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1 APAP (200-300 mg/kg) caused glutathione depletion and pr
2 APAP administration began at 0 h and continued to 'ALF',
3 APAP overdose induces autophagy, which attenuates APAP-i
4 APAP overdose induces massive hepatocyte necrosis, necro
5 APAP pretreatment inhibited activation of the early step
6 APAP treatment inhibited complex II activity ex vivo, bu
7 APAP treatment resulted in PKC-alpha translocation to mi
8 APAP-ALF survivors had significantly lower serum FABP1 l
9 APAP-induced (300 mg/kg) liver injury in mice was accomp
10 APAP-induced increases in CD11b(+)/Ly6C(hi) macrophages
11 APAP-induced liver toxicity was mirrored by significantl
12 IU/l vs. 7,585 +/- 5,336 IU/l, p = 0.0013), APAP-alone-treated mice vs. APAP + neostigmine-treated m
13 pha (184 +/- 23 vs. 130 +/- 33, p = 0.0086), APAP-alone-treated mice vs. APAP + neostigmine-treated m
35 tients are often administered acetaminophen (APAP), a CAR-activating ligand, in conjunction with an o
36 f autophagy protected against acetaminophen (APAP)-induced liver injury in mice by clearing damaged m
38 patocytes in ALF, and in both acetaminophen (APAP)- and carbon tetrachloride (CCl4)-treated mice.
39 gnaling pathways activated by acetaminophen (APAP) and insulin signaling in hepatocytes with or witho
40 s and patients suffering from acetaminophen (APAP, paracetamol)-induced acute liver failure (ALF) sho
46 me P-450 isoforms involved in acetaminophen (APAP) toxicity were examined in HepaRG cells treated wit
49 , and ALF etiologies included acetaminophen (APAP) hepatotoxicity (29%), indeterminate ALF (23%), idi
50 administered a 1:1 mixture of acetaminophen (APAP) and (13)C6-APAP resulted in mass spectra that cont
51 trasensitive determination of acetaminophen (APAP) in the presence of its common interference isoniaz
53 ntal or intentional misuse of acetaminophen (APAP) is the leading cause of acute liver failure in the
57 dney injury in the context of acetaminophen (APAP; paracetamol)-induced liver injury is an important
58 reement with in vivo studies, acetaminophen (APAP) toxicity was most profound in HUVEC mono-cultures;
62 R341H, or R341C in mice predisposes to acute APAP hepatotoxicity, thereby providing direct evidence f
65 xpression but increased JNK activation after APAP administration, which exacerbated APAP-induced live
66 y used drug, its potential application after APAP overdose in patients should be further explored.
67 poptotic signaling, hepatic cell death after APAP is generally considered necrotic in mice and in hum
69 als treated with morphine 3 or 6 hours after APAP treatment, as compared with animals treated concurr
70 tting of therapeutic treatment 2 hours after APAP, IL-22 supported protection in the context of subop
75 ocated to mitochondria in mouse livers after APAP treatment followed by mitochondrial protein ubiquit
76 gnificantly faster in CA diet-fed mice after APAP administration secondary to rapid cyclin D1 inducti
77 occurred in Parkin knock-out (KO) mice after APAP treatment based on electron microscopy analysis and
81 and increased hepatocyte proliferation after APAP treatment in their livers compared with WT mice.
82 ion of compensatory liver regeneration after APAP hepatotoxicity is critical for final recovery, but
83 kinase 3 (GSK3) in liver regeneration after APAP hepatotoxicity using a pharmacological inhibition s
84 gnaling pathways in liver regeneration after APAP overdose and highlighted canonical Wnt signaling as
85 vel role of GSK3 in liver regeneration after APAP overdose and identified GSK3 as a potential therape
90 athways involved in liver regeneration after APAP-induced acute liver injury using a novel incrementa
91 t the mechanisms of liver regeneration after APAP-induced ALF have not been extensively explored yet.
93 t activation of beta-catenin signaling after APAP overdose is associated with timely liver regenerati
96 ted ASMase(-/-) mice and hepatocytes against APAP hepatotoxicity, effects that were reversed by chlor
97 sion of UCP2 protected wildtype mice against APAP-induced hepatotoxicity in the absence of PPARalpha
100 tors (Ro-31-8245, Go6983), protected against APAP cytotoxicity despite sustained c-jun-N-terminal kin
101 tisense (ASO) in mice also protected against APAP-induced liver injury by inhibiting JNK activation.
102 s, and Parkin KO mice were protected against APAP-induced liver injury compared with wild type mice.
103 ion, p62 degradation), and protected against APAP-induced liver injury, even in the presence of susta
107 P treatment, resulting in protection against APAP-mediated hepatic insulin resistance and alterations
109 ating monocyte-derived macrophages aggravate APAP hepatotoxicity, and the pharmacological inhibition
111 duced by overdose of N-acetyl-p-aminophenol (APAP) and defined three distinct MF subsets that populat
112 ging solvent; and N-acetyl-para-aminophenol (APAP, or paracetamol), a hepatotoxic analgesic drug.
114 onist inhibited APAP induced hypothermia and APAP was without effect on body temperature in Trpa1(-/-
118 2G7 treatments significantly attenuated APAP-induced serum elevations of alanine aminotransferas
119 overdose induces autophagy, which attenuates APAP-induced liver cell death by removing damaged mitoch
120 r microsomes, which are known to bioactivate APAP to the reactive metabolite N-acetyl-p-benzoquinone
121 talk between signaling pathways triggered by APAP and insulin signaling in hepatocytes, which is in p
122 1 mixture of acetaminophen (APAP) and (13)C6-APAP resulted in mass spectra that contained "twin" ions
123 en (N-acetyl-p-aminophenol, APAP) and (13)C6-APAP were incubated with rat liver microsomes, which are
124 deficient mice, and a mouse model of chronic APAP treatment were used to examine the mechanisms invol
125 pathways were modulated in mice with chronic APAP treatment, resulting in protection against APAP-med
126 JNK 1 and 2 silencing in vivo decreased APAP-induced PKC-alpha translocation to mitochondria, su
128 h the exosome-rich fraction, whereas in DILI/APAP injury these miRNAs were present in the protein-ric
131 retic non-steroidal anti-inflammatory drugs, APAP elicits hypothermia in addition to its antipyretic
133 eased and prolonged JNK activation; elevated APAP protein adducts; K8 hyperphosphorylation at S74/S43
137 acrophages accumulate in the liver following APAP intoxication; moreover, Gal-3 plays a role in promo
140 -/-) hepatocytes display lower threshold for APAP-induced cell death and defective fusion of mitochon
141 Previous studies suggest that aside from APAP-induced direct damage to hepatocytes, the hepatic i
142 urthermore, allotransplantation of HPCs from APAP+ISO-treated mice to other APAP-injured mice improve
145 cient mice were significantly protected from APAP-induced liver injury, compared with wild-type mice.
147 ere significantly older, less likely to have APAP overdose, and had a lower overall 3-week survival c
151 sferase levels and histopathologic damage in APAP-induced liver injury, a process that coincided with
153 y, the data suggest that miRNA elevations in APAP toxicity represent a regulatory response to modify
154 entation are likely to be critical events in APAP hepatotoxicity in humans, resulting in necrotic cel
156 the role of reactive metabolite formation in APAP-induced chemical stress, both the hepatotoxicity an
158 bution of sterile postinjury inflammation in APAP-induced acute liver injury (APAP-ALI) and justifies
160 umulation was enhanced by P-gp inhibitors in APAP-treated animals, suggesting P-gp-mediated transport
161 onfirmed that necroptosis is not involved in APAP toxicity by using mixed lineage kinase domain-like
166 ombin generation was dramatically reduced in APAP-treated HPC(DeltaTF) mice compared with APAP-treate
169 xtraction by 25-hydroxycholesterol increased APAP-mediated mitophagy and protected ASMase(-/-) mice a
170 and activities, which resulted in increased APAP protein adduct formation, were observed in livers o
171 In contrast, a TRPA1 antagonist inhibited APAP induced hypothermia and APAP was without effect on
172 ammation in APAP-induced acute liver injury (APAP-ALI) and justifies development of anti-inflammatory
176 ales were injected i.p. with 50 or 250 mg/kg APAP or phosphate-buffered saline on gestation day 12.5;
179 cted localised bioluminescence in the liver (APAP) and kidneys (cisplatin) in vivo and ex vivo, whils
184 using an AMPK activator oppositely modulated APAP cytotoxicity, suggesting that p-AMPK and AMPK regul
188 sults do not support broad use of NAC in non-APAP PALF and emphasizes the importance of conducting co
191 only those adults with nonacetaminophen (non-APAP) acute liver failure (ALF) and grade 1-2 hepatic en
192 ren from birth through age 17 years with non-APAP ALF enrolled in the PALF registry were eligible to
195 eous, but not intrathecal, administration of APAP elicited a dose dependent decrease in body temperat
196 of yeast induced pyrexia, administration of APAP evoked a marked hypothermia in wildtype and Trpv1(-
197 eneration was not secondary to alteration of APAP-induced hepatotoxicity, which remained unchanged af
198 an clock in modulating the chronotoxicity of APAP, we used a conditional null allele of brain and mus
200 candidate for the accurate determination of APAP and INH within human fluids and pharmaceutical form
201 (ogen) does not contribute to development of APAP-induced liver injury and suggest rather that plasmi
203 tarting from 4 hours after 600 mg/kg dose of APAP, resulted in early initiation of liver regeneration
208 mechanisms involving PTP1B in the effects of APAP on glucose homeostasis and hepatic insulin signalin
209 ere less susceptible to the toxic effects of APAP, including parameters of oxidative stress and ATP d
210 se inhibitor that ameliorates the effects of APAP-induced acute liver failure in the mouse and theref
211 n together, our data imply that inclusion of APAP in a pain treatment regimen activates CAR at the BB
213 /Ly6C(lo) macrophages increased in livers of APAP-treated Gal-3(-/-) mice; this was associated with i
214 adduct formation, were observed in livers of APAP-treated NKT cell-deficient mice, compared to WT mic
215 oRNA-122 and completely abrogated markers of APAP-induced inflammation (tumor necrosis factor, monocy
220 nd that the reactive oxidative metabolite of APAP, N-acetyl-p-benzoquinoneimine (NAPQI), caused the s
221 a indicate that all the major metabolites of APAP and multiple low-abundance metabolites (e.g., aceta
222 te liver regeneration in the murine model of APAP induced liver injury, which was associated with a m
223 Using various strategies in a mouse model of APAP overdose, the authors demonstrate that platelets pa
226 iates the initial, ASK1-independent phase of APAP-induced JNK activation and thus promotes drug-induc
227 ll known, those that halt the progression of APAP liver disease and facilitate liver recovery are les
230 iO-SPEs were evaluated toward the sensing of APAP and INH in human serum, urine, saliva, and tablet s
231 ctrocatalytic activity toward the sensing of APAP and INH with an enhanced analytical signal (voltamm
232 our in vivo data suggest that chronic use of APAP may be associated with insulin resistance in the li
233 tested the effect of bile acid modulation on APAP hepatotoxicity using C57BL/6 mice, which were fed a
235 of HPCs from APAP+ISO-treated mice to other APAP-injured mice improved AILI, an effect antagonized b
238 infiltrate liver as early as 8-12 hours post-APAP overdose and form dense cellular clusters around ne
240 (10 mg/kg, IP, administered 90 minutes post-APAP) protected against hepatotoxicity, whereas mice tre
242 oxicity and liver injury at early times post-APAP overdose were unaffected by syndecan-1, suggesting
247 r data provide strong evidence that prenatal APAP interferes with maternal immune and endocrine adapt
248 on and hepatic platelet accumulation promote APAP-induced liver injury, independent of platelet PAR-4
249 could be a promising new approach to reduce APAP-induced liver injury, but requires complementary st
251 nti-CD41 antibody also significantly reduced APAP-mediated liver injury and thrombin generation, indi
252 of the hepatocyte clock dramatically reduces APAP bioactivation and toxicity in vivo and in vitro bec
254 151a-3p and miR-382-5p specifically reported APAP toxicity - being unaffected by drug-induced kidney
256 rmic activity was independent of TRPV1 since APAP evoked hypothermia was identical in wildtype and Tr
257 emical autophagic flux assays, we found that APAP induced autophagy both in the in vivo mouse liver a
266 ting that necroptosis does not contribute to APAP-induced necrosis and RIPK1 has a unique, independen
267 Mitochondrial dysfunction contributes to APAP-induced liver injury but the mechanism by which APA
270 ssion in cases of acute liver failure due to APAP overdose and should be validated in multicenter pro
271 susceptibility of ASMase(-/-) hepatocytes to APAP and the impairment in the formation of mitochondria
274 ic deletion of FcRn results in resistance to APAP-induced liver injury through increased albumin loss
276 Ucp2-null mice, however, were sensitive to APAP-induced hepatotoxicity despite activation of PPARal
279 LC accumulation determines susceptibility to APAP hepatotoxicity by modulating mitophagy, and imply t
285 r cells (KC) were significantly reduced upon APAP challenge and started recovering by self-renewal at
286 33, p = 0.0086), APAP-alone-treated mice vs. APAP + neostigmine-treated mice) and histopathological s
287 /l, p = 0.0013), APAP-alone-treated mice vs. APAP + neostigmine-treated mice), inflammatory cytokine
288 uced liver injury but the mechanism by which APAP causes hepatocyte toxicity is not completely unders
293 ignificantly decreased in dams injected with APAP, accompanied by a morphologically altered placenta.
297 Subsequently, control mice were treated with APAP (350 mg/kg) followed by the beta-adrenoceptor agoni
299 st hepatotoxicity, whereas mice treated with APAP alone developed massive centrilobular necrosis and
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