Selenium-Chitosan Protects Porcine Endometrial Epithelial Cells from Zearalenone-induced Apoptosis via the JNK/SAPK Signaling Pathway

• Published in: Biological trace element research Vol. 202; no. 5; pp. 2075 - 2084
• Main Authors: Wang, Huanhuan, She, Fuze, Chen, Fu, Li, Kun, Qin, Shunyi
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.05.2024; Springer Nature B.V
• Subjects: Animals; Apoptosis; Biochemistry; Biomedical and Life Sciences; Biotechnology; Brief Report; c-Jun protein; Cell cycle; Chitosan; Chitosan - pharmacology; Damage; Endometrium; Epithelial cells; Epithelial Cells - metabolism; Epithelium; G1 phase; G2 phase; Gene expression; JNK Mitogen-Activated Protein Kinases - metabolism; JNK protein; Kinases; Life Sciences; MAP kinase; MAP Kinase Signaling System; Membrane potential; Nutrition; Oncology; p53 Protein; Proteins; Reactive oxygen species; Reactive Oxygen Species - metabolism; Selenium; Selenium - metabolism; Selenium - pharmacology; Signal Transduction; Swine; Transcription factors; Zearalenone; Zearalenone - metabolism; Zearalenone - toxicity; Reactive oxygen species; Cell cycle; Zearalenone; Selenium-chitosan; Signaling pathway of JNK/SAPK; Porcine endometrial epithelial cells; Mitochondrial membrane potential; Apoptosis
• ISSN: 0163-4984; 1559-0720
• DOI: 10.1007/s12011-023-03816-8

This study was designed to assess whether selenium-chitosan (Se-CTS) can protect porcine endometrial epithelial cells (PEECs) against damage and apoptosis induced by zearalenone (ZEA) via modulating the JNK/SAPK signaling pathway. The cell cycle, mitochondrial membrane potential (MMP), reactive oxygen species (ROS), and apoptosis rates of porcine endometrial epithelial cells were determined, as well as the expression levels of genes related to the SAPK/JNK signaling pathway. The results showed that 3.0 µmol/L Se-CTS decreased the percentage of ZEA-induced G1 phase in PEECs ( P  < 0.01), whereas 1.5 and 3.0 µmol/L Se-CTS increased the percentage of ZEA-induced percentage of G2 phase of PEECs ( P  < 0.01). Further, Se-CTS at 1.5 and 3.0 µmol/L improved the ZEA-induced decrease in MMP ( P  < 0.01), whereas Se-CTS at 0.5, 1.5, and 3.0 µmol/L reduced the increase in ROS levels and apoptosis rate induced by ZEA in PEECs ( P  < 0.01 or P  < 0.05). Furthermore, 3.0 µmol/L Se-CTS ameliorated the increase in the expression of c-Jun N-terminal kinase (JNK), apoptosis signal–regulated kinase (ASK1), and c-Jun induced by ZEA ( P  < 0.01) and the reduction in mitogen-activated protein kinase kinase 4 (MKK4) and protein 53 (p53) expression ( P  < 0.01), while 1.5 µmol/L Se-CTS improved the expression of ASK1 and c-Jun induced by ZEA ( P  < 0.05). The results proved that Se-CTS alleviates ZEA-induced cell cycle stagnation, cell mitochondrial damage, and cell apoptosis via decreasing ZEA-produced ROS and modulating the JNK/SAPK signaling pathway.