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nac-n-acetyl-l-cysteine

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Meeting Abstracts
Journal: Diabetes
Diabetes 1999;48(12):2398–2406
Published: 01 December 1999
... the involvement of oxidative stress in the progression of pancreatic beta-cell dysfunction in type 2 diabetes and to evaluate the potential usefulness of antioxidants in the treatment of type 2 diabetes. We used diabetic C57BL/KsJ-db/db mice, in whom antioxidant treatment (N-acetyl-L-cysteine [NAC], vitamins C...
Journal Articles
Journal: Diabetes
Diabetes 2006;55(6):1614–1624
Published: 01 June 2006
... phosphorylation. Antioxidant N-acetyl-l-cysteine (NAC) prevented mercury-induced insulin secretion inhibition and Akt phosphorylation but not increased PI3K activity. Inhibition of PI3K/Akt activity with PI3K inhibitor or by expressing the dominant-negative p85 or Akt prevented mercury-induced...
Journal Articles
Journal: Diabetes
Diabetes 2004;53(1):129–140
Published: 01 January 2004
... insulinoma cells. The effects of oxidative stress caused by OA and potential protective effects of N-acetyl-l-cysteine (NAC), a scavenger of reactive oxygen species (ROS), on global gene expression and β-cell function were investigated. Long-term exposure of MIN6 cells to OA led...
Meeting Abstracts
Journal: Diabetes
Diabetes 2019;68(Supplement_1):387-P
Published: 01 June 2019
...AMIR MOHEET; ANJALI KUMAR; LISA COLES; NATHAN RUBIN; LYNN E. EBERLY; ELIZABETH R. SEAQUIST Impaired awareness of hypoglycemia (IAH) is common in diabetes. Administration of N-acetyl cysteine (NAC) during episodes of hypoglycemia (HG) prevents the development of IAH in rodents (Fioramonti 2013...
Meeting Abstracts
Journal: Diabetes
Diabetes 2018;67(Supplement_1):242-OR
Published: 01 July 2018
... by behavioral optomotry. In R28 retinal cells in culture, hyperglycemic conditions increased REDD1 expression, ROS levels, and cell death. However, addition of the antioxidant N-acetyl-L-cysteine (NAC) to culture medium was sufficient to prevent the increase in ROS and cell death in response to hyperglycemic...
Images
Effects of <em><span class="search-highlight">N</em></span>-<span class="search-highlight">acetyl</span>-<sc><span class="search-highlight">l</span></sc>-<span class="search-highlight">cysteine</span>, genistein, PD9805...
Published: 01 June 2001
FIG. 3. Effects of N-acetyl-l-cysteine, genistein, PD98059, and SB203580 on NF-κB stimulation by CML-HSA. THP-1 cells transfected with the NF-κB reporter were preincubated with the antioxidant N-acetyl-l-cysteine (NAC, 500 μmol/l), a tyrosine kinase inhibitor genistein (100 μmol/l), an MEK-1 inhibitor (PD98059, 50 μmol/l), or a p38 inhibitor (SB203580, 10 μmol/l) at 37°C for 30 min. The cells were then exposed to 100 μg/ml CML-HSA for another 1 h and lysates were assayed for luciferase activity. NF-κB reporter activity with HSA treatment was defined as 100%. All values represent the means ± SE of at least three independent experiments (*P < 0.05). FIG. 3. Effects of N-acetyl-l-cysteine, genistein, PD98059, and SB203580 on NF-κB stimulation by CML-HSA. THP-1 cells transfected with the NF-κB reporter were preincubated with the antioxidant N-acetyl-l-cysteine (NAC, 500 μmol/l), a tyrosine kinase inhibitor genistein (100 μmol/l), an MEK-1 inhibitor (PD98059, 50 μmol/l), or a p38 inhibitor (SB203580, 10 μmol/l) at 37°C for 30 min. The cells were then exposed to 100 μg/ml CML-HSA for another 1 h and lysates were assayed for luciferase activity. NF-κB reporter activity with HSA treatment was defined as 100%. All values represent the means ± SE of at least three independent experiments (*P < 0.05). More
Journal Articles
Journal: Diabetes
Diabetes 2007;56(4):930–939
Published: 01 April 2007
... characterize this phenotype. Oxidative stress induced by aminotriazole (ATZ) was sufficient to stimulate Ub-protein aggregate formation. Furthermore, the addition of the antioxidants N-acetyl cysteine (NAC) and taurine resulted in a significant decrease in formation of Ub-protein aggregates in high...
Images
Hypoxia increased ROS generation but did not activate protein tyrosine phos...
Published: 01 January 2009
FIG. 4. Hypoxia increased ROS generation but did not activate protein tyrosine phosphatases. A: 3T3-L1 adipocytes were incubated with DCFH-DA for 30 min before being incubated for 16 h in normoxia or hypoxia, in the absence or presence of N-acetyl cysteine (10 mmol/l). Adipocytes were lysed, and fluorescence was measured. Results are expressed as the fold of stimulation compared with controls. Data are the means ± SE of three independent experiments performed in triplicate. B: 3T3-L1 adipocytes were incubated in normoxia (21% O2) or hypoxia (1% O2) for 16 h before being stimulated for 5 min with insulin (100 nmol/l). Total phosphatase activity was determined by the dephosphorylation of the synthetic substrate pNPP (para-nitrophenyl phosphate) compared with the activity of CIP (calf intestine phosphatase). Data are the means ± SE of three independent experiments performed in triplicate. C: 3T3-L1 adipocytes were incubated in normoxia or hypoxia for 16 h in the absence or presence of 2 mmol/l vanadate. Adipocytes were stimulated with insulin (100 nmol/l) for 5 min, and cell lysates were analyzed by immunoblots with indicated antibodies. A representative experiment of three independent experiments is shown. Ins, insulin; NAC, N-acetyl cysteine; prot, protein; pTyr, phosphorylated tyrosine. ***P < 0.001. FIG. 4. Hypoxia increased ROS generation but did not activate protein tyrosine phosphatases. A: 3T3-L1 adipocytes were incubated with DCFH-DA for 30 min before being incubated for 16 h in normoxia or hypoxia, in the absence or presence of N-acetyl cysteine (10 mmol/l). Adipocytes were lysed, and fluorescence was measured. Results are expressed as the fold of stimulation compared with controls. Data are the means ± SE of three independent experiments performed in triplicate. B: 3T3-L1 adipocytes were incubated in normoxia (21% O2) or hypoxia (1% O2) for 16 h before being stimulated for 5 min with insulin (100 nmol/l). Total phosphatase activity was determined by the dephosphorylation of the synthetic substrate pNPP (para-nitrophenyl phosphate) compared with the activity of CIP (calf intestine phosphatase). Data are the means ± SE of three independent experiments performed in triplicate. C: 3T3-L1 adipocytes were incubated in normoxia or hypoxia for 16 h in the absence or presence of 2 mmol/l vanadate. Adipocytes were stimulated with insulin (100 nmol/l) for 5 min, and cell lysates were analyzed by immunoblots with indicated antibodies. A representative experiment of three independent experiments is shown. Ins, insulin; NAC, N-acetyl cysteine; prot, protein; pTyr, phosphorylated tyrosine. ***P < 0.001. More
Journal Articles
Journal: Diabetes
Diabetes 2007;56(7):1783–1791
Published: 01 July 2007
..., glucose-stimulated insulin secretion GSSG, oxidized glutathione HNE, 4-hydroxynonenal HO-1, heme oxygenase 1 MGO, methylglyoxal NAC, N-acetyl-L-cysteine NQO-1, NAD(P)H:quinone oxidoreductase 1 Nrf2, transcription factor NF-E2–related factor 2 ·O2, superoxide PEG...
Includes: Supplementary data
Journal Articles
Journal: Diabetes
Diabetes 2005;54(7):2179–2187
Published: 01 July 2005
... endothelial cell HUVEC, human umbilical vein endothelial cell NAC, N-acetyl-l-cysteine PTP, permeability transition pore ROS, reactive oxygen species tBH, tert-butylhydroperoxide Diabetes is a worldwide leading cause of morbidity and mortality, and the management...
Images
Sensitivity of WT and mutant GK to elevated oxidative stress. <em>A</em>...
Published: 13 November 2011
FIG. 4. Sensitivity of WT and mutant GK to elevated oxidative stress. A: GSH content of MIN6, primary hepatocytes (Hep), and H4IIE cells was determined using an enzyme-recycling assay. Results are expressed as nanomoles per milligram protein. Means are ± SEM of three independent experiments. ***P < 0.005 relative to MIN6. BF: MIN6 cells were transiently transfected with 0.6 μg/well (WT, W99R) or 1.2 μg/well (V62M, G72R, S263P, and G264S) of myc-GK and cultured for 24 h. Cells were treated with 100 μmol/L diamide plus 100 μmol/L SNP or 10 μmol/L MEN at 5 mmol/L glucose for 1 h. BD: Parallel incubations were performed for determination of GSH, H2O2, and NO and expressed as fold change relative to control. Means are ± SEM of four independent experiments. *P < 0.05, **P < 0.01, ***P < 0.005 relative to absence of SNP/MEN. E and F: GK activity was determined using a spectrophotometric method and expressed relative to absence of SNP/MEN. Means are ± SEM of four (SNP) or five (MEN) independent experiments. *P < 0.05, **P < 0.01, ***P < 0.005 relative to WT; #P < 0.05 relative to absence of MEN. G: Untreated MIN6 cells were cultured in the presence of 2 mmol/L N-acetyl cysteine (NAC) for 24 h followed by a 1-h incubation with 100 μmol/L diamide and 5 μmol/L MEN. GK activity was determined using a spectrophotometric method and expressed relative to absence of MEN/NAC. Means are ± SEM of four independent experiments. **P < 0.01, effect of MEN. H: Untreated MIN6 cells were cultured in the presence of 10 μmol/L GKA-S (inactive) or GKA-R (active) for 24 h followed by incubation with 100 μmol/L diamide and increasing concentrations of MEN (5, 7.5, and 10 μmol/L) for 1 h. GK activity was determined using a spectrophotometric method and expressed relative to control. Means are ± SEM of four independent experiments. *P < 0.05, **P < 0.01, ***P < 0.005, effect of GKA-R. FIG. 4. Sensitivity of WT and mutant GK to elevated oxidative stress. A: GSH content of MIN6, primary hepatocytes (Hep), and H4IIE cells was determined using an enzyme-recycling assay. Results are expressed as nanomoles per milligram protein. Means are ± SEM of three independent experiments. ***P < 0.005 relative to MIN6. B–F: MIN6 cells were transiently transfected with 0.6 μg/well (WT, W99R) or 1.2 μg/well (V62M, G72R, S263P, and G264S) of myc-GK and cultured for 24 h. Cells were treated with 100 μmol/L diamide plus 100 μmol/L SNP or 10 μmol/L MEN at 5 mmol/L glucose for 1 h. B–D: Parallel incubations were performed for determination of GSH, H2O2, and NO and expressed as fold change relative to control. Means are ± SEM of four independent experiments. *P < 0.05, **P < 0.01, ***P < 0.005 relative to absence of SNP/MEN. E and F: GK activity was determined using a spectrophotometric method and expressed relative to absence of SNP/MEN. Means are ± SEM of four (SNP) or five (MEN) independent experiments. *P < 0.05, **P < 0.01, ***P < 0.005 relative to WT; #P < 0.05 relative to absence of MEN. G: Untreated MIN6 cells were cultured in the presence of 2 mmol/L N-acetyl cysteine (NAC) for 24 h followed by a 1-h incubation with 100 μmol/L diamide and 5 μmol/L MEN. GK activity was determined using a spectrophotometric method and expressed relative to absence of MEN/NAC. Means are ± SEM of four independent experiments. **P < 0.01, effect of MEN. H: Untreated MIN6 cells were cultured in the presence of 10 μmol/L GKA-S (inactive) or GKA-R (active) for 24 h followed by incubation with 100 μmol/L diamide and increasing concentrations of MEN (5, 7.5, and 10 μmol/L) for 1 h. GK activity was determined using a spectrophotometric method and expressed relative to control. Means are ± SEM of four independent experiments. *P < 0.05, **P < 0.01, ***P < 0.005, effect of GKA-R. More
Journal Articles
Journal: Diabetes
Diabetes 2001;50(6):1495–1504
Published: 01 June 2001
...FIG. 3. Effects of N-acetyl-l-cysteine, genistein, PD98059, and SB203580 on NF-κB stimulation by CML-HSA. THP-1 cells transfected with the NF-κB reporter were preincubated with the antioxidant N-acetyl-l-cysteine (NAC, 500 μmol/l), a tyrosine kinase inhibitor...
Images
Inhibition of autophagic flux reduces eNOS dimerization and impairs endothe...
Published: 18 February 2022
Figure 2 Inhibition of autophagic flux reduces eNOS dimerization and impairs endothelial function by upregulating ROS. (AC) HUVECs were incubated with 10 µmol/L CQ or 10 nmol/L BafA1 for 3 or 12 h under FBS-free conditions. Western blotting was used to determine the protein expression of eNOS, p62, and LC3 (n = 8). (D) Treatment of db/m+ mouse aortas with 3-MA (10 mmol/L, 24 h), CQ (10 µmol/L, 24 h), or BafA1 (10 nmol/L, 16 h) impaired EDR (n = 4–5). % Phe tone is the percentage of tension with phenylephrine contraction. *P < 0.05 vs control. (E and F) Representative images showing mtROS generation using MitoSOX red staining in HUVECs after incubation with CQ (10 µmol/L, 24 h) and CQ plus mtROS scavenger Mito TEMPO (100 µmol/L, 24 h); n = 12–16. (G) DAF-DA staining results showing that 6-h treatment with CQ (10 µmol/L) inhibited 1 µmol/L A23187-induced NO production in HUVECs, which was attenuated by Mito TEMPO (100 µmol/L, 6 h); n = 5–6. *P < 0.05 vs. control; #P < 0.05 vs. CQ. (H) HUVECs were preincubated with Mito TEMPO (100 µmol/L), BH4 (100 µmol/L), and N-acetyl-l-cysteine (NAC; 2.5 mmol/L), then followed by treatment with BafA1 (10 nmol/L) for 12 h. Western blotting was used to determine the expression of eNOS. (I) Statistical analysis result of (H); n = 7–8. Results are reported as mean ± SD. Statistical analysis was performed using two-way repeated measures ANOVA followed by Tukey test for (D and G), and one-way ANOVA followed by Tukey test for (B, C, F, and I). More
Journal Articles
Journal: Diabetes
Diabetes 2007;56(6):1534–1543
Published: 01 June 2007
...), and GW3965 was kindly provided by Dr. Peter Tontonoz (University of California, Los Angeles, CA). Cerulenin was purchased from Sigma Aldrich (Saint Louis, MO), and N-acetyl-l-cysteine (NAC) was purchased from Calbiochem. Pancreatic islets were isolated from Otsuka Long-Evans...
Includes: Supplementary data
Journal Articles
Journal: Diabetes
Diabetes 2003;52(7):1843–1850
Published: 01 July 2003
... aortic endothelial cell ICAM-1, intercellular adhesion molecule-1 LOX-1, lectin-like oxLDL receptor-1 MAPK, mitogen-activated protein kinase NAC, N-acetyl-l-cysteine NF, nuclear factor NP-40, Nonidet P-40 oxLDL, oxidized LDL PKC, protein kinase C PMSF, phenylmethylsulfonyl...
Journal Articles
Journal: Diabetes
Diabetes 2005;54(5):1506–1513
Published: 01 May 2005
... endothelial cell LA, linoleic acid LOX-1, lectin-like oxidized LDL receptor-1 NAC, N-acetyl-l-cysteine oxLDL, oxidized LDL NF, nuclear factor PKC, protein kinase C SR, scavenger receptor Endothelial dysfunction (ED), a characteristic feature of early-state atherosclerosis...
Journal Articles
Journal: Diabetes
Diabetes 2020;69(8):1650–1661
Published: 22 May 2020
... , De Backer   WA . Antioxidant and anti-inflammatory efficacy of NAC in the treatment of COPD: discordant in vitro and in vivo dose-effects: a review . Pulm Pharmacol Ther   2007 ; 20 : 9 – 22 4. Awad   N , Khatib   N , Ginsberg   Y , et al . N-acetyl-cysteine (NAC) attenuates...
Journal Articles
Journal: Diabetes
Diabetes 2007;56(2):394–403
Published: 01 February 2007
... 2007 GLUT4myc, c-myc epitope–tagged GLUT4 IRS, insulin receptor substrate NAC, N-acetyl-l-cysteine PAK, p21-activated kinase PI, phosphatidylinositol siRNA, small interfering RNA Insulin promotes dietary glucose disposal into skeletal muscle through recruitment...
Includes: Supplementary data
Journal Articles
Journal: Diabetes
Diabetes 2006;55(11):2939–2949
Published: 01 November 2006
...-7082, diphenyleneiodonium chloride, and N-acetyl-l-cysteine (NAC) were purchased from Calbiochem. hTNFα was purchased from R&D Systems. 3T3-L1 preadipocytes were grown to confluence in Dulbecco’s modified Eagle’s medium (DMEM) supplemented with 10% bovine calf serum (Gibco...
Includes: Supplementary data
Journal Articles
Journal: Diabetes
Diabetes 2018;67(1):78–84
Published: 27 October 2017
... described ( 14 ). N-acetyl-l-cysteine (NAC) (Sigma-Aldrich, Saint-Quentin-Fallavier, France) treatment was initiated at embryonic day 9.5 (E9.5) until E13.5, and at E12.5 until E19.5. Tissues were fixed in 10% formalin and processed for immunohistochemistry, as described previously...
Includes: Supplementary data