P101 Attenuated Cyclophosphamide-Induced Liver Injury in Mice by Regulating the Nrf2/ARE Signaling Pathway.

Cyclophosphamide causes side effects in cancer patients, including hepatotoxicity. Probiotics have recently emerged as potential approaches for the administration of many diseases. This study aimed to evaluate the protective effects of P101 against cyclophosphamide-induced liver injury and elucidate the underlying mechanism.

Polystyrene Microplastics Induced Ovarian Toxicity in Juvenile Rats Associated with Oxidative Stress and Activation of the PERK-eIF2α-ATF4-CHOP Signaling Pathway.

Numerous reports confirm that microplastics exposure could induce reproductive toxicity in mammals. However, the effects of microplastics exposure during juveniles on ovarian apoptosis through oxidative and endoplasmic reticulum (ER) stresses remains unclear, which is the focus of our study. In the present study, female rats (4 weeks old) were exposed to polystyrene microplastics (PS-MPs, 1 μm) at different dosages (0, 0.

Effects of microplastic and engineered nanomaterials on inflammatory bowel disease: A review.

Many microplastics and engineered nanomaterials (ENMs) exist in the daily environment. The intestinal impact of these exogenous fine particles on inflammatory bowel disease (IBD) people may be unpredictable. In this paper, we reviewed the recent progress in the effect of microplastics and ENMs on IBD individuals.

Lactiplantibacillus plantarum P101 alleviates alcoholic liver injury by modulating the Nrf2/HO-1 pathway in mice.

Aims: The occurrence of alcoholic liver injury is related to the oxidative stress. Bacteria for alleviating alcoholic related liver injury have received widespread attention. Study aims to investigate the alleviated efficacy of Lactiplantibacillus plantarum (L.

Male reproductive toxicity of polystyrene microplastics: Study on the endoplasmic reticulum stress signaling pathway.

Microplastics (MPs) have raised health concerns in public for its potential reproductive toxicity. In this study, we subjected the Kunming mice to 0.01, 0.

High-fat diet in mice led to increased severity of spermatogenesis impairment by lead exposure: perspective from gut microbiota and the efficacy of probiotics.

Background: The mechanism of multifactorial spermatogenesis impairment is unclear. This study aimed to investigate the reproductive toxicity of lead (Pb) in mice fed a high-fat diet (HFD) and to delineate the important role of gut microbiota.

Results: Results showed that, compared with mice fed a normal diet (ND), Pb exposure caused more severe spermatogenesis impairment in HFD-fed mice, including decreased sperm count and motility, seminiferous tubule injury, serum and intratesticular testosterone decline, and downregulated expression level of spermatogenesis-related genes.

Zinc Oxide Particles Can Cause Ovarian Toxicity by Oxidative Stress in Female Mice Model.

Introduction: Zinc oxide nanoparticles (ZnO NPs) participate in all aspects of our lives, but with their wide application, more and more disadvantages are exposed. The goal of this study was to investigate the toxicity of ZnO NPs in female mice ovaries and explore its potential mechanism.

Methods: In this study, adult female mice were orally exposed to 0, 100, 200, and 400 mg/kg ZnO NPs for 7 days.

Lead exposure exacerbates adverse effects of HFD on metabolic function via disruption of gut microbiome, leading to compromised barrier function and inflammation.

Purpose: The toxicity of lead (Pb) has been intensively studied, while the adverse effects in the population on a high-fat diet (HFD) remain unclear. This study compared the different biologic effects of Pb in CHOW and HFD-fed mice and investigated the important role that gut microbiota may play.

Methods: C57BL/6 mice were fed a CHOW diet and HFD with or without 1 g/L Pb exposure through drinking water for 8 weeks.

SARS-CoV-2 infection threatening intestinal health: A review of potential mechanisms and treatment strategies.

The outbreak of the COVID-19 pandemic has brought great problems to mankind, including economic recession and poor health. COVID-19 patients are frequently reported with gastrointestinal symptoms such as diarrhea and vomiting in clinical diagnosis. Maintaining intestinal health is the key guarantee to maintain the normal function of multiple organs, otherwise it will be a disaster.

Microplastics-perturbed gut microbiota triggered the testicular disorder in male mice: Via fecal microbiota transplantation.

Microplastics (MPs), an emerging environmental pollutant, have been clarified to induce testicular disorder in mammals. And the current studies have delineated a correlation between gut microbiota and male reproduction. However, it's still unclear whether gut microbiota gets involved in MPs-induced reproductive toxicity.

Polystyrene microplastics exacerbated liver injury from cyclophosphamide in mice: Insight into gut microbiota.

Microplastics (MPs) have infiltrated human food system globally, and the latent health risks have been well-described. However, the impact of pre-consumed MPs on liver resistance to foreign robust stimuli remains unclear. In this study, we developed a mouse model drinking roughly 18 and 180 μg/kg/day polystyrene MPs for 90 days, then intraperitoneally injected mice with 80 mg/kg cyclophosphamide (CTX) to investigate whether chronic pre-exposure to MPs aggravates hepatoxicity induced by CTX.

Combination of Houttuynia cordata polysaccharide and Lactiplantibacillus plantarum P101 alleviates acute liver injury by regulating gut microbiota in mice.

Background: Polysaccharides and probiotics can play an outstanding role in the treatment of liver disease by regulating gut microbiota. Recently, the combined therapeutic effect of probiotics and polysaccharides has attracted the attention of researchers. Houttuynia cordata polysaccharide (HCP) combined with Lactiplantibacillus plantarum P101 was used to prevent carbon tetrachloride (CCl )-induced acute liver injury (ALI) in mice, and its effect on gut microbiota regulation was explored.

Pre-Exposure to TiO2-NPs Aggravates Alcohol-Related Liver Injury by Inducing Intestinal Barrier Damage in Mice.

The wide application of titanium dioxide nanoparticles (TiO2-NPs) and the increase in opportunities for its release into the environment undoubtedly compound the potential of these materials to harm people. Research on the effects of pre-exposure to TiO2-NPs on disease development is scarce. The purpose of this work was to assess whether pre-exposure to TiO2-NPs (20 and 200 mg/kg) for 28 days aggravates the development of alcohol-related liver injury in mice.

Inhibition of testosterone synthesis induced by oral TiO NPs is associated with ROS-MAPK(ERK1/2)-StAR signaling pathway in SD rat.

Titanium dioxide nanoparticles (TiO NPs) have been widely used in food, medical, and other fields; their reproductive toxicity has been reported in numerous studies. However, the relevant toxicity mechanism still requires further exploration. In this paper, the effect of oral exposure to 500 mg/kg TiO NPs (anatase and rutile) in adult male SD rats was studied over 3 and 7 days.

GG Ameliorated Long-Term Exposure to TiO Nanoparticles Induced Microbiota-Mediated Liver and Colon Inflammation and Fructose-Caused Metabolic Abnormality in Metabolism Syndrome Mice.

A huge number of titanium dioxide nanoparticles (TiO NPs) exist in confectionery foods, which is a high-risk factor for development of diet-induced metabolism syndrome (MetS). In this study, we built a high fructose drinking-induced MetS mouse model, and oral intake of 20 mg/kg TiO NPs was administered for 8 weeks. Significant pathological changes and inflammatory factors of overproduction were detected in the liver and colon.

Foodborne TiO Nanoparticles Induced More Severe Hepatotoxicity in Fructose-Induced Metabolic Syndrome Mice via Exacerbating Oxidative Stress-Mediated Intestinal Barrier Damage.

The hazard of titanium dioxide nanoparticles (TiO NPs) in diseased population should be given focus due to the huge number of these NPs in foods and medicine. This study aimed to evaluate the stronger biological adverse effect of oral exposure to TiO NPs in a fructose-induced metabolic syndrome mouse model. Compared to the normal mice, low-dose (2 mg/kg) TiO NPs did not cause severe hepatotoxicity.

Protective Effect of GG on TiO Nanoparticles-Induced Oxidative Stress Damage in the Liver of Young Rats.

The potential toxicity of titanium dioxide nanoparticles (TiO NPs) to mammals has become a widespread concern. Young individuals exposed to TiO NPs have a higher risk than adults. In this study, the protective effects of GG (LGG) on liver toxicity in young rats induced by TiO NPs were explored.

Toxic effects of TiO NPs in the blood-milk barrier of the maternal dams and growth of offspring.

Titanium dioxide nanoparticles (TiO NPs) are amongst the most frequently used nanomaterial in everyday consumer products, and their widespread applications have raised concerns of the consequent deleterious effects on human health, particularly to vulnerable populations, such as lactating females remains elusive. Therefore, this study was initiated to investigate the detrimental effects and toxic mechanisms induced by TiO NPs in maternal dams and offspring during the lactation period. Dams were randomly divided into three groups.

Restraining the TiO nanoparticles-induced intestinal inflammation mediated by gut microbiota in juvenile rats via ingestion of Lactobacillus rhamnosus GG.

Human were given a lot of opportunities to ingest TiO NPs in the environment. Children have low, sensitive intestinal tolerance, and they could be exposed to higher levels of TiO NPs than adults. Few studies have been conducted on the interaction between TiO NPs and juvenile intestine phase models.