ArticleJournal of food and drug analysis2017
Extract from Mulberry (Morus australis) leaf decelerate acetaminophen induced hepatic inflammation involving downregulation of myeloid differentiation factor 88 (MyD88) signals.
Article in Journal of food and drug analysis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- Absence of IκBβ/NFκB signaling does not attenuate acetaminophen-induced hepatic injury.Anatomical record (Hoboken, N.J. : 2007) · 2025Article
- Effect of Fermented Mulberry Leaves on Gut Health of Finishing Pigs.Animals : an open access journal from MDPI · 2024Article
- Effect of Dietary Supplemented with Mulberry Leaf Powder on Growth Performance, Serum Metabolites, Antioxidant Property and Intestinal Health of Weaned Piglets.Antioxidants (Basel, Switzerland) · 2023Article
- Sericultural By-Products: The Potential for Alternative Therapy in Cancer Drug Design.Molecules (Basel, Switzerland) · 2023Review
- APAP-Induced IκBβ/NFκB Signaling Drives Hepatic Il6 Expression and Associated Sinusoidal Dilation.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Camellia japonica diminishes acetaminophen-induced acute liver failure by attenuating oxidative stress in mice.Environmental science and pollution research international · 2021Article
- Anti-inflammatory effects ofInternational journal of medical sciences · 2021Article
- Development and evaluation of an automated multi-channel multiplug filtration cleanup device for pesticide residue analysis on mulberry leaves and processed tea.RSC advances · 2020Article
- Corilagin reduces acetaminophen-induced hepatotoxicity through MAPK and NF-American journal of translational research · 2020Article
- Endoplasmic Reticulum Stress-Induced Resistance to Doxorubicin Is Reversed by Mulberry Leaf Polyphenol Extract in Hepatocellular Carcinoma through Inhibition of COX-2.Antioxidants (Basel, Switzerland) · 2019Article
- The protective efficacy of soursop fruit extract against hepatic injury associated with acetaminophen exposure is mediated through antioxidant, anti-inflammatory, and anti-apoptotic activities.Environmental science and pollution research international · 2019Article
- Anti-Inflammatory Effects of High Hydrostatic Pressure Extract of Mulberry (Molecules (Basel, Switzerland) · 2019Article
- Mito-tempo protects against acute liver injury but induces limited secondary apoptosis during the late phase of acetaminophen hepatotoxicity.Archives of toxicology · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acetaminophen (APAP) induced inflammation and oxidative stress can cause cell death to induce liver damage. The antioxidative and anti-inflammatory effect of Mulberry (Morus australis) leaf extract (MLE) was shown in previous studies. In this study, we investigated the modulation of MLE on APAP induced inflammation and oxidative stress in rat liver injury or liver cancer cell (HepG2). Wistar rat was fed orally with MLE (0.5% or 1.0 %) for 1 week, and then, 900 mg/kg of APAP was injected intraperitoneally (i.p.). Pretreatment of MLE decreased obvious foci of inflammatory cell infiltration in liver. It also reduced the expression of inflammatory parameters including cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and nuclear factor kappa B (NF-κB) in liver. Treating with MLE increased the antioxidative enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase. Giving APAP to HepG2 hepatocyte was conducted to elucidate the mechanism of MLE or its functional components. The result showed that APAP upregulated hepatic protein expression of (myeloid differentiation factor 88) MyD88, nuclear factor kappa B (NF-kB), inhibitor of kappa B (IkB), c-Jun N-terminal kinases (JNK), and receptor interacting proteins (RIP1 and RIP3). Pretreatment of MLE, gallic acid (GA), gallocatechin gallate (GCG), or protocatechuic acid (PCA) suppressed the indicated protein expression. These findings confirmed that MLE has the potential to protect liver from APAP-induced inflammation, and the protecting mechanism might involve decreasing oxidative stress and regulating the innate immunity involving MyD88.
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