Carvacrol modulates antioxidant enzymes, DNA integrity, and apoptotic markers in zearalenone-exposed fetal rat liver DOI
Mohammed Eleyan,

Mohammed R. Zughbur,

Mohamed Hussien

и другие.

Drug and Chemical Toxicology, Год журнала: 2024, Номер unknown, С. 1 - 10

Опубликована: Ноя. 13, 2024

Maternal exposure to zearalenone (ZEA), a mycotoxin, can impact fetal liver development. This study investigated the protective effects of carvacrol (CRV) against ZEA-induced damage. Thirty-two pregnant rats were allocated four groups (eight rats/group); control, CRV (75 mg/kg), ZEA (5 and co-treated group (ZEA + CRV). The animals given their doses during gestation period. revealed significant increase in malondialdehyde (MDA) level liver. In contrast, glutathione S-transferase (GST), superoxide dismutase (SOD), catalase (CAT) activities, besides (GSH) levels, decreased ZEA-intoxicated rats. Additionally, increased expression pro-apoptotic genes (P53, Bax, caspase-9), elevated immunoreactivity caspase-3, anti-apoptotic Bcl-2, induced severe fatty degeneration, congestion, necrosis comet assays DNA damage, as evidenced by reduced head content tail moment ZEA-exposed Surprisingly, co-treatment with significantly mitigated hepatic lipid peroxidation, antioxidant disturbance, apoptosis, damage after maternal ZEA. These findings highlight potential promising approach mitigate ZEA-associated developmental hepatotoxicity.

Язык: Английский

Chrysin mitigates diclofenac-induced hepatotoxicity by modulating oxidative stress, apoptosis, autophagy and endoplasmic reticulum stress in rats DOI
Behçet Varışlı, Cüneyt Çağlayan, Fatih Mehmet Kandemir

и другие.

Molecular Biology Reports, Год журнала: 2022, Номер 50(1), С. 433 - 442

Опубликована: Ноя. 7, 2022

Язык: Английский

Процитировано

34

Cadmium neurotoxicity and therapeutic strategies DOI
Shuangquan Wen, Liang Wang

Journal of Biochemical and Molecular Toxicology, Год журнала: 2024, Номер 38(3)

Опубликована: Март 1, 2024

Abstract Cadmium (Cd) is a multitarget, carcinogenic, nonessential environmental pollutant. Due to its toxic effects at very low concentrations, lengthy biological half‐life, and excretion rate, exposure Cd carries concern. Prolonged causes severe injury the nervous system of both humans animals. Nevertheless, precise mechanisms responsible for neurotoxic have yet be fully elucidated. The accurate chemical mechanism potentially entails destruction metal‐ion homeostasis, inducing oxidative stress, apoptosis, autophagy. Here we review evidence corresponding strategies protect against Cd‐induced central injury.

Язык: Английский

Процитировано

7

Carvacrol enhances anti-tumor activity and mitigates cardiotoxicity of sorafenib in thioacetamide-induced hepatocellular carcinoma model through inhibiting TRPM7 DOI

Eman H. Yousef,

Nada F. Abo El‐Magd,

Amal M. El Gayar

и другие.

Life Sciences, Год журнала: 2023, Номер 324, С. 121735 - 121735

Опубликована: Май 2, 2023

Язык: Английский

Процитировано

13

Plant Monoterpenes and Essential Oils as Potential Anti-Ageing Agents: Insights from Preclinical Data DOI Creative Commons
Mónica Zuzarte, Cátia Sousa, Jorge M. Alves-Silva

и другие.

Biomedicines, Год журнала: 2024, Номер 12(2), С. 365 - 365

Опубликована: Фев. 4, 2024

Ageing is a natural process characterized by time-dependent decline of physiological integrity that compromises functionality and inevitably leads to death. This also quite relevant in major human pathologies, being primary risk factor neurodegenerative diseases, metabolic disorders, cardiovascular diseases musculoskeletal disorders. Bearing this mind, it not surprising research aiming at improving health during has burst the last decades. Importantly, hallmarks ageing phenotype have been identified, knowledge for future studies towards identification putative pharmaceutical targets, enabling development preventive/therapeutic strategies improve longevity. In context, aromatic plants emerged as source potential bioactive volatile molecules, mainly monoterpenes, with many referring their anti-ageing potential. Nevertheless, an integrated review on current lacking, several approaches studying isolated or overall effect, without depicting possible mechanisms action. Herein, we aim provide updated systematization monoterpenes recently proposed hallmarks, highlight main action already well chemical entity–activity relations. By gathering categorizing available scattered information, identify important gaps could help pave way field.

Язык: Английский

Процитировано

5

Mechanism of evodiamine blocking Nrf2/MAPK pathway to inhibit apoptosis of grass carp hepatocytes induced by DEHP DOI

Yutian Lei,

Wenyue Zhang,

Meichen Gao

и другие.

Comparative Biochemistry and Physiology Part C Toxicology & Pharmacology, Год журнала: 2022, Номер 263, С. 109506 - 109506

Опубликована: Ноя. 8, 2022

Язык: Английский

Процитировано

19

Protective Effects of Carvacrol on Mercuric Chloride‐Induced Lung Toxicity Through Modulating Oxidative Stress, Apoptosis, Inflammation, and Autophagy DOI Creative Commons
Berna Eriten, Sefa Küçükler, Cihan Gür

и другие.

Environmental Toxicology, Год журнала: 2024, Номер 39(12), С. 5227 - 5237

Опубликована: Авг. 6, 2024

ABSTRACT Mercuric chloride (HgCl 2 ) is extremely toxic to both humans and animals. It could be absorbed via ingestion, inhalation, skin contact. Exposure HgCl can cause severe health effects, including damages the gastrointestinal, respiratory, central nervous systems. The purpose of this work was explore if carvacrol (CRV) protect rats lungs from damage caused by . Intraperitoneal injections at a dose 1.23 mg/kg body weight were given either alone or in conjunction with oral CRV administration doses 25 50 for 7 days. study included biochemical histological techniques examine lung tissue's oxidative stress, apoptosis, inflammation, autophagy processes. ‐induced reductions GSH levels antioxidant enzymes (SOD, CAT, GPx) activity enhanced co‐administration. Furthermore, MDA lowered CRV. inflammatory mediators NF‐κB, IκB, NLRP3, TNF‐α, IL‐1β, IL6, COX‐2, iNOS all reduced When exposed , apoptotic Bax, caspase‐3, Apaf1, p53, caspase‐6, caspase‐9 increased, but antiapoptotic Bcl‐2 after treatment. decreased Beclin‐1, LC3A, LC3B, which turn damage. After treatment, higher pathological observed terms alveolar septal thickening, congestion, edema, cell infiltration compared control group while ameliorated these effects. Consequently, preventing increases stress corresponding autophagy, disturbance tissue integrity tissues, might seen as useful therapeutic alternative.

Язык: Английский

Процитировано

4

Metabolomic modelling and neuroprotective effects of carvacrol against acrylamide toxicity in rat's brain and sciatic nerve DOI Creative Commons
Durmuş HATİPOĞLU,

Ates M. Burak,

Senturk Goktug

и другие.

Clinical and Experimental Pharmacology and Physiology, Год журнала: 2024, Номер 51(3)

Опубликована: Янв. 20, 2024

Abstract The study aimed to investigate the harmful effects of acrylamide (AA), which forms in carbohydrate‐rich foods at temperatures above 120°C, on central and peripheral nervous systems evaluate potential neuroprotective carvacrol (CRV). Male Wistar Albino rats were subjected AA (40 mg/kg/bw/day) CRV (50 for 15 days. Following last administration, evaluations revealed disrupted gait, heightened thermal sensitivity altered paw withdrawal thresholds AA‐exposed rats. Notably, reduced glutathione (GSH) raised malondialdehyde (MDA) levels both brain sciatic nerve tissues. nuclear factor erythroid 2‐related 2 (Nrf2), caspase 3 κB (NF‐κB) gene expressions while decreasing NR4A2. co‐administration mitigated gait abnormalities, elevated GSH lowered MDA also modulated expression, reducing Nrf2 NF‐κB increasing Histopathological signs AA‐induced neurodegeneration glial fibrillary acidic protein observed tissues rectified with simultaneous administration CRV, thereby demonstrating efficacy regions. This is pioneering CRV's against neurotoxicity systems, effectively addressing limitations literature. In conclusion, nerve, significantly mitigating this neurotoxicity. novel research underscores promise as a agent adverse systems.

Язык: Английский

Процитировано

3

The Ameliorative Effect of Naringenin on Fenamiphos Induced Hepatotoxicity and Nephrotoxicity in a Rat Model: Oxidative stress, Inflammatory markers, Biochemical, Histopathological, Immunohistochemical and Electron Microscopy Study DOI
Hatice Karaboduk, Çağlar Adıgüzel, Fatma Gökçe Apaydın

и другие.

Food and Chemical Toxicology, Год журнала: 2024, Номер 192, С. 114911 - 114911

Опубликована: Авг. 10, 2024

Язык: Английский

Процитировано

3

The Effect of Selenium Against Cadmium-Induced Nephrotoxicity in Rats: The Role of the TRPM2 Channel DOI Creative Commons
Ömer Faruk Keleş, Mehmet Hafit Bayir, Hacı Ahmet Çiçek

и другие.

Toxics, Год журнала: 2025, Номер 13(2), С. 87 - 87

Опубликована: Янв. 24, 2025

This study investigated the protective effect of selenium (Se) in a cadmium (Cd)-induced nephrotoxicity model rats and role TRPM2 channel this mechanism. For purpose, Cd (25 mg/kg orally), Se (0.5 i.p.), 2-aminoethoxydiphenyl borate (2-APB), antagonist, (3 i.p.) were administered to every day for 5 days. At end study, kidney tissues analysed using histological biochemical methods. A histopathological examination revealed congestion, tubular degeneration, necrosis, glomerular adhesion group. However, these lesions significantly reduced + 2-APB groups, while group showed appearance similar control Immunohistochemical analysis that Caspase-3, Bax, expression was higher group, levels lower treatment groups (p < 0.05). Among received Cd, urea, creatinine, TOS, TNF-α, IL-1β at highest level TAS lowest The modulated parameters; however, compared brought closer These findings indicated targeting inactivation together with could alleviate Cd-induced nephrotoxicity.

Язык: Английский

Процитировано

0

Alleviating effect of antioxidants on combined chromium and cadmium-induced neurotoxicity and apoptosis by activating the Nrf2-keap1 and associated pathway in Swiss albino mice DOI
Swapnil Tripathi,

Dharati Parmar,

S.H. Raval

и другие.

Metabolic Brain Disease, Год журнала: 2025, Номер 40(4)

Опубликована: Апрель 4, 2025

Язык: Английский

Процитировано

0