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Baicalin Attenuates H(2)O(2)-Induced Oxidative Stress by Regulating the AMPK/Nrf2 Signaling Pathway in IPEC-J2 Cells
Oxidative stress can adversely affect the health status of the body, more specifically by causing intestinal damage by disrupting the permeability of the intestinal barrier. This is closely related to intestinal epithelial cell apoptosis caused by the mass production of reactive oxygen species (ROS)...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10253293/ https://www.ncbi.nlm.nih.gov/pubmed/37298392 http://dx.doi.org/10.3390/ijms24119435 |
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author | Liang, Jiahua Zhou, Ying Cheng, Xinyi Chen, Jiaqi Cao, Huabin Guo, Xiaoquan Zhang, Caiying Zhuang, Yu Hu, Guoliang |
author_facet | Liang, Jiahua Zhou, Ying Cheng, Xinyi Chen, Jiaqi Cao, Huabin Guo, Xiaoquan Zhang, Caiying Zhuang, Yu Hu, Guoliang |
author_sort | Liang, Jiahua |
collection | PubMed |
description | Oxidative stress can adversely affect the health status of the body, more specifically by causing intestinal damage by disrupting the permeability of the intestinal barrier. This is closely related to intestinal epithelial cell apoptosis caused by the mass production of reactive oxygen species (ROS). Baicalin (Bai) is a major active ingredient in Chinese traditional herbal medicine that has antioxidant, anti-inflammatory, and anti-cancer properties. The purpose of this study was to explore the underlying mechanisms by which Bai protects against hydrogen peroxide (H(2)O(2))-induced intestinal injury in vitro. Our results indicated that H(2)O(2) treatment caused injury to IPEC-J2 cells, resulting in their apoptosis. However, Bai treatment attenuated H(2)O(2)-induced IPEC-J2 cell damage by up-regulating the mRNA and protein expression of ZO-1, Occludin, and Claudin1. Besides, Bai treatment prevented H(2)O(2)-induced ROS and MDA production and increased the activities of antioxidant enzymes (SOD, CAT, and GSH-PX). Moreover, Bai treatment also attenuated H(2)O(2)-induced apoptosis in IPEC-J2 cells by down-regulating the mRNA expression of Caspase-3 and Caspase-9 and up-regulating the mRNA expression of FAS and Bax, which are involved in the inhibition of mitochondrial pathways. The expression of Nrf2 increased after treatment with H(2)O(2), and Bai can alleviate this phenomenon. Meanwhile, Bai down-regulated the ratio of phosphorylated AMPK to unphosphorylated AMPK, which is indicative of the mRNA abundance of antioxidant-related genes. In addition, knockdown of AMPK by short-hairpin RNA (shRNA) significantly reduced the protein levels of AMPK and Nrf2, increased the percentage of apoptotic cells, and abrogated Bai-mediated protection against oxidative stress. Collectively, our results indicated that Bai attenuated H(2)O(2)-induced cell injury and apoptosis in IPEC-J2 cells through improving the antioxidant capacity through the inhibition of the oxidative stress-mediated AMPK/Nrf2 signaling pathway. |
format | Online Article Text |
id | pubmed-10253293 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-102532932023-06-10 Baicalin Attenuates H(2)O(2)-Induced Oxidative Stress by Regulating the AMPK/Nrf2 Signaling Pathway in IPEC-J2 Cells Liang, Jiahua Zhou, Ying Cheng, Xinyi Chen, Jiaqi Cao, Huabin Guo, Xiaoquan Zhang, Caiying Zhuang, Yu Hu, Guoliang Int J Mol Sci Article Oxidative stress can adversely affect the health status of the body, more specifically by causing intestinal damage by disrupting the permeability of the intestinal barrier. This is closely related to intestinal epithelial cell apoptosis caused by the mass production of reactive oxygen species (ROS). Baicalin (Bai) is a major active ingredient in Chinese traditional herbal medicine that has antioxidant, anti-inflammatory, and anti-cancer properties. The purpose of this study was to explore the underlying mechanisms by which Bai protects against hydrogen peroxide (H(2)O(2))-induced intestinal injury in vitro. Our results indicated that H(2)O(2) treatment caused injury to IPEC-J2 cells, resulting in their apoptosis. However, Bai treatment attenuated H(2)O(2)-induced IPEC-J2 cell damage by up-regulating the mRNA and protein expression of ZO-1, Occludin, and Claudin1. Besides, Bai treatment prevented H(2)O(2)-induced ROS and MDA production and increased the activities of antioxidant enzymes (SOD, CAT, and GSH-PX). Moreover, Bai treatment also attenuated H(2)O(2)-induced apoptosis in IPEC-J2 cells by down-regulating the mRNA expression of Caspase-3 and Caspase-9 and up-regulating the mRNA expression of FAS and Bax, which are involved in the inhibition of mitochondrial pathways. The expression of Nrf2 increased after treatment with H(2)O(2), and Bai can alleviate this phenomenon. Meanwhile, Bai down-regulated the ratio of phosphorylated AMPK to unphosphorylated AMPK, which is indicative of the mRNA abundance of antioxidant-related genes. In addition, knockdown of AMPK by short-hairpin RNA (shRNA) significantly reduced the protein levels of AMPK and Nrf2, increased the percentage of apoptotic cells, and abrogated Bai-mediated protection against oxidative stress. Collectively, our results indicated that Bai attenuated H(2)O(2)-induced cell injury and apoptosis in IPEC-J2 cells through improving the antioxidant capacity through the inhibition of the oxidative stress-mediated AMPK/Nrf2 signaling pathway. MDPI 2023-05-29 /pmc/articles/PMC10253293/ /pubmed/37298392 http://dx.doi.org/10.3390/ijms24119435 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Liang, Jiahua Zhou, Ying Cheng, Xinyi Chen, Jiaqi Cao, Huabin Guo, Xiaoquan Zhang, Caiying Zhuang, Yu Hu, Guoliang Baicalin Attenuates H(2)O(2)-Induced Oxidative Stress by Regulating the AMPK/Nrf2 Signaling Pathway in IPEC-J2 Cells |
title | Baicalin Attenuates H(2)O(2)-Induced Oxidative Stress by Regulating the AMPK/Nrf2 Signaling Pathway in IPEC-J2 Cells |
title_full | Baicalin Attenuates H(2)O(2)-Induced Oxidative Stress by Regulating the AMPK/Nrf2 Signaling Pathway in IPEC-J2 Cells |
title_fullStr | Baicalin Attenuates H(2)O(2)-Induced Oxidative Stress by Regulating the AMPK/Nrf2 Signaling Pathway in IPEC-J2 Cells |
title_full_unstemmed | Baicalin Attenuates H(2)O(2)-Induced Oxidative Stress by Regulating the AMPK/Nrf2 Signaling Pathway in IPEC-J2 Cells |
title_short | Baicalin Attenuates H(2)O(2)-Induced Oxidative Stress by Regulating the AMPK/Nrf2 Signaling Pathway in IPEC-J2 Cells |
title_sort | baicalin attenuates h(2)o(2)-induced oxidative stress by regulating the ampk/nrf2 signaling pathway in ipec-j2 cells |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10253293/ https://www.ncbi.nlm.nih.gov/pubmed/37298392 http://dx.doi.org/10.3390/ijms24119435 |
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