N-acetylcysteine attenuates TNF-α induced changes in secretion of interleukin-6, plasminogen activator inhibitor-1 and adiponectin from 3T3-L1 adipocytes

Araki, Shunsuke; Dobashi, Kazushige; Kubo, Kazuyasu; Yamamoto, Yukiyo; Asayama, Kohtaro; Shirahata, Akira

doi:10.1016/j.lfs.2006.08.004

Cited by 46 publications

(43 citation statements)

References 47 publications

(55 reference statements)

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“…Blocking of NFκB with an IκB super-repressor abolished the activating effects of abovementioned treatments in the presence and absence of PBMCs. It is important to note that NAC had inhibitory effect on TNF-α treated cells as shown previously [30]. and in Fig.…”

Section: Increased Function Of Nuclear Nfκb By Nacsupporting

confidence: 77%

N-acetylcysteine protects dental pulp stromal cells from HEMA-induced apoptosis by inducing differentiation of the cells

Paranjpe

Cacalano

Hume

et al. 2007

Free Radical Biology and Medicine

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Resin based materials are now widely used in dental restorations. While the use of these materials is aesthetically appealing in patients, they carry the risk of local and systemic adverse effects. The potential risks are direct damage to the cells and induction of immune-based hypersensitivity reactions. Dental Pulp Stromal Cells (DPSCs) and oral keratinocytes are the major cell types which may come in contact with dental resins such as 2-hydroxyethyl methacrylate (HEMA) after dental restorations. Here we show that N-acetyl cysteine (NAC) inhibits HEMA induced apoptotic cell death and restores the function of DPSCs and oral epithelial cells. NAC inhibits HEMA mediated toxicity through induction of differentiation in DPSCs since the genes for dentin sialoprotein (DSP), Osteopontin (OPN), Osteocalcin (OCN), and Alkaline Phosphatase (ALP) which are induced during differentiation are also induced by NAC. Unlike NAC, Vitamin E and C which known anti-oxidant compounds failed to prevent either HEMA mediated cell death or decrease in VEGF secretion by human DPSCs. More importantly, when added either alone or in combination with HEMA Vitamin E and Vitamin C did not increase the gene expression for OPN, and in addition Vitamin E inhibited the protective effect of NAC on DPSCs. NAC inhibited HEMA mediated decrease in NFκB activity thus, providing survival mechanism for the cells. Overall, the studies reported in this paper indicated that undifferentiated DPSCs have exquisite sensitivity to HEMA induced cell death, and their differentiation by NAC resulted in an increased NFκB activity which might have provided the basis for their increased protection from HEMA mediated functional loss and cell death.

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Section: Increased Function Of Nuclear Nfκb By Nacsupporting

confidence: 77%

N-acetylcysteine protects dental pulp stromal cells from HEMA-induced apoptosis by inducing differentiation of the cells

Paranjpe

Cacalano

Hume

et al. 2007

Free Radical Biology and Medicine

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“…It is interesting in our findings that NAC alone slightly decreased ROS levels of preadipocytes and adipocytes by 10 and 25%, respectively, while it significantly increased GSH levels of preadipocytes and adipocytes by 25 and 42%. One of the possible explanations for the lesser effect of NAC on ROS than GSH production is that the distinct types of antioxidant enzymes (i. e., catalase, NADPH oxidase, xanthine oxidase, and superoxide dismutase) and factors (i. e., NFjB and adiponectin) [28,42] may affect ROS and GSH production in 3T3-L1 cells at varying levels. This explanation is supported by the facts that NAC suppressed tumor necrosis factor a-decreased superoxide dismutase and catalase in 3T3-L1 adipocytes [28] and that NAC reversed the effects of H 2 O 2 on the expression levels of adiponectin gene to normal levels in 3T3-L1 adipocytes [42].…”

Section: Discussionmentioning

confidence: 99%

“…Tea catechins were dissolved in 0.1% DMSO and sterile medium for cell treatment. According to the literature [28,29], which shows that N-acetyl-L-cysteine (NAC) and L-buthionine-[S,R]-sulfoximine (BSO) are respectively able to stimulate and inhibit GSH levels, we treated serumstarved 3T3-L1 cells with or without EGCG in the presence and absence of either NAC (5 -10 mM) or BSO (40 lM) for 8 h. In other experiments, we followed the method of Tachibana et al (24) and treated 3T3-L1 cells with either a rabbit polyclonal 67LR antibody (l5 lg/mL) or preimmu-nized NRS (as the control) for 1 h, and then stimulated them with or without EGCG (50 lM) for 8 h. After treatment, ROS and GSH levels were measured.…”

Section: Experimental Treatmentsmentioning

confidence: 99%

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The effects of green tea (–)‐epigallocatechin‐3‐gallate on reactive oxygen species in 3T3‐L1 preadipocytes and adipocytes depend on the glutathione and 67 kDa laminin receptor pathways

Wang

Chang

Hsiao

et al. 2009

Molecular Nutrition Food Res

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Green tea (-)-epigallocatechin-3-gallate (EGCG) is known as to regulate obesity and fat cell activity. However, little information is known about the effects of EGCG on oxidative reactive oxygen species (ROS) of fat cells. Using 3T3-L1 preadipocytes and adipocytes, we found that EGCG increased ROS production in dose- and time-dependent manners. The concentration of EGCG that increased ROS levels by 180-500% was approximately 50 muM for a range of 8-16 h of treatment. In contrast, EGCG dose- and time-dependently decreased the amount of intracellular glutathione (GSH) levels. EGCG was more effective than (-)-epicatechin, (-)-epicatechin-3-gallate, and (-)-epigallocatechin in changing ROS and GSH levels. This suggests a catechin-specific effect. To further examine the relation of GSH to ROS as altered by EGCG, we observed that exposure of preadipocytes and adipocytes to N-acetyl-L-cysteine (a GSH precursor) blocked the EGCG-induced increases in ROS levels and decreases in GSH levels. These observations suggest a GSH-dependent effect of EGCG on ROS production. While EGCG was demonstrated to alter levels of ROS and GSH, its signaling was altered by an EGCG receptor (the so-called 67 kDa laminin receptor(67LR)) antiserum, but not by normal rabbit serum. These data suggest that EGCG mediates GSH and ROS levels via the 67LR pathway.

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“…In addition to amifostine, our choices of other likely candidates were the thiol-containing antioxidants n-acetyl cysteine (NAC) and pyrrolidine dithiocarbamate (PDTC), both of which inhibit nuclear factor-kB activation and nuclear translocation and thereby the transcription of many cytokines, chemokines and adhesion molecules. 13,14 We 9,10 and others 11,12 have demonstrated the critical role of tumor necrosis factor a and interleukin-1b in pathogenesis of aGVHD. We tested their administration prior to lethal total body irradiation (TBI) and allogeneic bone marrow (BM)/spleen transplantation in our standard protocol that typically leads to fatal aGVHD.…”

Section: Introductionmentioning

confidence: 93%

Amifostine prior to lethal irradiation prevents allogeneic bone marrow engraftment in mice

Thompson

Asmis

Chu

et al. 2008

Bone Marrow Transplant

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N-acetylcysteine attenuates TNF-α induced changes in secretion of interleukin-6, plasminogen activator inhibitor-1 and adiponectin from 3T3-L1 adipocytes

Cited by 46 publications

References 47 publications

N-acetylcysteine protects dental pulp stromal cells from HEMA-induced apoptosis by inducing differentiation of the cells

N-acetylcysteine protects dental pulp stromal cells from HEMA-induced apoptosis by inducing differentiation of the cells

The effects of green tea (–)‐epigallocatechin‐3‐gallate on reactive oxygen species in 3T3‐L1 preadipocytes and adipocytes depend on the glutathione and 67 kDa laminin receptor pathways

Amifostine prior to lethal irradiation prevents allogeneic bone marrow engraftment in mice

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