In vivo protective effect against ethanol metabolism and liver injury of oyster (Crassostrea Gigas) extracts obtained via subcritical water processing

Maltol, a food-flavoring agent and Maillard reaction product formed during the processing of red ginseng (Panax ginseng, C.A. Meyer), has been confirmed to exert a hepatoprotective effect in alcohol-induced oxidative damage in mice. However, its beneficial effects on acetaminophen (APAP)-induced hepatotoxicity and the related molecular mechanisms remain unclear. The purpose of this article was to investigate the protective effect and elucidate the mechanisms of action of maltol on APAP-induced liver injury in vivo. Maltol was administered orally at 50 and 100 mg/kg daily for seven consecutive days, then a single intraperitoneal injection of APAP (250 mg/kg) was performed after the final maltol administration. Liver function, oxidative indices, inflammatory factors—including serum alanine and aspartate aminotransferases (ALT and AST), tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), liver glutathione (GSH), superoxide dismutase (SOD), malondialdehyde (MDA), cytochrome P450 E1 (CYP2E1) and 4-hydroxynonenal (4-HNE) were measured. Results demonstrated that maltol possessed a protective effect on APAP-induced liver injury. Liver histological changes and Hoechst 33258 staining also provided strong evidence for the protective effect of maltol. Furthermore, a maltol supplement mitigated APAP-induced inflammatory responses by increasing phosphorylated nuclear factor-kappa B (NF-κB), inhibitor kappa B kinase α/β (IKKα/β), and NF-kappa-B inhibitor alpha (IκBα) in NF-κB signal pathways. Immunoblotting results showed that maltol pretreatment downregulated the protein expression levels of the B-cell-lymphoma-2 (Bcl-2) family and caspase and altered the phosphorylation of phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) in a dose-dependent manner. In conclusion, our findings clearly demonstrate that maltol exerts a significant liver protection effect, which may partly be ascribed to its anti-inflammatory and anti-apoptotic action via regulation of the PI3K/Akt signaling pathway.

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Protective Effect of Eckol against Acute Hepatic Injury Induced by Carbon Tetrachloride in Mice

Marine Drugs ◽

10.3390/md16090300 ◽

2018 ◽

Vol 16 (9) ◽

pp. 300 ◽

Cited By ~ 8

Author(s):

Shulan Li ◽

Juan Liu ◽

Mengya Zhang ◽

Yuan Chen ◽

Tianxing Zhu ◽

...

Keyword(s):

Carbon Tetrachloride ◽

Liver Injury ◽

Protective Effect ◽

Acute Liver Injury ◽

Treated Group ◽

Terminal Deoxynucleotidyl Transferase ◽

Enhanced Expression ◽

Pre Treatment

Several in vitro studies have shown the potential hepatoprotective properties of eckol, a natural phlorotannin derived from the brown alga. However, the in vivo hepatoprotective potential of eckol has not been determined. In this study, we performed an in vivo study to investigate the protective effect of eckol and its possible mechanisms on the carbon tetrachloride (CCl4)-induced acute liver injury model in mice. Results revealed that eckol pre-treatment at the dose of 0.5 and 1.0 mg/kg/day for 7 days significantly suppressed the CCl4-induced increases of alanine transaminase (ALT) and aspartate aminotransferase (AST) levels in serum and meliorated morphological liver injury. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) analysis showed that the number of positive apoptotic hepatocytes in the eckol-treated group was lower than that in the CCl4 model group. Western blotting analysis also demonstrated the enhanced expression of bcl-2 and suppressed expression of cleaved caspase-3 by eckol. The CCl4-induced oxidative stress in liver was significantly ameliorated by eckol, which was characterized by reduced malondialdehyde (MDA) formations, and enhanced superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities and glutathione (GSH) content. Moreover, the CCl4-induced elevations of pro-inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 were markedly suppressed in the eckol-treated group. However, eckol enhanced the level of IL-10, a potent anti-inflammatory cytokine, and recruited CD11c+ dendritic cells into the liver tissues of CCl4-treated mice. These results indicated that eckol has the protective effect on CCl4-induced acute liver injury via multiple mechanisms including anti-apoptosis, anti-oxidation, anti-inflammation and immune regulation.

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Protective effect of dioscin against thioacetamide-induced acute liver injury via FXR/AMPK signaling pathway in vivo

Biomedicine & Pharmacotherapy ◽

10.1016/j.biopha.2017.10.153 ◽

2018 ◽

Vol 97 ◽

pp. 481-488 ◽

Cited By ~ 21

Author(s):

Lingli Zheng ◽

Lianhong Yin ◽

Lina Xu ◽

Yan Qi ◽

Hua Li ◽

...

Keyword(s):

Liver Injury ◽

Protective Effect ◽

Signaling Pathway ◽

Acute Liver Injury ◽

Ampk Signaling

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Corrigendum to “Protective effect of dioscin against thioacetamide-induced acute liver injury via FXR/AMPK signaling pathway in vivo” [Biomed. Pharmacother. 97 (2018) 481–488]

Biomedicine & Pharmacotherapy ◽

10.1016/j.biopha.2019.109448 ◽

2019 ◽

Vol 120 ◽

pp. 109448 ◽

Cited By ~ 1

Author(s):

Lingli Zheng ◽

Lianhong Yin ◽

Lina Xu ◽

Yan Qi ◽

Hua Li ◽

...

Keyword(s):

Liver Injury ◽

Protective Effect ◽

Signaling Pathway ◽

Acute Liver Injury ◽

Ampk Signaling

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Dynamic evaluation of the protective effect of Dendrobium officinale polysaccharide on acute alcoholic liver injury mice in vitro and in vivo by NIR fluorescence imaging

Analytical and Bioanalytical Chemistry ◽

10.1007/s00216-021-03546-7 ◽

2021 ◽

Author(s):

Gang Nie ◽

Yu Zhang ◽

Zhihong Zhou ◽

Jingya Xu ◽

Huiling Wang ◽

...

Keyword(s):

Liver Injury ◽

Protective Effect ◽

Fluorescence Imaging ◽

Dendrobium Officinale ◽

Alcoholic Liver Injury ◽

Dynamic Evaluation ◽

Nir Fluorescence

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Yi-Qi-Jian-Pi Formula Suppresses RIPK1/RIPK3-Complex-Dependent Necroptosis of Hepatocytes Through ROS Signaling and Attenuates Liver Injury in Vivo and in Vitro

Frontiers in Pharmacology ◽

10.3389/fphar.2021.658811 ◽

2021 ◽

Vol 12 ◽

Author(s):

Feixia Wang ◽

Li Tang ◽

Baoyu Liang ◽

Chun Jin ◽

Liyuan Gao ◽

...

Keyword(s):

Protein Kinase ◽

Liver Injury ◽

Protective Effect ◽

Molecular Mechanisms ◽

Positive Role ◽

Interacting Protein ◽

Ros Signaling ◽

Tnf Α

Acute-on-chronic liver failure (ACLF) is described as a characteristic of acute jaundice and coagulation dysfunction. Effective treatments for ACLF are unavailable and hence are urgently required. We aimed to define the effect of Yi-Qi-Jian-Pi Formula (YQJPF) on liver injury and further examine the molecular mechanisms. In this study, we established CCl4-, LPS-, and d-galactosamine (D-Gal)-induced ACLF rat models in vivo and LPS- and D-Gal-induced hepatocyte injury models in vitro. We found that YQJPF significantly ameliorates liver injury in vivo and in vitro that is associated with the regulation of hepatocyte necroptosis. Specifically, YQJPF decreased expression of receptor-interacting protein kinase 1 (RIPK1), receptor-interacting protein kinase 3 (RIPK3) and pseudokinase mixed lineage kinase domain-like (MLKL) to inhibit the migration of RIPK1 and RIPK3 into necrosome. YQJPF also reduces the expression of inflammatory cytokines IL-6, IL-8, IL-1β, and TNF-α, which were regulated by RIPK3 mediates cell death. RIPK1 depletion was found to enhance the protective effect of YQJPF. Furthermore, we showed that YQJPF significantly downregulates the mitochondrial reactive oxygen species (ROS) production and mitochondrial depolarization, with ROS scavenger, 4-hydroxy-TEMPO treatment recovering impaired RIPK1-mediated necroptosis and reducing the expression of IL-6, IL-8, IL-1β, and TNF-α. In summary, our study revealed the molecular mechanism of protective effect of YQJPF on hepatocyte necroptosis, targeting RIPK1/RIPK3-complex-dependent necroptosis via ROS signaling. Overall, our results provided a novel perspective to indicate the positive role of YQJPF in ACLF.

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Protective effect of free phenolics from Lycopus lucidus Turcz. root on carbon tetrachloride-induced liver injury in vivo and in vitro

Food & Nutrition Research ◽

10.29219/fnr.v62.1398 ◽

2018 ◽

Vol 62 (0) ◽

Cited By ~ 1

Author(s):

Yue-Hong Lu ◽

Cheng-Rui Tian ◽

Chun-Yan Gao ◽

Wen-Jing Wang ◽

Wen-Yi Yang ◽

...

Keyword(s):

Carbon Tetrachloride ◽

Liver Injury ◽

Protective Effect ◽

Free Phenolics ◽

Lycopus Lucidus

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Protective Effect of Dihydrokaempferol on Acetaminophen-Induced Liver Injury by Activating the SIRT1 Pathway

The American Journal of Chinese Medicine ◽

10.1142/s0192415x21500324 ◽

2021 ◽

pp. 1-14

Author(s):

Jiaqi Zhang ◽

Cheng Hu ◽

Xiulong Li ◽

Li Liang ◽

Mingcai Zhang ◽

...

Keyword(s):

Liver Injury ◽

Protective Effect ◽

Western Blotting ◽

Inflammatory Responses ◽

Chinese Herbs ◽

Western World ◽

Dependent Manner ◽

Stress Injury

Acetaminophen (APAP) overdose is the leading cause of acute liver failure (ALF) in the Western world, with limited treatment opportunities. 3,5,7,4[Formula: see text]-Tetrahydroxyflavanone (Dihydrokaempferol, DHK, Aromadendrin) is a flavonoid isolated from Chinese herbs and displays high anti-oxidant and anti-inflammatory capacities. In this study, we investigated the protective effect by DHK against APAP-induced liver injury in vitro and in vivo and the potential mechanism of action. Cell viability assays were used to determine the effects of DHK against APAP-induced liver injury. The levels of reactive oxygen species (ROS), serum alanine/aspartate aminotransferases (ALT/AST), liver myeloperoxidase (MPO), and malondialdehyde (MDA) were measured and analyzed to evaluate the effects of DHK on APAP-induced liver injury. Western blotting, immunofluorescence staining, RT-PCR, and Transmission Electron Microscope were carried out to detect the signaling pathways affected by DHK. Here, we found that DHK owned a protective effect on APAP-induced liver injury with a dose-dependent manner. Meanwhile, Western blotting showed that DHK promoted SIRT1 expression and autophagy, activated the NRF2 pathway, and inhibited the translocation of nuclear p65 (NF-[Formula: see text]B) in the presence of APAP. Furthermore, SIRT1 inhibitor EX-527 aggravated APAP-induced hepatotoxicity when treating with DHK. Molecular docking results suggested potential interaction between DHK and SIRT1. Taken together, our study demonstrates that DHK protects against APAP-induced liver injury by activating the SIRT1 pathway, thereby promoting autophagy, reducing oxidative stress injury, and inhibiting inflammatory responses.

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