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The Associated Regulatory Mechanisms of Zinc Lactate in Redox Balance and Mitochondrial Function of Intestinal Porcine Epithelial Cells
Joint Authors
Li, Tiejun
Tang, Wenjie
Yang, Lingyuan
Long, Jing
Li, Jianzhong
He, Liuqin
Li, Shuwei
Kuang, Shengyao
Feng, Yanzhong
Chen, Heshu
Du, Zhiliang
Yin, Yulong
Li, Fenglan
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-15, 15 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2020-12-18
Country of Publication
Egypt
No. of Pages
15
Main Subjects
Abstract EN
Zinc lactate (ZnLA) is a new organic zinc salt which has antioxidant properties in mammals and can improve intestinal function.
This study explored the effects of ZnLA and ZnSO4 on cell proliferation, Zn transport, antioxidant capacity, mitochondrial function, and their underlying molecular mechanisms in intestinal porcine epithelial cells (IPEC-J2).
The results showed that addition of ZnLA promoted cell proliferation, inhibited cell apoptosis and IL-6 secretion, and upregulated the mRNA expression and concentration of MT-2B, ZNT-1, and CRIP, as well as affected the gene expression and activity of oxidation or antioxidant enzymes (e.g., CuZnSOD, CAT, and Gpx1, GSH-PX, LDH, and MDA), compared to ZnSO4 or control.
Compared with the control, ZnLA treatment had no significant effect on mitochondrial membrane potential, whereas it markedly increased the mitochondrial basal OCR, nonmitochondrial respiratory capacity, and mitochondrial proton leakage and reduced spare respiratory capacity and mitochondrial reactive oxygen (ROS) production in IPEC-J2 cells.
Furthermore, ZnLA treatment increased the protein expression of Nrf2 and phosphorylated AMPK, but reduced Keap1 and p62 protein expression and autophagy-related genes LC3B-1 and Beclin mRNA abundance.
Under H2O2-induced oxidative stress conditions, ZnLA supplementation markedly reduced cell apoptosis and mitochondrial ROS levels in IPEC-J2 cells.
Moreover, ZnLA administration increased the protein expression of Nrf2 and decreased the protein expression of caspase-3, Keap1, and p62 in H2O2-induced IPEC-J2 cells.
In addition, when the activity of AMPK was inhibited by Compound C, ZnLA supplementation did not increase the protein expression of nuclear Nrf2, but when Compound C was removed, the activities of AMPK and Nfr2 were both increased by ZnLA treatment.
Our results indicated that ZnLA could improve the antioxidant capacity and mitochondrial function in IPEC-J2 cells by activating the AMPK-Nrf2-p62 pathway under normal or oxidative stress conditions.
Our novel finding also suggested that ZnLA, as a new feed additive for piglets, has the potential to be an alternative for ZnSO4.
American Psychological Association (APA)
Tang, Wenjie& Long, Jing& Li, Tiejun& Yang, Lingyuan& Li, Jianzhong& He, Liuqin…[et al.]. 2020. The Associated Regulatory Mechanisms of Zinc Lactate in Redox Balance and Mitochondrial Function of Intestinal Porcine Epithelial Cells. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-15.
https://search.emarefa.net/detail/BIM-1205705
Modern Language Association (MLA)
Tang, Wenjie…[et al.]. The Associated Regulatory Mechanisms of Zinc Lactate in Redox Balance and Mitochondrial Function of Intestinal Porcine Epithelial Cells. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-15.
https://search.emarefa.net/detail/BIM-1205705
American Medical Association (AMA)
Tang, Wenjie& Long, Jing& Li, Tiejun& Yang, Lingyuan& Li, Jianzhong& He, Liuqin…[et al.]. The Associated Regulatory Mechanisms of Zinc Lactate in Redox Balance and Mitochondrial Function of Intestinal Porcine Epithelial Cells. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-15.
https://search.emarefa.net/detail/BIM-1205705
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1205705