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  • Research Article   
  • Cell Mol Biol,
  • DOI: 10.4172/1165-158X.1000211

SP-A Induces Preterm Birth through Promoting Oxidative Stress via Upregulating STOX1

Xiafang Li1* and Chunnian Zhang2
1Department of Obstetrics, Ganzhou People’s Hospital, Ganzhou, Jiangxi, 341000, China
2Department of Obstetrics and Gynecology, Ganzhou People’s Hospital, Ganzhou, Jiangxi, 341000, China
*Corresponding Author : Xiafang Li, Department of Obstetrics, Ganzhou People’s Hospital, No. 16 Meiguan Avenue, Zhanggong District, Ganzhou, Jiangxi, 341000, China, Tel: +86-0797-5889551, Email: xiaf_l0302@126.com

Received Date: Sep 08, 2021 / Accepted Date: Oct 05, 2021 / Published Date: Oct 12, 2021

Abstract

Preterm birth is the leading cause of infant mortality. The mechanisms that instigate preterm birth remain elusive and this makes it difficult to predict or prevent preterm birth. In this study, we found that SP-A induced the pathological damage to placenta and promoted preterm birth. Mechanismly, SP-A promoted the expression of STOX1 which further promoted the oxidative stress in placenta through inhibiting the activities of series antioxidant enzymes including SOD, CAT1 and GSH-Px. SP-A also induced dysregulation of arginine metabolism through inhibiting NOS2 and ARG2. Overexpression of STOX1 aggravated SP-A induced oxidative stress, pathological damage and preterm birth, whereas knockdown of STOX1 alleviated SP-A induced oxidative stress, pathological damage and preterm birth. Our study uncovers that SP-A induces preterm birth through promoting oxidative stress via upregulating STOX1, which provides new targets for prediction and prevention of preterm birth.

Keywords: Antioxidant, Enzymes, Corticotropin-releasing hormone, Placental cells, Oxidative stress, Necrosis, Apoptosis

Citation: Li X, Zhang C (2021) SP-A Induces Preterm Birth through Promoting Oxidative Stress via Upregulating STOX1. Cell Mol Biol 67: 211. Doi: 10.4172/1165-158X.1000211

Copyright: © 2021 Li X, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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