The active components and potential mechanisms of Wuji Wan in the treatment of ethanol-induced gastric ulcer: An integrated metabolomics, network pharmacology and experimental validation DOI Creative Commons

Tiantai Wu,

Huan Zhang, Yang Jin

et al.

Journal of Ethnopharmacology, Journal Year: 2024, Volume and Issue: 326, P. 117901 - 117901

Published: Feb. 8, 2024

Wuji Wan (WJW) is a traditional Chinese medicine formula that can be found in the "Prescriptions of Taiping Benevolent Dispensary" has been employed treating gastric discomfort, burning epigastric pain, and reflux for hundreds years shown promise ulcers (GUs). However, active components mechanism action against GUs remain unclear. The aim this study was to explore WJW elucidate underlying involved GUs. Initially, cell viability measured by counting kit 8 (CCK-8) assay evaluate efficacy WJW-containing serum vitro. ulcer index, inhibition rate, hematoxylin staining (H&E), periodic acid-Schiff (PAS) were used therapeutic effect vivo. Subsequently, levels inflammatory factors oxidative stress determined using an enzyme-linked immunosorbent assays (ELISA) on vitro vivo samples. Additionally, UPLC-Q Exactive Plus Orbitrap HRMS analyze absorbed into blood its metabolites. Network pharmacology metabolomics subsequently identify targets pathways. Real-time quantitative PCR (RT‒qPCR) Western blotting verify mRNA protein key Finally, identified molecular docking binding stability targets. ameliorated ethanol-induced damage GES-1 cells promoted healing. reduced IL-6, TNF-α, MDA, LDH while increasing IL-10, SOD, T-AOC cells. Moreover, treatment resulted decreased MDA increased PGE2, NO rats. In addition, eight blood. network results revealed 192 common entry GUs, KEGG analysis apoptosis signaling pathways main activity Metabolomic screening 13 differential There 23 components, metabolites, with TNF (TNF-α), AKT1, PTGS2 (COX2) MAPK1. significantly inhibited expression Bax, Caspase-9, Caspase-3, cleaved COX2, p-p44/42 MAPK promoting Bcl-2 p-AKT1. Molecular are berberine, palmatine, coptisine, evodiamine, rutaecarpine, evocarpine, paeoniflorin. reduces inflammation injury inhibits paper, we provide new strategy exploring formulas diseases based target mechanisms.

Language: Английский

A comprehensive review on human health effects of chromium: insights on induced toxicity DOI
Hooshyar Hossini, Behnaz Shafie,

Amir Dehghan Niri

et al.

Environmental Science and Pollution Research, Journal Year: 2022, Volume and Issue: 29(47), P. 70686 - 70705

Published: Aug. 30, 2022

Language: Английский

Citations

203

Mechanism of chromium-induced toxicity in lungs, liver, and kidney and their ameliorative agents DOI Open Access
Rituraj Chakraborty, Kaviyarasi Renu, Mohamed Ahmed Eladl

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2022, Volume and Issue: 151, P. 113119 - 113119

Published: May 24, 2022

Heavy metal Chromium (Cr), can adversely affect humans and their health if accumulated in organs of the body, such as lungs, liver, kidneys. Cr (VI) is highly toxic has a higher solubility water than (III). One most common routes for exposure through inhalation associated with lung, kidney damage, widespread dermatitis, GI tract human lung cancer, cardiomyopathies, cardiovascular disease. The increase ROS production been attributed to damage caused by toxicity. Cr-induced ROS-mediated oxidative stress seen cause redox imbalance affecting antioxidant system balance body. Nrf2 pathway dysregulation implicated same. Deregulation histone acetylation methylation observed, together gene genes p16, MGMT, APC, hMLH1, also miR-143 repression. Several ultra-structural changes have observed following (VI)-toxicity, including rough ER dilation, alteration mitochondrial membrane nuclear membrane, pycnotic nuclei formation, cytoplasm vacuolization. A significant change was metabolism lipid, glucose, protein after Cr. Cr-toxicity leads immune dysregulations expression IL-8, IL-4, IgM, lymphocytes, leukocytes among others. P53, well pro-and anti-apoptotic proteins, are involved apoptosis. These damages be alleviated via agents that restore balance, regulate Nrf-2 levels, or proteins while decreasing pro-apoptotic proteins.

Language: Английский

Citations

107

A review of chromium (Cr) epigenetic toxicity and health hazards DOI

Mahalaxmi Iyer,

Uttpal Anand,

Thiruvenkataswamy Saranya

et al.

The Science of The Total Environment, Journal Year: 2023, Volume and Issue: 882, P. 163483 - 163483

Published: April 17, 2023

Language: Английский

Citations

94

Biogeochemical behaviour and toxicology of chromium in the soil-water-human nexus: A review DOI Creative Commons
Wael I. Mortada, Ali El‐Naggar, Ahmed Mosa

et al.

Chemosphere, Journal Year: 2023, Volume and Issue: 331, P. 138804 - 138804

Published: May 1, 2023

Language: Английский

Citations

57

Toxicological effects of deltamethrin on quail cerebrum: Weakened antioxidant defense and enhanced apoptosis DOI
Jiayi Li, Huijie Jiang, Pengfei Wu

et al.

Environmental Pollution, Journal Year: 2021, Volume and Issue: 286, P. 117319 - 117319

Published: May 6, 2021

Language: Английский

Citations

86

Exploring the liver fibrosis induced by deltamethrin exposure in quails and elucidating the protective mechanism of resveratrol DOI Creative Commons
Siyu Li, Xiaoyan Zheng, Xiaoya Zhang

et al.

Ecotoxicology and Environmental Safety, Journal Year: 2020, Volume and Issue: 207, P. 111501 - 111501

Published: Nov. 3, 2020

Deltamethrin (DLM) is widely used in agriculture and the prevention of human insect-borne diseases. However, molecular mechanism DLM induced liver injury remains unclear to date. This study investigated potential that fibrosis quails. Japanese quails received resveratrol (500 mg/kg) daily with or without (45 exposure for 12 weeks. Histopathology, transmission electron microscopy, biochemical indexes, TUNEL, quantitative real-time PCR, western blot analysis were performed. hepatic steatosis, oxidative stress, inflammation, apoptosis. Most importantly, Nrf2/TGF-β1/Smad3 signaling pathway played an important role on DLM-induced Interestingly, addition resveratrol, Nrf2 activator, alleviates stress inflammation response by activating Nrf2, thereby inhibits Collectively, these findings demonstrate chronic induces via expression inhibition apoptosis, then results activation NF-κB/TNF-α TGF-β1/Smad3 pathway.

Language: Английский

Citations

81

Hexavalent chromium induced heart dysfunction via Sesn2-mediated impairment of mitochondrial function and energy supply DOI

Daqian Yang,

Qingyue Yang,

Ning Fu

et al.

Chemosphere, Journal Year: 2020, Volume and Issue: 264, P. 128547 - 128547

Published: Oct. 7, 2020

Language: Английский

Citations

80

The link between deacetylation and hepatotoxicity induced by exposure to hexavalent chromium DOI Creative Commons
Qingyue Yang, Bing Han, Siyu Li

et al.

Journal of Advanced Research, Journal Year: 2021, Volume and Issue: 35, P. 129 - 140

Published: April 8, 2021

Hexavalent chromium (Cr(VI)), one of the toxic heavy metals, poses a serious threat to human and animal health. Protein acetylation regulates structure function most proteins in variety ways. However, hepatotoxicity Cr(VI) whether it is related deacetylation remains largely unknown.We aimed explore link between silent information regulator two ortholog 1 (Sirt1) induced by exposure, better clarify biological mechanism liver injury Cr(VI).We established model K2Cr2O7 injecting rats intraperitoneally for 35 days continuously adding resveratrol (Res) further hepatotoxicity.The results revealed that inflammatory response apoptosis hepatocytes. Furthermore, reduced Sirt1 expression inhibited downstream key transcription factors, including nuclear factor erythroid 2-related 2 (Nrf2), Forkhead box O3 (FOXO3), factor-kappa B (NF-κB). Conversely, when Res was administered as an activator Sirt1, enhanced, were significantly alleviated.In summary, this work firstly demonstrates induces rat inhibiting which positive significance protecting natural environment health from chronic Cr poisoning.

Language: Английский

Citations

77

Hexavalent chromium induces renal apoptosis and autophagy via disordering the balance of mitochondrial dynamics in rats DOI
Xiaoyan Zheng, Siyu Li, Jiayi Li

et al.

Ecotoxicology and Environmental Safety, Journal Year: 2020, Volume and Issue: 204, P. 111061 - 111061

Published: Aug. 1, 2020

Language: Английский

Citations

75

Harmful Effects of Inorganic Mercury Exposure on Kidney Cells: Mitochondrial Dynamics Disorder and Excessive Oxidative Stress DOI
Biqi Han,

Zhanjun Lv,

Xue‐Min Han

et al.

Biological Trace Element Research, Journal Year: 2021, Volume and Issue: 200(4), P. 1591 - 1597

Published: May 31, 2021

Language: Английский

Citations

74