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Drug: Acetaminophen

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Total 23 results found since Jan 2013.

Metabolic modulation of acetaminophen-induced hepatotoxicity by osteopontin.
In conclusion, this study clearly defines the cell source of OPN induction in response to APAP treatment, provides a novel insight into the metabolic role of OPN to APAP overdose, and suggests an Opn-targeted therapeutic strategy for the treatment or prevention of APAP-induced hepatotoxicity. PMID: 29735980 [PubMed - as supplied by publisher]
Source: Cellular and Molecular Immunology - May 7, 2018 Category: Molecular Biology Authors: Wen Y, Wang C, Gu J, Yu C, Wang K, Sun X, Sun Y, Wu H, Tong Y, Xia Q, Kong X Tags: Cell Mol Immunol Source Type: research

Baicalein and baicalin alleviate acetaminophen-induced liver injury by activating Nrf2 antioxidative pathway: the involvement of ERK1/2 and PKC.
This study investigated the protection of baicalin and its aglycone baicalein against APAP-induced hepatotoxicity and its mechanism. Baicalein and baicalin alleviated APAP-induced hepatotoxicity both in vitro and in vivo. Moreover, baicalin-provided this protection was not diminished in hepatocytes or mice treated with β-glucuronidase inhibitor. Results of liver glutathione (GSH) and reactive oxygen species (ROS) formation demonstrated the alleviation of baicalein and baicalin on APAP-induced liver oxidative stress injury. Baicalein and baicalin induced the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) ...
Source: Biochemical Pharmacology - January 12, 2018 Category: Drugs & Pharmacology Authors: Shi L, Hao Z, Zhang S, Wei M, Lu B, Wang Z, Ji L Tags: Biochem Pharmacol Source Type: research

Blockade of Notch signaling promotes acetaminophen-induced liver injury
This study was designed to investigate the role of Notch signaling in the regulation of innate immune responses in acetaminophen (APAP)-induced liver injury. Using a mouse model of APAP-induced liver injury, wild-type (WT) and toll-like receptor 4 knockout (TLR4 KO) mice were injected intraperitoneally with APAP or PBS. Some animals were injected with γ-secretase inhibitor DAPT or DMSO vehicle. For the in vitro study, bone marrow-derived macrophages (BMMs) were transfected with Notch1 siRNA, TLR4 siRNA, and non-specific (NS) siRNA and stimulated with LPS. Indeed, paracetamol/acetaminophen-induced liver damage was worse af...
Source: Immunologic Research - March 12, 2017 Category: Allergy & Immunology Source Type: research

Activation of GR but not PXR by Dexamethasone Attenuated Acetaminophen Hepatotoxicities via Fgf21 Induction.
In conclusion, via GR activation, DEX induced Fgf21 expression in mouse liver and human hepatoma cells. PMID: 28088388 [PubMed - as supplied by publisher]
Source: Toxicology - January 10, 2017 Category: Toxicology Authors: Vispute SG, Bu P, Le Y, Cheng X Tags: Toxicology Source Type: research

Caffeic acid prevents acetaminophen-induced liver injury by activating the Keap1-Nrf2 antioxidative defense system.
In conclusion, we demonstrated that CA prevented APAP-induced hepatotoxicity by decreasing Keap1 expression, inhibiting binding of Keap1 to Nrf2, and thus activating Nrf2 and leading to increased expression of antioxidative signals including HO-1 and NQO1. PMID: 26721592 [PubMed - as supplied by publisher]
Source: Free Radical Biology and Medicine - December 23, 2015 Category: Biology Authors: Pang C, Zheng Z, Shi L, Sheng Y, Wei H, Wang Z, Ji L Tags: Free Radic Biol Med Source Type: research

The Involvement of p62-Keap1-Nrf2 antioxidative signaling pathway and JNK in the protection of natural flavonoid quercetin against hepatotoxicity.
Abstract Quercetin, one of the most abundant dietary flavonoids, is reported to have protective function against various hepatotoxicants-induced hepatotoxicity. The present study aims to investigate the critical role of nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidative signaling pathway in the protection of quercetin against hepatotoxicity. Quercetin prevented the cytotoxicity induced by a variety of hepatotoxicants including clivorine (Cliv), acetaminophen (APAP), ethanol, carbon tetrachloride (CCl4), and toosendanin (TSN) in human normal liver L-02 cells. Quercetin induced the nuclear translocatio...
Source: Free Radical Biology and Medicine - April 13, 2015 Category: Biology Authors: Ji LL, Sheng YC, Zheng ZY, Shi L, Wang ZT Tags: Free Radic Biol Med Source Type: research

Salvianolic acid B protects against acetaminophen hepatotoxicity by inducing Nrf2 and phase II detoxification gene expression via activation of the PI3K and PKC signaling pathways
Publication date: Available online 24 December 2014 Source:Journal of Pharmacological Sciences Author(s): Musen Lin , Xiaohan Zhai , Guangzhi Wang , Xiaofeng Tian , Dongyan Gao , Lei Shi , Hang Wu , Qing Fan , Jinyong Peng , Kexin Liu , Jihong Yao Acetaminophen (APAP) is used drugs worldwide for treating pain and fever. However, APAP overdose is the principal cause of acute liver failure in Western countries. Salvianolic acid B (SalB), a major water-soluble compound extracted from Radix Salvia miltiorrhiza, has well-known antioxidant and anti-inflammatory actions. We aimed to evaluate the ability of SalB to protect again...
Source: Journal of Pharmacological Sciences - December 25, 2014 Category: Drugs & Pharmacology Source Type: research

Acid-degradable cationic poly(ketal amidoamine) for enhanced RNA interference in vitro and in vivo.
Abstract Efficient delivery of small interfering RNA (siRNA) is one of major challenges in the successful applications of siRNA in clinic. In the present study, we report a new acid-degradable poly(ketal amidoamine) (PKAA) as a siRNA carrier, which has high delivery efficiency and low cytotoxicity. PKAA was designed to have acid-cleavable ketal linkages in the backbone of cationic biodegradable poly(amidoamine). PKAA efficiently self-assembled with siRNA to form nanocomplexes with a diameter of 200 nm and slightly positive charges, which are stable under physiological conditions, but rapidly release siRNA at ac...
Source: Biomacromolecules - December 16, 2012 Category: Biochemistry Authors: Lim H, Noh J, Kim Y, Kim H, Kim J, Khang G, Lee D Tags: Biomacromolecules Source Type: research