Effect of Ginkgo biloba extract on the expressions of Cox-2 and GST-Pi in rats with hepatocellular carcinoma risk

Ou, Chao; Zhao, Haiping; Su, Jianjia; Cao, Ji; Guo-jian, LI; Li, Le‐Qun

doi:10.4314/ahs.v14i1.7

Cited by 6 publications

(2 citation statements)

References 27 publications

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“…The levels of proteins that represent assembly of the NLRP3 inflammasome, such as NLRP3, caspase recruitment domain (ASC) and p10 (the active form of caspase 1), and symbolize activation, such as IL-1β and GSDMD, in liver tissue were enhanced in AFs-exposed mice, and the features of pyroptosis, which are characterized by pyroptosis bodies in the early stage and membrane rupture in the terminal stage, were observed. Notably, dephosphorylation of COX-2 plays a role in the activation of the NLRP3 inflammasome via protein phosphatase 2 A (PP2A)-B55δ induced by AFs and alters its ER localization and ER-associated degradation (ERAD) ( Ou et al, 2014 ; Zhang et al, 2019 ).…”

Section: Afs Amplify Hepatotoxicity In the Shape Of A Vice Feedback Lmentioning

confidence: 99%

Contamination of Aflatoxins Induces Severe Hepatotoxicity Through Multiple Mechanisms

et al. 2021

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Aflatoxins (AFs) are commonly contaminating mycotoxins in foods and medicinal materials. Since they were first discovered to cause “turkey X” disease in the United Kingdom in the early 1960s, the extreme toxicity of AFs in the human liver received serious attention. The liver is the major target organ where AFs are metabolized and converted into extremely toxic forms to engender hepatotoxicity. AFs influence mitochondrial respiratory function and destroy normal mitochondrial structure. AFs initiate damage to mitochondria and subsequent oxidative stress. AFs block cellular survival pathways, such as autophagy that eliminates impaired cellular structures and the antioxidant system that copes with oxidative stress, which may underlie their high toxicities. AFs induce cell death via intrinsic and extrinsic apoptosis pathways and influence the cell cycle and growth via microribonucleic acids (miRNAs). Furthermore, AFs induce the hepatic local inflammatory microenvironment to exacerbate hepatotoxicity via upregulation of NF-κB signaling pathway and inflammasome assembly in the presence of Kupffer cells (liver innate immunocytes). This review addresses the mechanisms of AFs-induced hepatotoxicity from various aspects and provides background knowledge to better understand AFs-related hepatoxic diseases.

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Section: Afs Amplify Hepatotoxicity In the Shape Of A Vice Feedback Lmentioning

confidence: 99%

Contamination of Aflatoxins Induces Severe Hepatotoxicity Through Multiple Mechanisms

et al. 2021

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“…HBx decreased mitochondrial membrane potential and ATP, and up‐regulated COX‐2 in vitro . Moreover, the expression of COX‐2 was also increased in the liver of AFB1‐treated rats and chicken . Therefore, there seemed to be a close, yet not totally understood, and complex interaction among COX‐2, mitochondrial dysfunction, necrosome formation and lipid accumulation in hepatocytes co‐exposed to HBx and AFB1.…”

Section: Introductionmentioning

confidence: 99%

HBx combined with AFB1 triggers hepatic steatosis via COX‐2‐mediated necrosome formation and mitochondrial dynamics disorder

Chen

Lin

Han

et al. 2019

J Cellular Molecular Medi

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Hepatitis B virus (HBV) infection and aflatoxin B1 (AFB1) exposure have been recognized as independent risk factors for the occurrence and exacerbation of hepatic steatosis but their combined impacts and the potential mechanisms remain to be further elucidated. Here, we showed that exposure to AFB1 impaired mitochondrial dynamics and increased intracellular lipid droplets (LDs) in the liver of HBV‐transgenic mice in vivo and the hepatitis B virus X protein (HBx)‐expressing human hepatocytes both ex vivo and in vitro. HBx combined with AFB1 exposure also up‐regulated receptor interaction protein 1 (RIP1), receptor interaction protein 3 (RIP3) and activated mixed lineage kinase domain like protein (MLKL), providing evidence of necrosome formation in the hepatocytes. The shift of the mitochondrial dynamics towards imbalance of fission and fusion was rescued when MLKL was inhibited in the HBx and AFB1 co‐treated hepatocytes. Most importantly, based on siRNA or CRISPR/Cas9 system, we found that the combination of HBx and AFB1 exposure increased cyclooxygenase‐2 (COX‐2) to mediate up‐regulation of RIP3 and dynamin‐related protein 1 (Drp1), which in turn promoted location of RIP3‐MLKL necrosome on mitochondria, subsequently exacerbated steatosis in hepatocytes. Taken together, these findings advance the understanding of mechanism associated with HBx and AFB1‐induced hepatic necrosome formation, mitochondrial dysfunction and steatosis and make COX‐2 a good candidate for treatment.

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The effect of EGB on proliferation of gastric carcinoma SGC7901 cells

et al. 2015

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Effect of Ginkgo biloba extract on the expressions of Cox-2 and GST-Pi in rats with hepatocellular carcinoma risk

Cited by 6 publications

References 27 publications

Contamination of Aflatoxins Induces Severe Hepatotoxicity Through Multiple Mechanisms

Contamination of Aflatoxins Induces Severe Hepatotoxicity Through Multiple Mechanisms

HBx combined with AFB1 triggers hepatic steatosis via COX‐2‐mediated necrosome formation and mitochondrial dynamics disorder

The effect of EGB on proliferation of gastric carcinoma SGC7901 cells

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