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The role of ANXA5 in DBP-induced oxidative stress through ERK/Nrf2 pathway

Lei Zhang1, Zhiqiang Qin1, Ran Li1

  • 1Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210009, China.

Environmental Toxicology and Pharmacology
|August 13, 2019
PubMed

Insights

Annexin A5 (ANXA5) protects male reproductive cells from Di-N-butylphthalate (DBP) toxicity by activating the ERK/Nrf2 antioxidant pathway. This finding highlights ANXA5 as a potential therapeutic target against DBP-induced oxidative stress.

Area of Science:

  • Reproductive Toxicology
  • Cell Biology
  • Molecular Biology

Background:

  • Di-N-butylphthalate (DBP) is an endocrine disruptor with known toxicity to the male reproductive system.
  • The antioxidative Nrf2 pathway is crucial in mitigating DBP-induced oxidative stress.
  • Annexin A5 (ANXA5), highly expressed in testicular cells, is upregulated by DBP exposure.

Purpose of the Study:

  • To investigate the role of ANXA5 in DBP-induced oxidative stress in mouse Leydig and Sertoli cells.
  • To elucidate the mechanism by which ANXA5 exerts its protective effects against DBP.
  • To determine the involvement of the ERK/Nrf2 pathway in ANXA5-mediated protection.

Main Methods:

  • Exposure of mouse Leydig and Sertoli cells to varying concentrations of DBP.
  • Assessment of oxidative stress markers (ROS, MDA, SOD) using DHE staining and ELISA.
  • Analysis of protein expression (ANXA5, Nrf2, NQO1, HO-1, ERK/P-ERK) via Western blot and ELISA.
  • Utilisation of an ERK inhibitor to investigate pathway involvement.

Main Results:

  • DBP exposure confirmed to induce oxidative stress in testicular cells.
  • DBP altered Nrf2 pathway activation and ANXA5 levels.
  • Overexpression of ANXA5 activated the Nrf2/HO-1/NQO1 antioxidant pathway, reducing DBP-induced oxidative stress.
  • ANXA5 increased ERK phosphorylation, and this effect was reversed by an ERK inhibitor.

Conclusions:

  • ANXA5 plays a protective role against DBP-induced oxidative stress in testicular Leydig and Sertoli cells.
  • The protective mechanism involves the activation of the ERK/Nrf2/antioxidant pathway.
  • ANXA5 represents a potential therapeutic target for mitigating DBP reproductive toxicity.
Keywords:
ANXA5AnnexinDi-N-butylphthalateERK/Nrf2Oxidative stress

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