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N-acetylcysteine inhibits induction of nitric oxide synthase in 3T3-L1 adipocytes.
J UOEH 2007; 29(4):417-29JU

Abstract

The present study was designed to determine whether N-acetylcysteine (NAC), a potent antioxidant, modulates nitric oxide (NO) production stimulated by lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF-alpha) in adipocytes. Stimulation by the combination of 5 microg/ml of LPS and 100 ng/ml of TNF-alpha (LT) significantly enhanced NO production in 3T3-L1 adipocytes. Preincubation of the cells with NAC (5-20 mM) for 24 h suppressed the increased NO production in a dose-dependent manner. The production of NO was decreased by 49% at the concentration of 20 mM of NAC. The decrease in NO production by NAC was accompanied by a decrease in inducible nitric oxide synthase (iNOS) protein, detected by immunoblot analysis, and iNOS mRNA, determined by real-time reverse-transcriptase coupled polymerase chain reaction analysis. Nuclear factor-kappa B (NF-kappa B) was significantly activated by LT-treatment, while the pretreatment with 20 mM of NAC prevented the activity by 42%. Pyrrolidine dithiocarbamate (PDTC), a NF-kappaB inhibitor, also inhibited the LT-mediated NO production dose-dependently. One hundred microM of PDTC inhibited the NO production by 46%. We also investigated the effect of NAC and PDTC on the production of interleukein-6 (IL-6), which is regulated transcriptionally by NF-kappa B in 3T3-L1 adipocytes. IL-6 production was markedly increased by LT stimulus, and the enhanced secretion of IL-6 was suppressed in a dose-dependent manner by pretreatment with NAC or PDTC. These results suggest that NAC regulates iNOS expression and NO production in adipocytes through the modulating activation of NF-kappa B.

Authors+Show Affiliations

Department of Pediatrics, School of Medicine, University of Occupational and Environmental Health, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18170962

Citation

Araki, Shunsuke, et al. "N-acetylcysteine Inhibits Induction of Nitric Oxide Synthase in 3T3-L1 Adipocytes." Journal of UOEH, vol. 29, no. 4, 2007, pp. 417-29.
Araki S, Dobashi K, Kubo K, et al. N-acetylcysteine inhibits induction of nitric oxide synthase in 3T3-L1 adipocytes. J UOEH. 2007;29(4):417-29.
Araki, S., Dobashi, K., Kubo, K., Kawagoe, R., Yamamoto, Y., & Shirahata, A. (2007). N-acetylcysteine inhibits induction of nitric oxide synthase in 3T3-L1 adipocytes. Journal of UOEH, 29(4), pp. 417-29.
Araki S, et al. N-acetylcysteine Inhibits Induction of Nitric Oxide Synthase in 3T3-L1 Adipocytes. J UOEH. 2007 Dec 1;29(4):417-29. PubMed PMID: 18170962.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - N-acetylcysteine inhibits induction of nitric oxide synthase in 3T3-L1 adipocytes. AU - Araki,Shunsuke, AU - Dobashi,Kazushige, AU - Kubo,Kazuyasu, AU - Kawagoe,Rinko, AU - Yamamoto,Yukiyo, AU - Shirahata,Akira, PY - 2008/1/4/pubmed PY - 2008/2/15/medline PY - 2008/1/4/entrez SP - 417 EP - 29 JF - Journal of UOEH JO - J. UOEH VL - 29 IS - 4 N2 - The present study was designed to determine whether N-acetylcysteine (NAC), a potent antioxidant, modulates nitric oxide (NO) production stimulated by lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF-alpha) in adipocytes. Stimulation by the combination of 5 microg/ml of LPS and 100 ng/ml of TNF-alpha (LT) significantly enhanced NO production in 3T3-L1 adipocytes. Preincubation of the cells with NAC (5-20 mM) for 24 h suppressed the increased NO production in a dose-dependent manner. The production of NO was decreased by 49% at the concentration of 20 mM of NAC. The decrease in NO production by NAC was accompanied by a decrease in inducible nitric oxide synthase (iNOS) protein, detected by immunoblot analysis, and iNOS mRNA, determined by real-time reverse-transcriptase coupled polymerase chain reaction analysis. Nuclear factor-kappa B (NF-kappa B) was significantly activated by LT-treatment, while the pretreatment with 20 mM of NAC prevented the activity by 42%. Pyrrolidine dithiocarbamate (PDTC), a NF-kappaB inhibitor, also inhibited the LT-mediated NO production dose-dependently. One hundred microM of PDTC inhibited the NO production by 46%. We also investigated the effect of NAC and PDTC on the production of interleukein-6 (IL-6), which is regulated transcriptionally by NF-kappa B in 3T3-L1 adipocytes. IL-6 production was markedly increased by LT stimulus, and the enhanced secretion of IL-6 was suppressed in a dose-dependent manner by pretreatment with NAC or PDTC. These results suggest that NAC regulates iNOS expression and NO production in adipocytes through the modulating activation of NF-kappa B. SN - 0387-821X UR - https://www.unboundmedicine.com/medline/citation/18170962/N_acetylcysteine_inhibits_induction_of_nitric_oxide_synthase_in_3T3_L1_adipocytes_ L2 - http://www.medicalonline.jp/meteo_linkout.php?issn=0387-821X&volume=29&issue=4&spage=417 DB - PRIME DP - Unbound Medicine ER -