Cecropin A Alleviates LPS-Induced Oxidative Stress and Apoptosis of Bovine Endometrial Epithelial Cells
Dairy cows receiving a prolonged high-concentrate diet express an elevated concentration of lipopolysaccharides (LPSs) in the peripheral blood circulation, accompanied by a series of systemic inflammatory responses; however, the specific impacts of inflammation are yet to be determined. Cecropin-lik...
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MDPI AG
2024-02-01
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author | Yu Zhao Yang Zhang Mingkun Sun Bowen Li Yuqiong Li Song Hua |
author_facet | Yu Zhao Yang Zhang Mingkun Sun Bowen Li Yuqiong Li Song Hua |
author_sort | Yu Zhao |
collection | DOAJ |
description | Dairy cows receiving a prolonged high-concentrate diet express an elevated concentration of lipopolysaccharides (LPSs) in the peripheral blood circulation, accompanied by a series of systemic inflammatory responses; however, the specific impacts of inflammation are yet to be determined. Cecropin-like antimicrobial peptides have become a research hotspot regarding antimicrobial peptides because of their excellent anti-inflammatory activities, and cecropin A is a major member of the cecropin family. To elucidate the mechanism of cecropin A as anti-inflammatory under the condition of sub-acute ruminal acidosis (SARA) in dairy cows, we induced inflammation in bEECs with LPS (10 µg/mL) and then added cecropin A (25 µM). Afterwards, we detected three categories of indexes including oxidative stress indices, inflammation-related genes, and apoptosis-related genes in bovine endometrial epithelial cells (bEECs). The results indicated that cecropin A has the ability to reduce inflammatory factors TNF-α, IL-1β, and IL-8 and inhibit the MAPK pathway to alleviate inflammation. In addition, cecropin A is able to reduce reactive oxygen species (ROS) levels and alleviates LPS-induced oxidative stress and mitochondrial dysfunction by downregulating NADPH Oxidase (NOX), and upregulating catalase (CAT), glutathione peroxidase (GPX), and superoxide dismutase (SOD). Furthermore, cecropin A demonstrates the ability to inhibit apoptosis by suppressing the mitochondrial-dependent apoptotic pathway, specifically Fas/FasL-caspase-8/-3. The observed increase in the Bcl-2/Bax ratio, a known apoptosis regulator, further supports this finding. In conclusion, our study presents novel solutions for addressing inflammatory responses associated with SARA. |
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spelling | doaj.art-2bea1f2905b146849f2bec7ec902a3582024-03-12T16:38:15ZengMDPI AGAnimals2076-26152024-02-0114576810.3390/ani14050768Cecropin A Alleviates LPS-Induced Oxidative Stress and Apoptosis of Bovine Endometrial Epithelial CellsYu Zhao0Yang Zhang1Mingkun Sun2Bowen Li3Yuqiong Li4Song Hua5College of Veterinary Medicine, Northwest A&F University, Yangling 712100, ChinaCollege of Veterinary Medicine, Northwest A&F University, Yangling 712100, ChinaCollege of Veterinary Medicine, Northwest A&F University, Yangling 712100, ChinaCollege of Veterinary Medicine, Northwest A&F University, Yangling 712100, ChinaLaboratory Institute of Animal Science, Ningxia Academy of Agricultural and Forestry Sciences, Yinchuan 750000, ChinaCollege of Veterinary Medicine, Northwest A&F University, Yangling 712100, ChinaDairy cows receiving a prolonged high-concentrate diet express an elevated concentration of lipopolysaccharides (LPSs) in the peripheral blood circulation, accompanied by a series of systemic inflammatory responses; however, the specific impacts of inflammation are yet to be determined. Cecropin-like antimicrobial peptides have become a research hotspot regarding antimicrobial peptides because of their excellent anti-inflammatory activities, and cecropin A is a major member of the cecropin family. To elucidate the mechanism of cecropin A as anti-inflammatory under the condition of sub-acute ruminal acidosis (SARA) in dairy cows, we induced inflammation in bEECs with LPS (10 µg/mL) and then added cecropin A (25 µM). Afterwards, we detected three categories of indexes including oxidative stress indices, inflammation-related genes, and apoptosis-related genes in bovine endometrial epithelial cells (bEECs). The results indicated that cecropin A has the ability to reduce inflammatory factors TNF-α, IL-1β, and IL-8 and inhibit the MAPK pathway to alleviate inflammation. In addition, cecropin A is able to reduce reactive oxygen species (ROS) levels and alleviates LPS-induced oxidative stress and mitochondrial dysfunction by downregulating NADPH Oxidase (NOX), and upregulating catalase (CAT), glutathione peroxidase (GPX), and superoxide dismutase (SOD). Furthermore, cecropin A demonstrates the ability to inhibit apoptosis by suppressing the mitochondrial-dependent apoptotic pathway, specifically Fas/FasL-caspase-8/-3. The observed increase in the Bcl-2/Bax ratio, a known apoptosis regulator, further supports this finding. In conclusion, our study presents novel solutions for addressing inflammatory responses associated with SARA.https://www.mdpi.com/2076-2615/14/5/768cecropin Alipopolysaccharideoxidative stressinflammationapoptosisendometrial epithelial cells |
spellingShingle | Yu Zhao Yang Zhang Mingkun Sun Bowen Li Yuqiong Li Song Hua Cecropin A Alleviates LPS-Induced Oxidative Stress and Apoptosis of Bovine Endometrial Epithelial Cells Animals cecropin A lipopolysaccharide oxidative stress inflammation apoptosis endometrial epithelial cells |
title | Cecropin A Alleviates LPS-Induced Oxidative Stress and Apoptosis of Bovine Endometrial Epithelial Cells |
title_full | Cecropin A Alleviates LPS-Induced Oxidative Stress and Apoptosis of Bovine Endometrial Epithelial Cells |
title_fullStr | Cecropin A Alleviates LPS-Induced Oxidative Stress and Apoptosis of Bovine Endometrial Epithelial Cells |
title_full_unstemmed | Cecropin A Alleviates LPS-Induced Oxidative Stress and Apoptosis of Bovine Endometrial Epithelial Cells |
title_short | Cecropin A Alleviates LPS-Induced Oxidative Stress and Apoptosis of Bovine Endometrial Epithelial Cells |
title_sort | cecropin a alleviates lps induced oxidative stress and apoptosis of bovine endometrial epithelial cells |
topic | cecropin A lipopolysaccharide oxidative stress inflammation apoptosis endometrial epithelial cells |
url | https://www.mdpi.com/2076-2615/14/5/768 |
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