The therapeutic detoxification of chlorogenic acid against acetaminophen-induced liver injury by ameliorating hepatic inflammation

Zheng, Zhiyong; Sheng, Yuchen; Ji, Lili

doi:10.1016/j.cbi.2015.05.023

Cited by 66 publications

(38 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The binding of endoligands like host cellular mRNA released from damaged cells to TLR-3 and/or TLR-4 promotes the expression of adaptor proteins including NF-κB, JNK and MyD88, which is followed by increasing cytokines and chemokines production [27, 28]. Zheng et al [29] reported that APAP enhanced liver expression of TLR-3, TLR-4 and MyD88, and facilitated hepatic inflammatory reactions. Our western blot data agreed that TLR-3, TLR-4, NF-κB, JNK and MyD88 were involved in APAP caused hepatotoxicity.…”

Section: Discussionmentioning

confidence: 99%

Alleviative effects from boswellic acid on acetaminophen-induced hepatic injury

Chen¹,

Hu²,

Yin³

2017

Biomedicine (Taipei)

View full text Add to dashboard Cite

Protective effects of boswellic acid (BA) against acetaminophen (APAP)-induced hepatotoxicity in Balb/ cA mice were examined. BA, at 0.05 or 0.1%, was supplied for 4 weeks. Acute liver injury was induced by APAP treatment. Results showed that BA intake increased hepatic BA bioavailability. APAP treatment decreased glutathione (GSH) level, increased reactive oxygen species (ROS) and oxidized glutathione (GSSG) production; and lowered activity and protein expression of glutathione reductase (GR) and heme oxygenase (HO)-1 in liver. BA intake at both doses alleviated subsequent APAP-induced oxidative stress by retaining GSH content, decreasing ROS and GSSG formations, reserving activity and expression of GR and HO-1 in liver, and lowering hepatic cytochrome P450 2E1 activity and expression. APAP treatment enhanced hepatic levels of interleukin-6, tumor necrosis factor-alpha and monocyte chemoattractant protein-1. BA pre-intake diminished APAP-induced release of those inflammatory cytokines and chemokines. APAP up-regulated hepatic protein expression of toll-like receptor (TLR)-3, TLR-4, MyD88, nuclear factor kappa B (NF-κB) p50, NF-κB p65 and JNK. BA pre-intake at both doses suppressed the expression of NF-κB p65 and p-JNK, and only at 0.1% down-regulated hepatic TLR-3, TLR-4 and MyD88 expression. APAP led to obvious foci of inflammatory cell infiltration in liver, determined by H&E stain. BA intake at both doses attenuated hepatic inflammatory infiltration. These findings support that boswellic acid is a potent hepato-protective agent.

show abstract

Section: Discussionmentioning

confidence: 99%

Alleviative effects from boswellic acid on acetaminophen-induced hepatic injury

Chen¹,

Hu²,

Yin³

2017

Biomedicine (Taipei)

View full text Add to dashboard Cite

show abstract

“…Clinically, when acetaminophen is administered beyond a therapeutic dose, the blood concentration reaches 150–200 mg/L within 0.5–4 h, resulting in acute liver failure . In such cases, many clinical manifestations will appear, such as appetite loss, nausea, and vomiting, and even mental symptoms along with hepatic encephalopathy and mental disorder, because of acetaminophen hepatotoxicity .…”

Section: Introductionmentioning

confidence: 99%

Preparation and in vitro evaluation of hydrophobic‐modified montmorillonite stabilized pickering emulsion for overdose acetaminophen removal

Zhang

Fan

et al. 2017

Can J Chem Eng

View full text Add to dashboard Cite

Pickering emulsion stabilized with hydrophobic‐modified montmorillonite (HMMT) was proposed for treating acute overdose acetaminophen intoxication, with a rapid removal rate, better stability, and good biocompatibility. The tiny HMMT was able to adsorb at the oil‐water interface of the Pickering emulsion to reduce the interfacial energy along with the formation of solid particle layer, in order to enhance the stability of the emulsion and improve the removal performance. With a fast removal rate, the detoxifying Pickering emulsion removed 0.5 g/L acetaminophen in the simulated gastric fluid to 0.13 g/L in 6 min, which is less than the intoxication content of 0.15 g/L, with a leakage ratio of lower than 4 % in simulated intestinal fluid over 4 h. Such a detoxifying emulsion was prepared at 55 °C with 2 % organoclay (HMMT) as the emulsifier, 6 % tributyl phosphate (TBP) as the extractant, and 0.1 mol/L NaOH as the inner phase in the volume ratio of 5:7. All the results denoted that the Pickering emulsion could be a promising candidate for the acute oral intoxication treatment.

show abstract

“…I read with interest the recent manuscript by Zheng et al (1) where the authors showed that treatment with chlorogenic acid (CGA) 1 h after an acetaminophen (APAP) overdose reduced liver injury. Since CGA attenuated hepatic MPO staining (indicator for neutrophil accumulation) and hepatic mRNA expression of various pro-inflammatory cytokines and chemokines, the authors concluded that the therapeutic use of CGA protected against APAP hepatotoxicity by preventing inflammatory injury mechanisms (1).…”

mentioning

confidence: 99%

“…Since CGA attenuated hepatic MPO staining (indicator for neutrophil accumulation) and hepatic mRNA expression of various pro-inflammatory cytokines and chemokines, the authors concluded that the therapeutic use of CGA protected against APAP hepatotoxicity by preventing inflammatory injury mechanisms (1). There are several fundamental concerns with the experimental design of these studies and the mechanistic conclusions.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Acetaminophen hepatotoxicity and sterile inflammation: The mechanism of protection of Chlorogenic acid

Jaeschke

2016

Chemico-Biological Interactions

View full text Add to dashboard Cite

Acetaminophen hepatotoxicity is characterized by extensive necrotic cell death and a sterile inflammatory response. A recent report suggested that a therapeutic intervention with chlorogenic acid, a dietary polyphenolic compound, protects against acetaminophen-induced liver injury by inhibiting the inflammatory injury. The purpose of this letter is to discuss a number of reasons why the protective mechanism of chlorogenic acid against acetaminophen hepatotoxicity does not involve an anti-inflammatory effect and provides an alternative explanation for the observed protection.

show abstract

The therapeutic detoxification of chlorogenic acid against acetaminophen-induced liver injury by ameliorating hepatic inflammation

Cited by 66 publications

References 46 publications

Alleviative effects from boswellic acid on acetaminophen-induced hepatic injury

Alleviative effects from boswellic acid on acetaminophen-induced hepatic injury

Preparation and in vitro evaluation of hydrophobic‐modified montmorillonite stabilized pickering emulsion for overdose acetaminophen removal

Acetaminophen hepatotoxicity and sterile inflammation: The mechanism of protection of Chlorogenic acid

Contact Info

Product

Resources

About