Chlorogenic acid ameliorates the heat stress-induced impairment of porcine Sertoli cells by suppressing oxidative stress and apoptosis

• Published in: Theriogenology Vol. 214; pp. 148 - 156
• Main Authors: Zhang, Shao-Xuan, Wang, Da-Li, Qi, Jia-Jia, Yang, Yu-Wei, Sun, Hao, Sun, Bo-Xing, Liang, Shuang
• Format: Journal Article
• Language: English
• Published: Elsevier Inc 15.01.2024
• Subjects: Apoptosis; Chlorogenic acid; Heat stress; Oxidative stress; Sertoli cells; Oxidative stress; Chlorogenic acid; Heat stress; Sertoli cells; Apoptosis
• ISSN: 0093-691X; 1879-3231
• DOI: 10.1016/j.theriogenology.2023.10.018

Sertoli cells are an important type of somatic cell in the testis that are in direct contact with spermatogonia in vivo and play an important role in the process of spermatogenesis. Chlorogenic acid (CGA) plays a pivotal role in the regulation of the mammalian cell heat stress response. For example, CGA treatment protects porcine oocytes from heat stress-induced apoptosis and prevents reduced embryo quality. However, the role of CGA treatment in protecting porcine testicular Sertoli cells against heat-induced damage has rarely been studied. This study aimed to identify the protective effects of CGA on oxidative stress and apoptosis in Sertoli cells under heat stress. The present results demonstrated that the addition of CGA significantly inhibited the accumulation of reactive oxygen species (ROS) and apoptosis in Sertoli cells induced by heat stress and decreased the expression of CASP3 protein and the BAX/BCL-2 protein ratio. CGA pretreatment also prevented the heat stress-induced reductions in the mitochondrial membrane potential, PCNA protein expression, and SOD and CAT activities. Moreover, CGA treatment reversed S phase cell cycle arrest and increased the HSP70 protein expression levels. Overall, these results suggest that oxidative damage participates in the inhibition of the proliferation of Sertoli cells and the increase in their apoptosis induced by heat stress, and the protective effects of CGA treatment on Sertoli cells under heat stress provide a theoretical basis for preventing heat stress injury in animals. •CGA ameliorated heat stress-induced intracellular ROS accumulation in porcine testicular Sertoli cells.•CGA inhibited heat stress-induced apoptosis in porcine testicular Sertoli cells.•CGA ameliorated heat stress-induced cell cycle arrest and mitochondrial dysfunction in porcine testicular Sertoli cells.