Diammonium glycyrrhizinate alleviates iron overload-induced liver injury in mice via regulating the gut-liver axis.

Background: Evidence indicates a close association between iron overload (IO) and the pathogenesis of chronic liver diseases, highlighting the potential for interventions targeted at IO to impede or decelerate the progression of chronic liver diseases. Diammonium glycyrrhizinate (DG), the medicinal form of glycyrrhizic acid, a principal constituent of licorice, has been clinically employed as a hepatoprotective agent; however, its protective effect against IO-induced liver injury and underlying molecular mechanisms remain elusive.

Purpose: The aim of the present study is to investigate the hepatoprotective effect of DG against IO-induced liver injury with a focus on the gut-liver axis.

Excess iron intake induced liver injury: The role of gut-liver axis and therapeutic potential.

Excessive iron intake is detrimental to human health, especially to the liver, which is the main organ for iron storage. Excessive iron intake can lead to liver injury. The gut-liver axis (GLA) refers to the bidirectional relationship between the gut and its microbiota and the liver, which is a combination of signals generated by dietary, genetic and environmental factors.

Insight into the regulation of NLRP3 inflammasome activation by mitochondria in liver injury and the protective role of natural products.

Due to high mortality rates and poor prognosis, liver injury remains one of the leading causes of mortality worldwide. Amounting evidence suggested that the activation of the nucleotide-binding oligomerization domain (NOD)-like receptor containing pyrin domain 3 (NLRP3) inflammasome, which promotes pro-interleukin-1β (pro-IL-1β) and pro-interleukin-18 (pro-IL-18) cleavage and maturation play a vital role in the occurrence and development of liver injury and liver disease. Mitochondrial dysfunction is a common co-occurring event in liver injury.

Effects of chronic realgar exposure on liver lipidome in mice and identification sensitive lipid biomarker model for realgar-induced liver damage.

Chronic or excessive use of realgar induced liver damage. The biomarkers and exact mechanism have not been fully investigated. We performed an untargeted lipidomics study to investigate the effects of realgar on liver lipidome in mice and explore the sensitive biomarker model of realgar induced liver damage.

Realgar Alleviated Neuroinflammation Induced by High Protein and High Calorie Diet in Rats via the Microbiota-Gut-Brain Axis.

Purpose: Gastrointestinal heat retention syndrome (GHRS) often occurs in adolescents, resulting into nervous system injury. Realgar, an arsenic mineral with neuroprotective effect, has been widely used to treat GHRS. However, its mechanism of action remains unknown.

An Experimental Study Reveals the Protective Effect of Autophagy against Realgar-Induced Liver Injury via Suppressing ROS-Mediated NLRP3 Inflammasome Pathway.

Realgar, a poisonous traditional Chinese medicine, has been shown to cause liver injury when used for long periods or overdoses. However, the underlying molecular mechanisms and therapeutic targets have not been fully elucidated. The aim of this study is to explore the role of autophagy in sub-chronic realgar exposure-induced liver injury.

Realgar facilitates the Nrf2-Keap1-p62 positive feedback signaling axis via MAPKs and AKT to interfere with autophagy-induced apoptosis and oxidative stress in the hippocampus.

Realgar, as a commonly used traditional Chinese medicine, exerts both pharmacological and biological effects. However, the mechanism by which it causes nervous system injury remains unclear. This study aimed to elucidate the specific mechanism underlying the hippocampal neurotoxicity caused by realgar.

Metabolic characteristics related to the hazardous effects of environmental arsenic on humans: A metabolomic review.

Arsenic (As) is a toxic metalloid exist ubiquitously in environment. Epidemiological studies and laboratory animal studies have verified that As damages multiple organs or tissues in the body and is associated with a variety of diseases. Changes in metabolites usually indicate disturbances in metabolic pathways and specific metabolites are considered as biomarkers of diseases or drugs/toxins or environmental effects.

Oxidative stress induced by realgar in neurons: p38 MAPK and ERK1/2 perturb autophagy and induce the p62-Keap1-Nrf2 feedback loop to activate the Nrf2 signalling pathway.

Ethnopharmacological Relevance: Due to the modernization of traditional Chinese medicine (TCM) and the influence of traditional medication habits (TCM has no toxicity or side effects), arsenic poisoning incidents caused by the abuse of realgar and realgar-containing Chinese patent medicines have occurred occasionally. However, the potential mechanism of central nervous system toxicity of realgar remains unclear.

Aim Of The Study: This study aimed to clarify the specific mechanism of realgar-induced neurotoxicity.

Sub-chronic exposure to realgar induces liver injury via upregulating the TXNIP/NLRP3 pathway and disturbing bile acid homeostasis in mice.

Ethnopharmacological Relevance: Realgar is a traditional Chinese medicine used in China for a long history. Long-time or excessive use of realgar causes liver injury. However, its underlying mechanism is not fully clarified.

Triclosan-induced glycolysis drives inflammatory activation in microglia via the Akt/mTOR/HIF 1α signaling pathway.

Exposure to triclosan (TCS) has been implicated in neurotoxicity including autism spectrum disorders in vivo and oxidative stress and cell apoptosis in vitro. Thus, the molecular mechanisms underlying TCS-induced neurotoxicity warrants further research. In this study, we try to address the mode of action that TCS induced the expression of inflammatory cytokines by shifting metabolism to glycolysis.

Liver metabonomics study on the protective effect of glycyrrhetinic acid against realgar-induced liver injury.

Glycyrrhetinic acid (GA) is the bioactive ingredient in Glycyrrhizae Radix et Rhizoma. Our previous study has reported that GA has protective effect on realgar-induced hepatotoxicity. However, the details of the hepatoprotective mechanisms of GA on realgar-induced liver injury remain to be elucidated.

Identification of neurotoxicity markers induced by realgar exposure in the mouse cerebral cortex using lipidomics.

Realgar is a traditional Chinese medicine containing arsenic and has neurotoxicity. This study used realgar exposure mice model, neurobehavioral tests, analytical chemistry, molecular biology and nontargeted lipidomics to explore the mechanism of realgar damages the nervous system. The arsenic contained in realgar passed through the BBB and accumulated in the brain.

Effects of realgar on GSH synthesis in the mouse hippocampus: Involvement of system XAG(-), system XC(-), MRP-1 and Nrf2.

Realgar is a type of mineral drug that contains arsenic and has neurotoxicity. Glutathione (GSH), which is the main antioxidant in the central nervous system, plays a key role in antioxidant defenses and the detoxification of arsenic. However, whether realgar interferes with the synthesis of GSH in the brain and the molecular mechanisms underlying its effects are largely unknown.

HNMR-based metabonomic study of sub-chronic hepatotoxicity induced by realgar.

Ethnopharmacological Relevance: Realgar has been used as a traditional Chinese medicine (TCM) for thousands of years. Recently, a number of realgar or realgar-containing medicines poisoning cases have been reported. However, the toxicological mechanism of realgar has not been clearly clarified.

Effects of Glycyrrhetinic Acid on GSH Synthesis Induced by Realgar in the Mouse Hippocampus: Involvement of System [Formula: see text], System [Formula: see text], MRP-1, and Nrf2.

Realgar, a type of mineral drug-containing arsenic, exhibits neurotoxicity. Brain glutathione (GSH) is crucial to protect the nervous system and to resist arsenic toxicity. Therefore, the main aim of this study was to explore the neurotoxic mechanisms of realgar and the protective effects of glycyrrhetinic acid (GA) by observing the effects of GA on the hippocampal GSH biosynthetic pathway after exposure to realgar.

Effect of realgar on extracellular amino acid neurotransmitters in hippocampal CA1 region determined by online microdialysis–dansyl chloride derivatization–high-performance liquid chromatography and fluorescence detection.

An online microdialysis (MD)–dansyl chloride (Dns) derivatization–high-performance liquid chromatography (HPLC) and fluorescence detection (FD) system was developed for simultaneous determination of eight extracellular amino acid neurotransmitters in hippocampus. The MD probe was implanted in hippocampal CA1 region. Dialysate and Dns were online mixed and derivatized.

An effective assessment of valproate sodium-induced hepatotoxicity with UPLC-MS and (1)HNMR-based metabonomics approach.

Valproate sodium is one of the most prescribed antiepileptic drugs. However, valproate sodium has various side effects, especially its toxicity on liver. Current markers for toxicity reflect mostly the late stages of tissue damage; thus, more efficient methods for toxicity evaluation are desired.

Metabonomic study of biochemical changes in urinary of type 2 diabetes mellitus patients after the treatment of sulfonylurea antidiabetic drugs based on ultra-performance liquid chromatography/mass spectrometry.

A metabonomic study on biochemical changes in the urine of type 2 diabetes mellitus (T2DM) patients after the treatment of sulfonylurea (SU) antidiabetic drugs was performed. An ultra-performance liquid chromatography/mass spectrometry (UPLC/MS) method was used to generate metabolic fingerprints for the metabonomic analysis of urinary samples obtained from 20 T2DM patients without any drug treatment and 20 T2DM patients treated with SU antidiabetic drugs and 20 normal glucose tolerance subjects. The resulting data were subjected to chemometric analysis (principal component analysis and partial least squares discriminant analysis) to investigate the effect of SU antidiabetic drugs on urinary metabolite profiles of T2DM patients.

Excitotoxicity Induced by Realgar in the Rat Hippocampus: the Involvement of Learning Memory Injury, Dysfunction of Glutamate Metabolism and NMDA Receptors.

Realgar is a type of mineral drug containing arsenic. The nervous system toxicity of realgar has received extensive attention. However, the underlying mechanisms of realgar-induced neurotoxicity have not been clearly elucidated.

[Effect of subchronic realgar exposure on Glu and Gln in infant rat brain].

Objective: To study the effect of realgar on Glu and Gln on rat brain tissues.

Methods: Forty-eight Wistar rats were divided into 4 groups randomly:control group,low dosage group, moderate dosage group and high dosage group. The treatment groups were treated with realgar by gastric perfusion at a dosage of 0.

Alteration of amino acid neurotransmitters in brain tissues of immature rats treated with realgar.

Realgar is a traditional Chinese medicine, which has been used for thousands of years and are claimed to have therapeutic effects. The toxicity from realgar or realgar-containing traditional medicines has raised public concern. However, the neurotoxicity induced by realgar is less reported.

Metabonomic study on 'Kidney-Yang Deficiency syndrome' and intervention effects of Rhizoma Drynariae extracts in rats using ultra performance liquid chromatography coupled with mass spectrometry.

This paper was designed to study metabonomic characters of the 'Kidney-Yang Deficiency syndrome' induced by high dose of hydrocortisone and the therapeutic effects of Rhizoma Drynariae, classic traditional Chinese medicine (TCM) in treating the syndrome. A urinary metabonomics method based on ultra-performance liquid chromatography coupled with mass spectrometry (UPLC/MS) was developed. The significant difference in metabolic profiling was observed from model group (hydrocortisone-induced group) compared with the pre-dose group (rats before hydrocortisone inducing) by using the principal components analysis (PCA).

Urinary metabonomic study on biochemical changes in chronic unpredictable mild stress model of depression.

Background: Depression is a prevalent complex psychiatric disorder and its pathophysiological mechanism is not yet well understood. We investigated the metabolic profiling of urine samples from depression model rats to find potential disease biomarkers and research pathology of depression.

Methods: An animal model of depression was produced by chronic unpredictable mild stress (CUMS).