Protein phosphatase 2A-B55β mediated mitochondrial p-GPX4 dephosphorylation promoted sorafenib-induced ferroptosis in hepatocellular carcinoma via regulating p53 retrograde signaling.

As a key endogenous negative regulator of ferroptosis, glutathione peroxidase 4 (GPX4) can regulate its antioxidant function through multiple post-translational modification pathways. However, the effects of the phosphorylation/dephosphorylation status of GPX4 on the regulation of inducible ferroptosis in hepatocellular carcinoma (HCC) remain unclear. To investigate the effects and molecular mechanism of GPX4 phosphorylation/dephosphorylation modification on ferroptosis in HCC cells.

Aflatoxin B1 exposure triggers hepatic lipotoxicity via p53 and perilipin 2 interaction-mediated mitochondria-lipid droplet contacts: An in vitro and in vivo assessment.

Aflatoxin B1 (AFB1) is one of the most toxic mycotoxins widely found in food contaminants, and its target organ is the liver. It poses a major food security and public health threat worldwide. However, the lipotoxicity mechanism of AFB1 exposure-induced liver injury remains unclear and requires further elucidation.

Rab7a-mTORC1 signaling-mediated cholesterol trafficking from the lysosome to mitochondria ameliorates hepatic lipotoxicity induced by aflatoxin B1 exposure.

Aflatoxin B1 (AFB1) is a common contaminant in many foodstuffs and is considered a public health concern worldwide due to its hepatotoxicity caused by lipid metabolism disorders. However, the molecular mechanism underlying AFB1-induced lipotoxicity-dependent liver injury via regulating cholesterol metabolism remains unclear. We established a cholesterol trafficking disorder-mediated hepatic lipotoxicity model with AFB1 mixture exposure in vitro (HepaRG and HepG2 cells, 1.

Effect of prenatal PFOS exposure on liver cell function in neonatal mice.

Perfluorooctane sulfonate (PFOS), a hepatotoxic pollutant, is detected in the human cord blood, and it may induce health risk to an embryo. In this study, we established intrauterine exposure to PFOS in mice to evaluate potential impacts of PFOS on postnatal day 1 (PND1) offspring through conducting biochemical tests, quantitative PCR, and immunostaining. As results, PFOS-exposed maternal mice showed marked hepatomegaly and induced liver steatosis in a high dose of 5 mg PFOS/kg.

Hepatoprotective benefits of vitamin C against perfluorooctane sulfonate-induced liver damage in mice through suppressing inflammatory reaction and ER stress.

Our previous studies show that vitamin C (VC) plays promising hepatoprotection in mice. Intrahepatic exposure of perfluorooctane sulfonate (PFOS) can induce dose-dependent cytotoxicity. However, pharmacology-based assessment of VC on PFOS remains uninvestigated.

Antihepatotoxic benefits of Poria cocos polysaccharides on acetaminophen-lesioned livers in vivo and in vitro.

In our previous study, preliminary data indicates that Poria cocos polysaccharides (PCP) shows beneficial hepatoprotection against acetaminophen (APAP)-induced liver injury in mice. However, biological molecular mechanism warrants to be further discussed. In current study, a number of biochemical tests and immunoassays were subjected to respective PCP-dosed mice in vivo and liver cells in vitro.

Immunophenotypes of Ductal Epithelial Cells in Advanced Pancreatic Ductal Adenocarcinoma.

Background/aims: In this report, we aimed to investigate the distribution and characterization of biomarker-immunolabeled ductal epithelium in advanced pancreatic ductal adenocarcinoma (PDAC).

Design: Eighteen patients with PDAC were medically diagnosed prior to being treated periodically. All clinical records were collected and assayed.

Prenatal exposure to perfluorooctanoic acid induces nerve growth factor expression in cerebral cortex cells of mouse offspring.

Previous studies have showed perfluorooctanoic acid (PFOA) inducing cytotoxicity in an organ. In addition, epidemiological data show that high level of PFOA in cord blood of a pregnant woman is detected. Therefore, we extrapolate that circulating PFOA may affect organogenesis in offspring, such as the brain.

Hepatoprotective effects exerted by Poria Cocos polysaccharides against acetaminophen-induced liver injury in mice.

Our study was to investigate the potential pharmacological activity of Poria Cocos polysaccharides (PCP) against acetaminophen (APAP)-induced liver injury in mice. PCP-dosed mice were used to conducting biochemical assays of serological liver enzyme (ALT), lactate dehydrogenase (LD), inflammatory cytokines (TNF-α, IL-6), and immunoassays for functional proteins in the livers. Consequently, APAP-exposed mice resulted in elevated levels of ALT, LD, TNF-α, IL-6 in sera.

Adverse bioeffect of perfluorooctanoic acid on liver metabolic function in mice.

Perfluorooctanoic acid (PFOA), a kind of manufactured material, is widely accumulated around environmental system and into wildlife, including human beings. Toxicologically, PFOA induces hepatomegaly (liver enlargement) in the dose- and time-dependent manners. However, biological mechanism of hepatotoxicity warrants to be further investigated.

Cytoprotective effects of glycyrrhetinic acid liposome against cyclophosphamide-induced cystitis through inhibiting inflammatory stress.

This study was designed to investigate the pharmacological efficacy of glycyrrhetinic acid liposome (GAL) against female mice with nonbacterial cystitis induced by cyclophosphamide (CPS). Mice in different groups were subjected to tests for lactate dehydrogenase (LD), cytokine contents (IL-6, TNF-α) in serum, and histological changes in bladder tissue and to immunoassays. As a result, cyclophosphamide-induced cystitis in mice showed an increased LD level in serum, and the contents of cytokines (IL-6, TNF-α) were elevated.

Biocharacterization of Heat Shock Protein 90 in Acetaminophen-Treated Livers Without Conspicuous Drug Induced Liver Injury.

Background/aims: Acetaminophen (APAP) refers to a medication used to manage pain and fever symptoms. Heat shock protein 90 (Hsp90) is to be expressed during various stresses, such as wound healing and tissue remodeling. Recently, it is discovered that Hsp90 is a potential modifier of cytogenesis.

Effect of acute exposure to PFOA on mouse liver cells in vivo and in vitro.

Increasingly, epidemiological evidences indicate chemosynthetic perfluorooctanoic acid (PFOA), an environmental pollutant, induces potential adverse effect on human health after long-term exposure. However, less study has been performed for assessment of acute effect of PFOA exposure on metabolic homeostasis. In experimental designs, PFOA-exposed liver cells in vivo and in vitro were used to discuss underlying mechanism related to PFOA-induced metabolic dysfunction.

MicroRNA-421 mediates immunosensitivity in late-stage human liver cancer.

This report showed the novel clinical evidence to evaluate the pathological predisposition of microRNA-421 (miR-421) on immuno-insufficiency to cancer progression of human hepatocellular carcinoma. Some hospitalized patients with liver cancer were recruited when they were diagnosed by clinical parameters. As expected, all patients were subjected to routine biochemical analysis and histocytological inspection prior to receiving medical treatment.

Clinical biocharacterization of immunophenotype in hepatocellular carcinoma patients.

In current observations, we investigated the clinical immunophenotypes in liver cells to assess the metastasic predisposition in advance hepatocellular carcinoma patients. In method, we harvested the clinically diagnosed data from 8 liver cancer subjects. Definitely, all patients were received standard chemotherapeutics when being confirmed as advanced liver cancer via clinical diagnosis.

FGF21 functions as a sensitive biomarker of APAP-treated patients and mice.

Acetaminophen (APAP) is a common medication that induces hepatocellular damage in a time- or dose-dependent manner. Fibroblast growth factor 21 (FGF21) exerts a series of biological effects, including cellular repair. Compared to clinical diagnosis parameters, we aimed to evaluate whether FGF21 can serve as a sensitive biomarker for APAP-induced liver impairment.

Valproate acid (VPA)-induced dysmetabolic function in clinical and animal studies.

Background: Valproate acid (VPA), a commonly used antiepileptic medicine, is found to be linked to developing dysmetabolic risk. However, the proposed mechanism remains completely unknown.

Methods: In this study, we collected data from patients with epilepsy and further investigated the preclinical study in mice.

Impact of perinatal exposure to acetaminophen on hepatocellular metabolic function in offspring.

Acetaminophen (APAP), an over the counter (OTC) medication, is widely used in antipyretic treatment. Although the risk of dose-dependent cytotoxicity has been known, the potential effect of perinatal exposure to acetaminophen on metabolic function in offspring remains uninvestigated. Therefore, we established a prenatally APAP-exposed pregnancy mouse model to assess the possible adverse effect on liver metabolic function in offspring.

Characterization of acetaminophen-induced cytotoxicity in target tissues.

Acetaminophen (APAP), commonly used in clinical prescription, has time- and dose-dependent side effects. Thus, further animal study warrants to be investigated to assess possible adverse effect of APAP application. Here, we conducted pre-clinical research to elucidate the molecular mechanism regarding APAP-mediated toxicological action.

Puerarin exerts the protective effect against chemical induced dysmetabolism in rats.

In this study, we aim to explore the potential benefits of puerarin on metabolic function of liver fibrosis (LF) rat induced by carbon tetrachloride (CCl), and to investigate with the underlying molecular mechanism targeted on liver and pancreas tissues. In methodology, The LF rats were prepared through intragastrically giving CCl twice each week (2ml/kg, v/w) for 8weeks, and dosed puerarin (20, 40mg/kg) were given three times each week via intraperitoneal injection. After being conducted with oral glucose tolerance test (OGTT), the blood samples of rat were harvested for biochemical tests, as well as the liver and pancreas were isolated for histological examination and biochemical assays.

Cantharidin-induced liver injuries in mice and the protective effect of vitamin C supplementation.

Cantharidin, a promising anti-cancer medication, is limitedly prescribed due to the risk of hepatic toxicity. Our previous study has shown that vitamin C (VC) acts as a potential hepatoprotective agent against chemical liver damage. Here we implemented further experiments to investigate the benefits of VC on cantharidin-induced liver injuries in mice.