodeling of local chromatin structure.
This work was supported by a grant from the National Institutes of Health, CA96810. 相似文献
16.
Rainer Voisard Nicola Huber Regine Baur Milorat Susa Oliver Ickrath Anton Both Wolfgang Koenig Vinzenz Hombach 《BMC molecular biology》2001,2(1):7-7
Background
Activation of nuclear factor-κB (NF-κB) is one of the key events in early atherosclerosis and restenosis. We hypothesized that tumor necrosis factor-α (TNF-α) induced and NF-κB mediated expression of intercellular adhesion molecule-1 (ICAM-1) can be inhibited by antisense RelA p65 and NF-κB1 p50 oligonucleotides (RelA p65 and NF-κB1 p50). 相似文献17.
Immunohistochemical localization of advanced glycation end-products (AGEs) and their receptor (RAGE) in polycystic and normal ovaries 总被引:2,自引:2,他引:0
Diamanti-Kandarakis E Piperi C Patsouris E Korkolopoulou P Panidis D Pawelczyk L Papavassiliou AG Duleba AJ 《Histochemistry and cell biology》2007,127(6):581-589
The aim of the present study was to investigate the localization/immunohistochemical distribution of AGEs and RAGE, as well
as their putative signalling mediator NF-κB in ovaries of women with polycystic ovary syndrome (PCOS) compared to normal.
Archival ovarian-tissue samples from biopsies of six women with PCOS and from six healthy of similar age women, were examined
immunohistochemically with monoclonal anti-AGEs, anti-RAGE and anti-NF-κB(p50/p65) specific antibodies. In healthy women,
AGE immunoreactivity was observed in follicular cell layers (granulosa and theca) and luteinized cells, but not in endothelial
cells. PCOS specimens displayed AGE immunoexpression in theca interna and granulosa cells as well as in endothelial cells,
but staining of granulosa cells was stronger than in that of normal ovaries. RAGE was highly expressed in normal and PCOS
tissues. Normal tissue exhibited no staining differences between granulosa cell layer and theca interna. However, in PCOS
ovaries, granulosa cells displayed stronger RAGE expression compared to theca interna cells in comparison to controls. NF-κB(p50/p65)
was expressed in the cytoplasm of theca interna and granulosa cells of both normal and PCOS ovaries; whereas the NF-κB p65
subunit was only observed in granulosa cells nuclei in PCOS tissue. In conclusion, these findings demonstrate for the first
time that RAGE and AGE-modified proteins with activated NF-κB are expressed in human ovarian tissue. Furthermore, a differential
qualitative distribution of AGE, RAGE and NF-κB p65 subunit was observed in women with PCOS compared to healthy controls,
where a stronger localization of both AGE and RAGE was observed in the granulosa cell layer of PCOS ovaries. 相似文献
18.
Nakaizumi A Horie T Kida T Kurimoto T Sugiyama T Ikeda T Oku H 《Cellular and molecular neurobiology》2012,32(1):95-106
Modulation of enzyme activity through nitrosylation has recently been identified as a new physiological activity of nitric
oxide (NO). We hypothesized that NO enhances the TNF-α-induced death of retinal neurons through a suppression of nuclear factor-κB
(NF-κB) by nitrosylation. In this study, cells from the RGC-5 line were exposed to different concentrations (2.0, 10, and
50 ng/ml) of TNF-α, and the degree of TNF-α-induced cell death was determined by the WST-8 assay and by flow cytometric measurements
of the externalization of phosphatidylserine. The effects of etanercept, a soluble TNFR-Fc fusion protein, and S-nitroso-N-penicillamine (SNAP), an NO donor, on the toxicity were determined. Experiments were also performed to determine whether
nitric oxide synthase (NOS) was associated with the toxicity of TNF-α. The activation of NF-κB was determined by the detection
of the p65 subunit in the nuclear extracts. Our results showed that exposure of RGC-5 cells to different concentrations of
TNF-α significantly decreased the number of living cells in a dose-dependent way. The death was partially due to apoptosis
with an externalization of phosphatidylserine, and the death was suppressed by etanercept. Exposure to TNF-α increased the
activation of NF-κB and the expression of iNOS. Although NF-κB inhibitors suppressed the increase of iNOS, they also potentiated
the TNF-α-induced death. Both L-NAME and aminoguanidine, both NOS inhibitors, rescued the cells from death. In contrast, addition
of SNAP caused nitrosylation of the inhibitory κB kinase, and suppressed the NF-κB activation and potentiated the TNF-α-induced
neurotoxicity. These results indicate that NO potentiates the neurotoxicity of TNF-α by suppressing NF-κB. 相似文献
19.
Pengfei Yu Qian Liu Kun Liu Kazumi Yagasaki Erxi Wu Guoying Zhang 《Cytotechnology》2009,59(3):219-229
Matrine has shown therapeutic and/or adjuvant therapeutic effects on the treatment of some patients with breast cancer. However,
its mechanisms of action are largely unknown. To disclose the mechanisms, we investigated in vitro and ex vivo effects of
matrine on the cancer cells. Our results confirmed that matrine significantly suppressed the proliferation of highly-metastatic
human breast cancer MDA-MB-231 cell line. Matrine displayed synergistic effects with existing anticancer agents celecoxib
(the inhibitor of cyclooxygenase-2), trichostatin A (the histone deacetylase inhibitor) and rosiglitazone against the proliferation
and VEGF excretions in MDA-MB-231 cells. Matrine induced the apoptosis and cell cycle arrest by reducing the ratios of Bcl-2/Bax
protein and mRNA levels in the cancer cells. Matrine significantly reduced the invasion, MMP-9/MMP-2 activation, Akt phosphorylation,
nuclear factor κB p-65 expression and DNA binding activity, and mRNA levels of MMP-9, MMP-2, EGF and VEGFR1 in MDA-MB-231 cells. Collectively,
our results suggest that matrine inhibits the cancer cell proliferation and invasion via EGF/VEGF-VEGFR1-Akt-NF-κB signaling pathway. 相似文献
20.
Effects of glutamine on the nuclear factor-kappaB signaling pathway of murine peritoneal macrophages
Marcelo Macedo Rogero Primavera Borelli Ricardo Ambrósio Fock Maria Carolina Borges Marco Aurélio Ramirez Vinolo Rui Curi Karina Nakajima Amanda Rabello Crisma Aline Domingas Ramos Julio Tirapegui 《Amino acids》2010,39(2):435-441
The aim of this study was to evaluate the effect of glutamine on the expression of proteins involved in the nuclear factor-kappaB
(NF-κB) signaling pathway of murine peritoneal macrophages. Since glutamine is essential for the normal functioning of macrophages,
it was hypothesized that in vitro glutamine supplementation would increase NF-κB activation. Peritoneal macrophages were pretreated
with glutamine (0, 0.6, 2 and 10 mM) before incubation with lipopolysaccharide (LPS), and the effects of glutamine on the
production of tumor necrosis factor-alpha and on the expression and activity of proteins involved in the NF-κB signaling pathway
were studied by an enzyme linked immuno-sorbent assay, Western blotting, and an electrophoretic mobility shift assay. Glutamine
treatment (2 and 10 mM) increased the activation of NF-κB in LPS-stimulated peritoneal macrophages (P < 0.05). In non-stimulated cells, glutamine treatment (2 and 10 mM) significantly reduced IκB-α protein expression (P < 0.05). Glutamine modulates NF-κB signaling pathway by reducing the level of IκB-α, leading to an increase in NF-κB within
the nucleus in peritoneal macrophages. 相似文献