Protective Effects of Carvacrol on Mercuric Chloride-Induced Lung Toxicity Through Modulating Oxidative Stress, Apoptosis, Inflammation, and Autophagy

IF 4.4 3区 医学 Q2 ENVIRONMENTAL SCIENCES
Berna Eriten, Sefa Kucukler, Cihan Gur, Adnan Ayna, Halit Diril, Cuneyt Caglayan
{"title":"Protective Effects of Carvacrol on Mercuric Chloride-Induced Lung Toxicity Through Modulating Oxidative Stress, Apoptosis, Inflammation, and Autophagy","authors":"Berna Eriten,&nbsp;Sefa Kucukler,&nbsp;Cihan Gur,&nbsp;Adnan Ayna,&nbsp;Halit Diril,&nbsp;Cuneyt Caglayan","doi":"10.1002/tox.24397","DOIUrl":null,"url":null,"abstract":"<p>Mercuric chloride (HgCl<sub>2</sub>) is extremely toxic to both humans and animals. It could be absorbed via ingestion, inhalation, and skin contact. Exposure to HgCl<sub>2</sub> can cause severe health effects, including damages to the gastrointestinal, respiratory, and central nervous systems. The purpose of this work was to explore if carvacrol (CRV) could protect rats lungs from damage caused by HgCl<sub>2</sub>. Intraperitoneal injections of HgCl<sub>2</sub> at a dose of 1.23 mg/kg body weight were given either alone or in conjunction with oral CRV administration at doses of 25 and 50 mg/kg body weight for 7 days. The study included biochemical and histological techniques to examine the lung tissue's oxidative stress, apoptosis, inflammation, and autophagy processes. HgCl<sub>2</sub>-induced reductions in GSH levels and antioxidant enzymes (SOD, CAT, and GPx) activity were enhanced by CRV co-administration. Furthermore, MDA levels were lowered by CRV. The inflammatory mediators NF-κB, IκB, NLRP3, TNF-α, IL-1β, IL6, COX-2, and iNOS were all reduced by CRV. When exposed to HgCl<sub>2</sub>, the levels of apoptotic Bax, caspase-3, Apaf1, p53, caspase-6, and caspase-9 increased, but the levels of antiapoptotic Bcl-2 reduced after CRV treatment. CRV decreased levels of Beclin-1, LC3A, and LC3B, which in turn decreased HgCl<sub>2</sub>-induced autophagy damage. After HgCl<sub>2</sub> treatment, higher pathological damage was observed in terms of alveolar septal thickening, congestion, edema, and inflammatory cell infiltration compared to the control group while CRV ameliorated these effects. Consequently, by preventing HgCl<sub>2</sub>-induced increases in oxidative stress and the corresponding inflammation, autophagy, apoptosis, and disturbance of tissue integrity in lung tissues, CRV might be seen as a useful therapeutic alternative.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"39 12","pages":"5227-5237"},"PeriodicalIF":4.4000,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/tox.24397","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Environmental Toxicology","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/tox.24397","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ENVIRONMENTAL SCIENCES","Score":null,"Total":0}
引用次数: 0

Abstract

Mercuric chloride (HgCl2) is extremely toxic to both humans and animals. It could be absorbed via ingestion, inhalation, and skin contact. Exposure to HgCl2 can cause severe health effects, including damages to the gastrointestinal, respiratory, and central nervous systems. The purpose of this work was to explore if carvacrol (CRV) could protect rats lungs from damage caused by HgCl2. Intraperitoneal injections of HgCl2 at a dose of 1.23 mg/kg body weight were given either alone or in conjunction with oral CRV administration at doses of 25 and 50 mg/kg body weight for 7 days. The study included biochemical and histological techniques to examine the lung tissue's oxidative stress, apoptosis, inflammation, and autophagy processes. HgCl2-induced reductions in GSH levels and antioxidant enzymes (SOD, CAT, and GPx) activity were enhanced by CRV co-administration. Furthermore, MDA levels were lowered by CRV. The inflammatory mediators NF-κB, IκB, NLRP3, TNF-α, IL-1β, IL6, COX-2, and iNOS were all reduced by CRV. When exposed to HgCl2, the levels of apoptotic Bax, caspase-3, Apaf1, p53, caspase-6, and caspase-9 increased, but the levels of antiapoptotic Bcl-2 reduced after CRV treatment. CRV decreased levels of Beclin-1, LC3A, and LC3B, which in turn decreased HgCl2-induced autophagy damage. After HgCl2 treatment, higher pathological damage was observed in terms of alveolar septal thickening, congestion, edema, and inflammatory cell infiltration compared to the control group while CRV ameliorated these effects. Consequently, by preventing HgCl2-induced increases in oxidative stress and the corresponding inflammation, autophagy, apoptosis, and disturbance of tissue integrity in lung tissues, CRV might be seen as a useful therapeutic alternative.

Abstract Image

香芹酚通过调节氧化应激、细胞凋亡、炎症和自噬对氯化汞诱发的肺毒性的保护作用
氯化汞(HgCl2)对人类和动物都有剧毒。可通过摄入、吸入和皮肤接触吸收。接触氯化汞会对健康造成严重影响,包括损害肠胃、呼吸和中枢神经系统。这项研究的目的是探讨香芹酚(CRV)能否保护大鼠的肺部免受 HgCl2 的损害。大鼠腹腔注射 1.23 毫克/千克体重的氯化汞,同时口服 25 毫克和 50 毫克/千克体重的香芹酚,连续 7 天。研究采用生化和组织学技术检测肺组织的氧化应激、细胞凋亡、炎症和自噬过程。氯化汞诱导的 GSH 水平和抗氧化酶(SOD、CAT 和 GPx)活性的降低在联合施用 CRV 后得到增强。此外,CRV 还能降低 MDA 水平。CRV 可降低炎症介质 NF-κB、IκB、NLRP3、TNF-α、IL-1β、IL6、COX-2 和 iNOS 的水平。当暴露于 HgCl2 时,凋亡因子 Bax、caspase-3、Apaf1、p53、caspase-6 和 caspase-9 的水平在 CRV 处理后升高,但抗凋亡因子 Bcl-2 的水平在 CRV 处理后降低。CRV降低了Beclin-1、LC3A和LC3B的水平,从而减少了HgCl2诱导的自噬损伤。与对照组相比,HgCl2 处理后观察到肺泡间隔增厚、充血、水肿和炎症细胞浸润等更高的病理损伤,而 CRV 可改善这些影响。因此,通过防止氯化汞诱导的氧化应激增加以及相应的炎症、自噬、细胞凋亡和肺组织完整性的破坏,CRV 可被视为一种有用的替代疗法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Environmental Toxicology
Environmental Toxicology 环境科学-毒理学
CiteScore
7.10
自引率
8.90%
发文量
261
审稿时长
4.5 months
期刊介绍: The journal publishes in the areas of toxicity and toxicology of environmental pollutants in air, dust, sediment, soil and water, and natural toxins in the environment.Of particular interest are: Toxic or biologically disruptive impacts of anthropogenic chemicals such as pharmaceuticals, industrial organics, agricultural chemicals, and by-products such as chlorinated compounds from water disinfection and waste incineration; Natural toxins and their impacts; Biotransformation and metabolism of toxigenic compounds, food chains for toxin accumulation or biodegradation; Assays of toxicity, endocrine disruption, mutagenicity, carcinogenicity, ecosystem impact and health hazard; Environmental and public health risk assessment, environmental guidelines, environmental policy for toxicants.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信