The antagonistic effect of caffeic acid phenethyl ester on cadmium‐caused pulmonary toxicity: MiR‐182‐5p/TLR4 axis

Abstract Cadmium (Cd) is a heavy metal toxic that can cause health problems including lung injury. This study was set out to meet the growing demand for effective treatment of lung diseases and explore the mechanism of caffeic acid phenethyl ester (CAPE, a natural phenolic acid) protect against Cd‐c...

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Main Authors: Rili Hao, Xing Zhou, Xiaqing Lv, Xiangyang Zhu, Yang Jiang, Dapeng Li
Format: Article
Language:English
Published: Wiley 2023-09-01
Series:Food Frontiers
Subjects:
Online Access:https://doi.org/10.1002/fft2.281
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author Rili Hao
Xing Zhou
Xiaqing Lv
Xiangyang Zhu
Yang Jiang
Dapeng Li
author_facet Rili Hao
Xing Zhou
Xiaqing Lv
Xiangyang Zhu
Yang Jiang
Dapeng Li
author_sort Rili Hao
collection DOAJ
description Abstract Cadmium (Cd) is a heavy metal toxic that can cause health problems including lung injury. This study was set out to meet the growing demand for effective treatment of lung diseases and explore the mechanism of caffeic acid phenethyl ester (CAPE, a natural phenolic acid) protect against Cd‐caused lung damage. In this study, CAPE significantly increased mice body weight, decreased lung W/D ratio, and alleviated histomorphological injury. CAPE mitigated CdCl2‐induced oxidative stress through Nrf2/HO‐1/NQO1 pathway, suppressed inflammation via MyD88/NF‐κB pathway, and alleviated apoptosis by modulating apoptosis mediators. CAPE also inhibited the CdCl2‐caused decreasing of TLR4 level and the increasing of miR‐182‐5p level, which is achieved by miR‐182‐5p sponging TLR4. Collectively, miR‐182‐5p is involved in CAPE against CdCl2‐caused lung damage by targeting TLR4. MiR‐182‐5p/TLR4 is a new pathway for inhibiting oxidative stress, apoptosis, and inflammation in CAPE‐mediated lung protection, which provides a novel avenue for treatment therapies.
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spelling doaj.art-f9e4b2c8cf9d43079a200f18b29c27e32023-09-29T05:33:43ZengWileyFood Frontiers2643-84292023-09-01431337134610.1002/fft2.281The antagonistic effect of caffeic acid phenethyl ester on cadmium‐caused pulmonary toxicity: MiR‐182‐5p/TLR4 axisRili Hao0Xing Zhou1Xiaqing Lv2Xiangyang Zhu3Yang Jiang4Dapeng Li5College of Food Science and Engineering, Shandong Agricultural UniversityKey Laboratory of Food Nutrition and Human Health in Universities of ShandongTaianP. R. ChinaCollege of Food Science and Engineering, Shandong Agricultural UniversityKey Laboratory of Food Nutrition and Human Health in Universities of ShandongTaianP. R. ChinaCollege of Food Science and Engineering, Shandong Agricultural UniversityKey Laboratory of Food Nutrition and Human Health in Universities of ShandongTaianP. R. ChinaCollege of Food Science and Engineering, Shandong Agricultural UniversityKey Laboratory of Food Nutrition and Human Health in Universities of ShandongTaianP. R. ChinaCollege of Food Science and Engineering, Shandong Agricultural UniversityKey Laboratory of Food Nutrition and Human Health in Universities of ShandongTaianP. R. ChinaCollege of Food Science and Engineering, Shandong Agricultural UniversityKey Laboratory of Food Nutrition and Human Health in Universities of ShandongTaianP. R. ChinaAbstract Cadmium (Cd) is a heavy metal toxic that can cause health problems including lung injury. This study was set out to meet the growing demand for effective treatment of lung diseases and explore the mechanism of caffeic acid phenethyl ester (CAPE, a natural phenolic acid) protect against Cd‐caused lung damage. In this study, CAPE significantly increased mice body weight, decreased lung W/D ratio, and alleviated histomorphological injury. CAPE mitigated CdCl2‐induced oxidative stress through Nrf2/HO‐1/NQO1 pathway, suppressed inflammation via MyD88/NF‐κB pathway, and alleviated apoptosis by modulating apoptosis mediators. CAPE also inhibited the CdCl2‐caused decreasing of TLR4 level and the increasing of miR‐182‐5p level, which is achieved by miR‐182‐5p sponging TLR4. Collectively, miR‐182‐5p is involved in CAPE against CdCl2‐caused lung damage by targeting TLR4. MiR‐182‐5p/TLR4 is a new pathway for inhibiting oxidative stress, apoptosis, and inflammation in CAPE‐mediated lung protection, which provides a novel avenue for treatment therapies.https://doi.org/10.1002/fft2.281cadmiumcaffeic acid phenethyl esterlung injurymiR‐182‐5p/TLR4 axis
spellingShingle Rili Hao
Xing Zhou
Xiaqing Lv
Xiangyang Zhu
Yang Jiang
Dapeng Li
The antagonistic effect of caffeic acid phenethyl ester on cadmium‐caused pulmonary toxicity: MiR‐182‐5p/TLR4 axis
Food Frontiers
cadmium
caffeic acid phenethyl ester
lung injury
miR‐182‐5p/TLR4 axis
title The antagonistic effect of caffeic acid phenethyl ester on cadmium‐caused pulmonary toxicity: MiR‐182‐5p/TLR4 axis
title_full The antagonistic effect of caffeic acid phenethyl ester on cadmium‐caused pulmonary toxicity: MiR‐182‐5p/TLR4 axis
title_fullStr The antagonistic effect of caffeic acid phenethyl ester on cadmium‐caused pulmonary toxicity: MiR‐182‐5p/TLR4 axis
title_full_unstemmed The antagonistic effect of caffeic acid phenethyl ester on cadmium‐caused pulmonary toxicity: MiR‐182‐5p/TLR4 axis
title_short The antagonistic effect of caffeic acid phenethyl ester on cadmium‐caused pulmonary toxicity: MiR‐182‐5p/TLR4 axis
title_sort antagonistic effect of caffeic acid phenethyl ester on cadmium caused pulmonary toxicity mir 182 5p tlr4 axis
topic cadmium
caffeic acid phenethyl ester
lung injury
miR‐182‐5p/TLR4 axis
url https://doi.org/10.1002/fft2.281
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