ライフサイエンスコーパス: N-acetylcysteine

1 3988, and oxidative stress was attenuated by N-acetylcysteine.

2 mediated relaxations, which were reversed by N-acetylcysteine.

3 ssure-dependent tone, which were annulled by N-acetylcysteine.

4 Another set of mice received the antioxidant N-acetylcysteine.

5 n of LKB1 and by incubation with antioxidant N-acetylcysteine.

6 f the phenotype by the antioxidant action of N-acetylcysteine.

7 ress program were blocked by the antioxidant N-acetylcysteine.

8 od and can be prevented with the antioxidant N-acetylcysteine.

9 defect, which is rescued by the antioxidant N-acetylcysteine.

10 lasmid that was prevented by the addition of N-acetylcysteine.

11 okine signaling 3), and antioxidants such as N-acetylcysteine.

12 eroxide, and these effects were inhibited by N-acetylcysteine.

13 substantially reduced in mice that received N-acetylcysteine.

14 She was treated with N-acetylcysteine.

15 the NOX subunit NOX2 and by the antioxidant N-acetylcysteine.

16 chronic treatment with the cystine prodrug, N-acetylcysteine.

17 ed HBEC and did not occur in the presence of N-acetylcysteine.

18 uld be partially reversed by the antioxidant N-acetylcysteine.

19 KO clones were cultivated in the presence of N-acetylcysteine.

20 processes were reversed by the antioxidant, N-acetylcysteine.

21 rolonged therapeutic efficacy as compared to N-acetylcysteine.

22 espiratory epithelium integrity with EGTA or N-acetylcysteine.

23 n of glutamate, alphaKG, or nucleobases with N-acetylcysteine.

24 ated by capsazepine, and by the antioxidant, N-acetylcysteine.

25 es in uterine arteries, which was blocked by N-acetylcysteine.

26 y CD4 T cells is improved by the antioxidant N-acetylcysteine.

27 bunit, which was restored in the presence of N-acetylcysteine.

28 N-acetylcysteine (3.3%) decreased biofilm biomass and ki

29 ) were observed, as well as increased use of N-acetylcysteine (48.9% vs. 69.3% overall; 15.8% vs. 49.

30 cysteamine bitartrate (60 mg/kg per day) and N-acetylcysteine (60 mg/kg per day) and were assessed ev

31 r studying the biochemical transformation of N-acetylcysteine, a commonly prescribed Cys supplement d

32 was performed for several small peptides and N-acetylcysteine, a drug administered intravenously to t

33 Supplementation of N-acetylcysteine, a glutathione precursor, conferred a p

34 ed cell death was rescued in the presence of N-acetylcysteine, a glutathione precursor.

35 el gating, and was attenuated by antioxidant N-acetylcysteine, a known scavenger of acrolein.

36 and (2) use the EAAC1(-/-) mouse to evaluate N-acetylcysteine, a membrane-permeable cysteine pro-drug

37 We posit that treatment with N-acetylcysteine, a precursor of glutathione, the larges

38 Treatment with N-acetylcysteine, a safe prodrug against oxidation, reve

39 We also show that N-acetylcysteine, a widely-used antioxidant, is a poor s

40 Perioperative fenoldopam and N-acetylcysteine abrogate the early postoperative declin

41 ncurrent administration of the ROS inhibitor N-acetylcysteine abrogated beta-catenin/HIF pathway acti

42 N-acetylcysteine accelerates amputation stump healing in

43 the toxin, whereas replenishing GSH level by N-acetylcysteine administration or activation of nuclear

44 Mice in posttreatment were treated with N-acetylcysteine after folic acid.

45 e JNK inhibitor SP600125, or the antioxidant N-acetylcysteine alleviated insulin resistance, demonstr

46 induced glutamatergic adaptations by chronic N-acetylcysteine also caused enduring inhibition of coca

47 Furthermore, the administration of N-acetylcysteine also prevented NF-kappaB activation, ne

48 lternative antioxidants (vitamin C, DTT, and N-acetylcysteine) also enhanced the chemotactic activity

49 Chemical chaperones or the antioxidant N-acetylcysteine ameliorated glucose tolerance and insul

50 Consistently, treatment with anti-oxidant N-acetylcysteine ameliorates muscle necrosis in Stra13-/

51 degeneration, and the unrelated anti-oxidant N-acetylcysteine ameliorates TAC-induced pathology.

52 ent study sought to evaluate the efficacy of N-acetylcysteine amide (NACA) eye drops in reversing the

53 r endothelial (HBMVEC) cells to test whether N-acetylcysteine amide (NACA), a novel antioxidant, prev

54 hypothesized that a novel thiol antioxidant, N-acetylcysteine amide (NACA), might ameliorate cellular

55 The potent antioxidant, N-acetylcysteine amide (NACA), reduces the severity of a

56 N-acetylcysteine amide eye drops were administered begin

57 BC1D24G501R mutant animals with antioxidants N-acetylcysteine amide or alpha-tocopherol as indicated

58 raperitoneally on postpartum day 10, whereas N-acetylcysteine amide was injected intraperitoneally on

59 re randomly divided into a control group, an N-acetylcysteine amide-only group, a sodium selenite-ind

60 N-acetylcysteine, an amino acid, seems to restore the ex

61 ponsible for changes in DICER, we found that N-acetylcysteine, an antioxidant and anti-aldehyde, prot

62 air, and to pretreatment with antioxidants (N-acetylcysteine and ascorbate) and placebo.

63 e effects could be reverted or aggravated by N-acetylcysteine and buthionine sulfoximine, respectivel

64 reatment of DCs or CSE with the antioxidants N-acetylcysteine and catalase.

65 the astroglial glutamate transporter GLT-1 (N-acetylcysteine and ceftriaxone) can decrease measures

66 b-treated mice were significantly reduced by N-acetylcysteine and completely eliminated by recombinan

67 Combined treatment with N-acetylcysteine and cyclic guanosine monophosphate sign

68 e mainly been assessed in adults and include N-acetylcysteine and dexamethasone.

69 ent on oxidative stress and the antioxidants N-acetylcysteine and glutathione (GSH) abrogated ULBP2/5

70 The antioxidants N-acetylcysteine and glutathione monoethyl ester inhibit

71 from modulation studies of glutathione using N-acetylcysteine and L-buthionine-sulfoximine indicate t

72 N-acetylcysteine and phosphoinositide 3-kinase (PI3K) in

73 Antioxidant N-acetylcysteine and recombinant ALR (rALR) both inhibit

74 All patients received a high dose of N-acetylcysteine and sodium bicarbonate solution.

75 Additional controls of n-acetylcysteine and sodium pyruvate were implemented to

76 pileptogenesis by a transient treatment with N-acetylcysteine and sulforaphane, which act to increase

77 ce for the potential roles of bortezomib and N-acetylcysteine, and explore new therapeutic approaches

78 uperior regenerability by each of ascorbate, N-acetylcysteine, and urate when compared to alpha-TOH.

79 In this work, water-dispersible N-acetylcysteine- and l-cysteine-stabilized palladium na

80 er/chlorobenzene two-phase system containing N-acetylcysteine as a reducing agent in the aqueous phas

81 Reactions conducted with ascorbate or N-acetylcysteine as a reductant under aerobic conditions

82 -phase peroxidation system containing excess N-acetylcysteine as a stoichiometric thiol reducing agen

83 Kras(G12D/+);Trp53(fl/fl) mice with 5E1 and N-acetylcysteine, as a ROS scavenger, decreased tumor DN

84 ed suppressor cells, whereas the antioxidant N-acetylcysteine attenuates the inhibitory effects of ph

85 ce in pre- + posttreatment were treated with N-acetylcysteine before folic acid and after folic acid.

86 ere treated with a subcutaneous injection of N-acetylcysteine before the folic acid injection.

87 orylation and activity, whereas antioxidants N-acetylcysteine, beta-naphthoflavone, and tertiary buty

88 In addition, the potent antioxidant N-acetylcysteine blocked EMT and expression of HIF-1alph

89 The antioxidant compound N-acetylcysteine blocked the curcumin-induced increased

90 eration of reactive oxygen species (ROS), as N-acetylcysteine blocked the induction of death receptor

91 rved similar antioxidant effects in WT mice: N-acetylcysteine blunted beta3-AR stimulation-induced br

92 New drugs including N-acetylcysteine, bortezomib, recombinant ADAMTS13, and

93 as rescued by treatment with the antioxidant N-acetylcysteine but not by p53 inactivation.

94 sed by the reactive oxygen species scavenger N-acetylcysteine but not by reducing agents or NO pathwa

95 although treatable by timely application of N-acetylcysteine, can be fatal.

96 thiols, including cysteine, dithiothreitol, N-acetylcysteine, captopril, bovine and human serum albu

97 N-Acetylcysteine, catalase, and l-N(G)-monomethyl argini

98 showed considerably reduced reactivity with N-acetylcysteine compared to the prototypical derivative

99 Pre-treatment with N-acetylcysteine completely reversed BSO+AUR-induced cel

100 Treatment with N-acetylcysteine could slow the progression of, but not

101 ibitable by pretreating the lymphocytes with N-acetylcysteine, cyclosporin A, or bongkrekic acid, emp

102 The effectiveness of the only antidote, N-acetylcysteine, declines rapidly after APAP ingestion,

103 Pretreatment with N-acetylcysteine decreases phosphorylation of p53 in cit

104 he treatment of trichotillomania, found that N-acetylcysteine demonstrated statistically significant

105 N-Acetylcysteine did not prevent ethanol-induced mortali

106 or sorbitol, quenching oxidative stress with N-acetylcysteine did suppress both SG formation and TDP-

107 JAK2V617F-mutant cells with the antioxidant N-acetylcysteine diminished reactive oxygen species (ROS

108 Treatment of mice with the antioxidant N-acetylcysteine diminishes PGC-1alpha variation observe

109 N-acetylcysteine, diphenyleneiodonium, and apocynin bloc

110 Treatment with the antioxidant N-acetylcysteine disrupts ROS-induced interaction of Mst

111 rted protection in the context of suboptimal N-acetylcysteine dosing.

112 N-acetylcysteine (dosing range, 1200-2400 mg/d) or place

113 N-acetylcysteine (dosing range, 1200-3000 mg/d) or place

114 he ability of the equine clinical treatments N-acetylcysteine, EDTA, and hydrogen peroxide to disrupt

115 The reducing agent N-acetylcysteine eliminated the effects of selenium on E

116 temperatures indicate that the -SH group of N-acetylcysteine enhances the rate of its hydrolysis by

117 combined with treatment with the antioxidant N-acetylcysteine, establishing that reactive oxygen spec

118 tress which was prevented by the antioxidant N-acetylcysteine (Eur J Neurosci.

119 Treatment with N-acetylcysteine from gestation on normalized most neuro

120 NPs: pharmacological (rescue with trolox and N-acetylcysteine), genetic (analysis of metal-sensitive

121 No adverse events occurred in the N-acetylcysteine group, and N-acetylcysteine was well to

122 nding EGF-like growth factor and antioxidant N-acetylcysteine had beneficial effects on epithelial wo

123 altered myocyte properties, the antioxidant N-acetylcysteine had broader effects in limiting glucose

124 Patients assigned to receive N-acetylcysteine had significantly greater reductions in

125 ture possible therapeutic approaches include N-acetylcysteine, hypothermia, liver assist devices, and

126 High-dose antioxidant treatment with N-acetylcysteine improved airspace caliber and attenuate

127 n-treated pregnant rats with the antioxidant N-acetylcysteine improved fetal survival but was deleter

128 nd are often steatotic, although addition of N-acetylcysteine improves the quality of the cells obtai

129 ere is controversy regarding the benefits of N-acetylcysteine in acute kidney injury.

130 The NACIAM trial (N-acetylcysteine in Acute Myocardial Infarction) examine

131 ffectiveness of Prednisone, Azathioprine and N-Acetylcysteine in Patients with IPF) clinical trial.

132 nergistically with the glutathione precursor N-acetylcysteine in preventing biliatresone-induced inju

133 The salutary effects of N-acetylcysteine in this mouse model provide an impetus

134 icipants (31 randomized to placebo and 35 to N-acetylcysteine) included in the analysis, 59 (89%) wer

135 Furthermore, N-acetylcysteine increased the levels of peroxiredoxin 3

136 n(III) tetrakis(4-benzoic acid)porphyrin and N-acetylcysteine increased the ratio of Akt to ERK phosp

137 by addition of nontoxic copper chelators or N-acetylcysteine, indicating a role for copper and react

138 nt fatty acid beta-oxidation, with S-nitroso-N-acetylcysteine induced site-specific S-nitrosylation o

139 ative stress was blocked by exposing mice to N-acetylcysteine, induction of liver UGT1A1 and CYP2B10

140 The cytoprotective antioxidant N-acetylcysteine inhibited Dp44mT-induced autophagosome

141 s treatment with the free radical scavenger, N-acetylcysteine, inhibited this effect.

142 In this study we show that the ROS scavenger N-acetylcysteine inhibits CSR.

143 However, three different N-acetylcysteine interventions neither significantly imp

144 echanism in RYR1-related myopathies and that N-acetylcysteine is a successful treatment modality ex v

145 ation therapy with cysteamine bitartrate and N-acetylcysteine is associated with delay of isoelectric

146 ombination of oral cysteamine bitartrate and N-acetylcysteine is beneficial for patients with neurona

147 N-acetylcysteine is more renoprotective than hydration a

148 Oral acetylcysteine (also known as N-acetylcysteine) is used with pirfenidone to treat idio

149 r agents (eg, riluzole, ketamine, memantine, N-acetylcysteine, lamotrigine, celecoxib, ondansetron) e

150 More importantly, the antioxidant, oral N-acetylcysteine led to amelioration of the muscle atrop

151 tates, reducing reactive oxygen species with N-acetylcysteine lessened protein aggregation and decrea

152 Treatment with the redox-active pharmaceutic N-acetylcysteine lowers gastric mucosal neutrophil infil

153 N-acetylcysteine may be protective against DILI while ta

154 eviously reported that phosphocysteamine and N-acetylcysteine mediate ceroid depletion in cultured ce

155 Timely administration of N-acetylcysteine (N-Ac) prevents the progression of seri

156 ) were treated in the presence or absence of N-acetylcysteine (NAC) administered 24 hours and 1 hour

157 of two structurally unrelated antioxidants: N-acetylcysteine (NAC) and melatonin.

158 roprobes after pharmacologic challenges with N-acetylcysteine (NAc) and MK-801.

159 se abolished by free radical scavenging with N-acetylcysteine (NAC) and Trolox.

160 such as glutathione ethyl ester (GSH-EE); or N-acetylcysteine (NAC) attenuate 15d-PGJ(2)-induced plat

161 tment with antioxidants alpha-tocopherol and N-acetylcysteine (NAC) attenuated paraquat-induced impla

162 cently, it was reported that the antioxidant N-acetylcysteine (NAC) decreased DMXAA-induced TNF-alpha

163 ting Nkx3.1 mutant mice with the antioxidant N-acetylcysteine (NAC) for 13 weeks post-weaning.

164 N-acetylcysteine (NAC) has anti-atherosclerotic effect w

165 The use of N-acetylcysteine (NAC) has been recently proposed as a p

166 Systemic N-acetylcysteine (NAC) has been shown to restore glutama

167 N-acetylcysteine (NAC) has been suggested to prevent rel

168 For decades, inhaled N-acetylcysteine (NAC) has been used as a mucolytic to r

169 combination of prednisone, azathioprine, and N-acetylcysteine (NAC) has been widely used as a treatme

170 N-Acetylcysteine (NAC) has been widely used in cell cult

171 so found that treatment with the antioxidant N-acetylcysteine (NAC) improved fetal survival in DHT+in

172 rmalities were all rescued by treatment with N-acetylcysteine (NAC) in diabetic females during gestat

173 N-acetylcysteine (NAC) is an antioxidant with reactive o

174 N-acetylcysteine (NAC) is an FDA-approved drug that has

175 N-acetylcysteine (NAC) is known to promote endothelial c

176 The glutathione (GSH) precursor N-acetylcysteine (NAC) is used to treat patients with AP

177 N-acetylcysteine (NAC) is widely used in patients with p

178 reatment with the anti-inflammatory compound N-acetylcysteine (NAC) on placental morphologic features

179 ypes, the in vivo effects of the antioxidant N-acetylcysteine (NAC) on two mouse models for NPC1 dise

180 ong administration of the potent antioxidant N-acetylcysteine (NAC) prevented acetaminophen-induced l

181 However, pretreatment with N-acetylcysteine (NAC) protects mouse and rat cells from

182 N-acetylcysteine (NAC) reduces oxidative damage and incr

183 nvestigate whether a donor pretreatment with N-acetylcysteine (NAC) reduces the incidence of DGF in a

184 atment of HMVEC-d cells with the antioxidant N-acetylcysteine (NAC) significantly inhibited KSHV entr

185 engers pyrrolidinedithiocarbamate (PDTC) and N-acetylcysteine (NAC) significantly inhibited ROS produ

186 ctric barrier discharge (DBD) plasma treated N-Acetylcysteine (NAC) solution against planktonic and b

187 Significant interaction was observed between N-acetylcysteine (NAC) therapy and rs3750920 within TOLL

188 We calibrated and applied an N-acetylcysteine (NAC) thiol reactivity assay as a surro

189 the efficient reversal by a typical antidote N-acetylcysteine (NAC) treatment of APAP-induced liver i

190 N-acetylcysteine (NAC) treatment prevents relapse in ani

191 N-acetylcysteine (NAC) was found to improve transplantat

192 The antioxidant N-acetylcysteine (NAC) was used to decrease ROS in both

193 ogether with 1 of 4 prophylactic regimes (1) N-acetylcysteine (NAC), (2) sodium bicarbonate (NaHCO3)

194 was to assess the feasibility of using oral N-acetylcysteine (NAC), a glutamatergic modulator and an

195 y continuous intracerebral administration of N-acetylcysteine (NAC), a ROS inhibitor.

196 Supplementation of N-acetylcysteine (NAC), a scavenger of reactive oxygen s

197 In rodents, N-acetylcysteine (NAC), a stimulator of the cystine-glut

198 N-Acetylcysteine (NAC), a strong antioxidant and ROS sca

199 N-acetylcysteine (NAC), a thiol-containing antioxidant,

200 e aim of this study was to determine whether N-acetylcysteine (NAC), an anti-inflammatory antioxidant

201 N-acetylcysteine (NAC), an antidote for acetaminophen po

202 Furthermore, N-acetylcysteine (NAC), an antioxidant and ROS scavenger

203 eiodonium (DPI), a flavoenzyme inhibitor, or N-acetylcysteine (NAC), an antioxidant.

204 N-acetylcysteine (NAC), an FDA-approved anti-mucolytic a

205 y zerumbone was abolished by glutathione and N-acetylcysteine (NAC), and this correlated with decreas

206 The oxygen radical scavenger, N-acetylcysteine (NAC), attenuates the chemotoxicity of

207 The only available treatment, N-acetylcysteine (NAC), has a limited time window of eff

208 into four groups for daily treatment: HBOT, N-acetylcysteine (NAC), HBO and NAC, and control (normox

209 vestigate the effect of a thiol antioxidant, N-acetylcysteine (NAC), in SSc.

210 ously showed that the glutathione precursor, N-acetylcysteine (NAC), prevented hypoglycemia-associate

211 ng a total of 10 strategies: saline, statin, N-acetylcysteine (NAC), sodium bicarbonate (NaHCO3), NAC

212 suggest that the over-the-counter supplement N-acetylcysteine (NAC), via glutamate modulation in the

213 Treatment of cells with N-acetylcysteine (NAC), which sequesters ROS, prevents a

214 hed by the antioxidant L-cysteine derivative N-acetylcysteine (NAC).

215 window of the only current treatment option, N-acetylcysteine (NAC).

216 on of ISO with the current standard of care, N-acetylcysteine (NAC).

217 tolerance, and efficacy of the GSH precursor N-acetylcysteine (NAC).

218 N-Acetylcysteine (NAC, a clinically approved mucolytic d

219 samples from 13 PALF survivors with APAPo + N-acetylcysteine (NAC, the frontline therapy for APAPo),

220 ntions (corticosteroids, pentoxifylline, and N-acetylcysteine [NAC], alone or in combination) with ea

221 C-5 non-cancerous cells with the antioxidant N-acetylcysteine or 2,2,6,6-tetramethylpiperidine-1-oxyl

222 plemented HCT 116 cells with the antioxidant N-acetylcysteine or 2,2,6,6-tetramethylpiperidine-1-oxyl

223 rtrophy and preserved systolic function with N-acetylcysteine or a placebo for 12 months (n=10 per gr

224 ment of CSE-knockout mice with NaHS, but not N-acetylcysteine or ezetimibe, inhibited the accelerated

225 armacological treatment with the antioxidant N-acetylcysteine or genetic disruption of the DNA damage

226 ntrast, reduction of adipose DNA damage with N-acetylcysteine or metformin ameliorated cellular senes

227 ibition of Th17 induction with ROS scavenger N-acetylcysteine or mitoquinone, a specific inhibitor fo

228 induced apoptosis was blocked by antioxidant N-acetylcysteine or NF-kappaB inhibitor via down-regulat

229 We focused on use of N-acetylcysteine or sodium bicarbonate for the preventio

230 of KB cells with antioxidants vitamin C and N-acetylcysteine or the pharmacological inhibitor PD1683

231 N-Acetylcysteine or tris(2-carboxylethyl)phosphine as co

232 prevented using reducing compounds, such as N-acetylcysteine or vitamin C, that enhance M. tuberculo

233 ellular level, the presence of antioxidants (N-acetylcysteine or vitamin E) significantly reduced the

234 g glutathione production with its precursor, N-acetylcysteine, or adding the reducing agent, dithioth

235 Administration of an antioxidant chemical, N-acetylcysteine, or ectopically overexpressing a reacti

236 gut microbiota, mice were aged, treated with N-acetylcysteine, or engineered to express the ROS scave

237 d medication (serotonin reuptake inhibitors, N-acetylcysteine, or naltrexone).

238 of RhoA-deficient mice with a ROS scavenger N-acetylcysteine partially restored thymocyte developmen

239 They randomly received N-acetylcysteine, physiologic saline, or sodium bicarbon

240 The greatest reduction in CIN was seen with N-acetylcysteine plus IV saline in patients receiving LO

241 atients receiving LOCM and with statins plus N-acetylcysteine plus IV saline.

242 However, N-acetylcysteine posttreatment worsened folic acid toxic

243 Glutathione levels did not increase in N-acetylcysteine posttreatment.

244 Glutathione levels decreased less in N-acetylcysteine pretreatment but also increased beginni

245 The survival rates in N-acetylcysteine pretreatment mice were significantly be

246 N-acetylcysteine pretreatment was effective in reducing

247 N-acetylcysteine produced these changes by inducing an e

248 Chronic treatment with N-acetylcysteine protects against mitochondrial oxidativ

249 Both CV-3988 and N-acetylcysteine reduced MS-WF-stimulated pneumococcal a

250 Exposure to the antioxidant N-acetylcysteine reduced oxidative stress and improved s

251 Treating mice in vivo with N-acetylcysteine reduces ROS levels, rescues HSC cycling

252 We propose that N-acetylcysteine represents the first potential therapeu

253 Intraperitoneal injection of the antioxidant N-acetylcysteine rescued defective follicle and oocyte d

254 Nurr1 in HEK293T cells, and the antioxidant N-acetylcysteine rescued from this effect.

255 tment of Paf(-/-) mice with the anti-oxidant N-acetylcysteine restored lymphoid progenitor numbers to

256 Treatment with N-acetylcysteine restored oxidized to total glutathione

257 thways of BCR-derived ROS with the scavenger N-acetylcysteine resulted in impaired in vitro BCR-induc

258 natal treatment of mice with the antioxidant N-acetylcysteine reversed the pollutant-induced increase

259 The antioxidant N-acetylcysteine reversed this phenotype, reducing both

260 retreated with vitamin E or sulforaphane and N-acetylcysteine; samples included A2E-free cells.

261 N-acetylcysteine seems to be beneficial for patients wit

262 The antioxidant N-acetylcysteine significantly inhibited ROS generation,

263 ntion (statin therapy, acetylsalicylic acid, N-acetylcysteine, sodium bicarbonate, off-pump coronary

264 Administration of N-acetylcysteine, sodium bicarbonate, or physiologic sal

265 N-acetylcysteine, sodium bicarbonate, statins, and ascor

266 ex I inhibitor-induced miR-663 expression by N-acetylcysteine suggested that reactive oxygen species

267 d a more general cytoprotective profile than N-acetylcysteine, suggesting a mechanism of action that

268 hat APAP-induced autophagy was suppressed by N-acetylcysteine, suggesting APAP mitochondrial protein

269 ide intermediate formed a stable adduct with N-acetylcysteine, suggesting that oxidative transformati

270 ndent inflammatory response was inhibited by N-acetylcysteine, suggesting that PRC may contribute to

271 the reactive oxygen species (ROS) scavenger N-acetylcysteine, suggesting that ROS contributes to mag

272 versed by its product lactate or antioxidant N-acetylcysteine, suggesting that Y10 phosphorylation-me

273 le cell disease treated with the antioxidant N-acetylcysteine suggests that cysteine disulfides, in p

274 tion and beta-oxidation products, as well as N-acetylcysteine, taurine and sulfo-conjugates in both r

275 e-treated with the oxygen radical scavenger, N-acetylcysteine, the NKA inhibitory activity of plumbag

276 minophen-induced liver injury at a time when N-acetylcysteine, the standard therapy, has no efficacy.

277 N-Acetylcysteine, theophylline, and other agents have sh

278 NA lesions was abrogated by the anti-oxidant N-acetylcysteine, this treatment did not alter the accum

279 Administration of N-acetylcysteine to control mice prevented VPA- and APAP

280 Fourteen healthy animals were given N-acetylcysteine to evaluate for toxicity and the other

281 infected murine macrophages, the addition of N-acetylcysteine to isoniazid treatment potentiated the

282 Addition of GSH or N-acetylcysteine to PBMCs selectively restored IL-12 and

283 for CRH5 but not AB12, MM cells, and in vivo N-acetylcysteine treatment eliminated these effects.

284 N-acetylcysteine treatment resulted in significant reduc

285 In addition, the N-acetylcysteine treatment significantly increased BKCa

286 Compared with placebo, N-acetylcysteine treatment was associated with significa

287 and demonstrate beneficial effects of early N-acetylcysteine treatment.

288 nical trial of prednisone, azathioprine, and N-acetylcysteine underwent HRCT at study start and finis

289 f patients "much or very much improved" with N-acetylcysteine use compared with 16% taking placebo (P

290 N-Acetylcysteine use was limited in this group, presumab

291 plain the variation from clinical studies of N-acetylcysteine use.

292 y, pretreatment with different antioxidants (N-acetylcysteine, vitamin E, or GSH ethyl ester) did not

293 HER-IPF, exposure to prednisone/azathioprine/N-acetylcysteine was associated with a higher composite

294 occurred in the N-acetylcysteine group, and N-acetylcysteine was well tolerated.

295 hen H(2)S-releasing compounds L-cysteine and N-acetylcysteine were added to the cell culture, the amo

296 and EAAC1(-/-) mice chronically treated with N-acetylcysteine were evaluated at serial time points fo

297 y, 15 of the 32 participants (47%) receiving N-acetylcysteine were much or very much improved compare

298 were mitigated by the free radical scavenger N-acetylcysteine, which also reverted phagocytosis to ba

299 xidant and redox regulator compounds such as N-acetylcysteine, which could be used preventively in yo

300 perone 4-phenyl butyric acid and antioxidant N-acetylcysteine, which significantly attenuate lewisite