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

2018 ◽  
Vol 62 (0) ◽  
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

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

Marine Drugs ◽  
2018 ◽  
Vol 16 (9) ◽  
pp. 300 ◽  
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.

Protective effect of the total flavonoids from Apocynum venetum L. on carbon tetrachloride-induced hepatotoxicity in vitro and in vivo

2018 ◽  
Vol 74 (2) ◽  
pp. 301-312 ◽  
Author(s):  
Wei Zhang ◽  
Zheng Dong ◽  
Xiujuan Chang ◽  
Cuihong Zhang ◽  
Guanghua Rong ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Protective Effect ◽  
Total Flavonoids ◽  
Apocynum Venetum

scholarly journals 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

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.

scholarly journals Inhibition of Oxidative Stress and ALOX12 and NF-κB Pathways Contribute to the Protective Effect of Baicalein on Carbon Tetrachloride-Induced Acute Liver Injury

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 976
Author(s):  
Chongshan Dai ◽  
Hui Li ◽  
Yang Wang ◽  
Shusheng Tang ◽  
Tony Velkov ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Protective Effect ◽  
Molecular Mechanisms ◽  
Acute Liver Injury ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Liver Tissues

This study investigates the protective effect of baicalein on carbon tetrachloride (CCl4)-induced acute liver injury and the underlying molecular mechanisms. Mice were orally administrated baicalein at 25 and 100 mg/kg/day for 7 consecutive days or ferrostatin-1 (Fer-1) at 10 mg/kg was i.p. injected in mice at 2 and 24 h prior to CCl4 injection or the vehicle. Our results showed that baicalein or Fer-1 supplementation significantly attenuated CCl4 exposure-induced elevations of serum alanine aminotransferase and aspartate aminotransferase, and malondialdehyde levels in the liver tissues and unregulated glutathione levels. Baicalein treatment inhibited the nuclear factor kappa-B (NF-κB) pathway, activated the erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway in liver tissues, and markedly improved CCl4-induced apoptosis, inflammation and ferroptosis in liver tissues exposed with CCl4. In vitro, baicalein treatment improved CCl4 -induced decreases of cell viabilities and knockdown of Nrf2 and arachidonate 12-lipoxygenase (ALOX12) genes partly abolished the protective effect of baicalein on CCl4 -induced cytotoxicity in HepG2 cells. In conclusion, our results reveal that baicalein supplementation ameliorates CCl4-induced acute liver injury in mice by upregulating the antioxidant defense pathways and downregulating oxidative stress, apoptosis, inflammation and ferroptosis, which involved the activation of Nrf2 pathway and the inhibition of ALOX12 and NF-κB pathways.

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

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.

Protective effect of Djulis ( Chenopodium formosanum ) and its bioactive compounds against carbon tetrachloride-induced liver injury, in vivo

2016 ◽  
Vol 26 ◽  
pp. 585-597 ◽  
Author(s):  
Chin-Chen Chu ◽  
Shih-Ying Chen ◽  
Charng-Cherng Chyau ◽  
Zi-Han Fu ◽  
Ching-Chih Liu ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Protective Effect ◽  
Bioactive Compounds

scholarly journals Antioxidant activities of anastatin A & B derivatives and compound 38c's protective effect in a mouse model of CCl4-induced acute liver injury

RSC Advances ◽  
2020 ◽  
Vol 10 (24) ◽  
pp. 14337-14346 ◽  
Author(s):  
Cen Xiang ◽  
Menglin Cao ◽  
Ai Miao ◽  
Feng Gao ◽  
Xuzhe Li ◽  
...  
Keyword(s):  
Antioxidant Activity ◽  
Liver Injury ◽  
Mouse Model ◽  
Protective Effect ◽  
Acute Liver Injury ◽  
Antioxidant Activities

Anastatins B derivative 38c both had good antioxidant activity in vitro and in vivo.

scholarly journals Protective effect of leaf extract of Ficus carica L. against carbon tetrachloride-induced hepatic toxicity in mice and HepG2 cell line

2021 ◽  
Vol 20 (1) ◽  
pp. 113-119
Author(s):  
Syeda Hira ◽  
Muhammad Gulfraz ◽  
S.M. Saqlan Naqvi ◽  
Rehmat Ullah Qureshi ◽  
Hina Gul
Keyword(s):  
Carbon Tetrachloride ◽  
Protective Effect ◽  
Hepg2 Cell ◽  
Leaf Extract ◽  
Treated Group ◽  
Ficus Carica ◽  
Protective Effects ◽  
Hepatoprotective Effects

Purpose: To determine the in vivo and in vitro hepatoprotective effects of Ficus carica.Methods: The methanol leaf extract of Ficus carica L was further fractionated into n-hexane, ethyl acetate and aqueous fractions. For in vivo study, male albino mice were divided into twelve groups. Hepatotoxicity was induced in the mice using carbon tetrachloride (CCl4). The extract of F. carica and its fractions were administered at doses of 200 and 400 mg/kg. Silymarin was used as standardhepatoprotective drug. The protective effects of the extract and fractions were determined via assay of biochemical parameters and antioxidant enzymes in the liver. The histopathology of the liver was also studied. Moreover, the in vitro hepatoprotective effect of the extract and fractions against CCl4-induced damage was determined in HepG2 cell line.Results: There were significant increases in the serum levels of liver biomarkers in CCl4-treated group, whereas treatments with plant extract and fractions significantly reduced the levels of these parameters (p < 0.05). In addition, results from histopathology revealed evidence of protective effect of Ficus carica through reversal of CCl4-induced decreases in the activities of liver antioxidant enzymes.Conclusion: These results indicate that methanol leaf extract of Ficus carica L. and its fractions exert significant and dose-dependent hepatoprotective effects in vivo and in vitro. Keywords: Ficus carica, Hepatoprotection, Carbon tetrachloride, Liver biomarkers

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