Chlorogenic Acid Ameliorates Damage Induced by Fluorene-9-Bisphenol in Porcine Sertoli Cells

被引:17
|
作者
Zhang, Shaoxuan [1 ]
Sun, Boxing [1 ]
Wang, Dali [1 ]
Liu, Ying [1 ]
Li, Jing [1 ]
Qi, Jiajia [1 ]
Zhang, Yonghong [1 ]
Bai, Chunyan [1 ]
Liang, Shuang [1 ]
机构
[1] Jilin Univ, Coll Anim Sci, Dept Anim Sci, Changchun, Peoples R China
来源
FRONTIERS IN PHARMACOLOGY | 2021年 / 12卷
关键词
chlorogenic acid; BPFL; porcine sertoli cells; ameliorates; impairments; ENDOPLASMIC-RETICULUM STRESS; UNFOLDED PROTEIN RESPONSE; OXIDATIVE STRESS; MOLECULAR-MECHANISMS; SIGNALING PATHWAYS; APOPTOSIS; AUTOPHAGY; SPERMATOGENESIS; MITOCHONDRIA; METABOLISM;
D O I
10.3389/fphar.2021.678772
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
4,4 '-(9-Fluorenylidene) diphenol (BPFL, also known as BHPF and fluorene-9-bisphenol) is a novel bisphenol A substitute that is used in the plastics industry as an organic synthesis intermediate and is a potential endocrine disruptor. However, the deleterious effects of BPFL on porcine Sertoli cells (SCs) and the possible underlying mechanisms are still unclear. Chlorogenic acid (CA) is a free radical scavenger in the cellular antioxidant system that prevents oxidative damage and apoptosis. In the present research, we found that BPFL induced impairments in porcine SCs in a dose-dependent manner and that CA protected porcine SCs against BPFL exposure-induced impairments. Cell viability, proliferation and apoptosis assay results revealed that BPFL exposure could inhibit porcine SC proliferation and induce apoptosis, while CA supplementation ameliorated the effects of BPFL. Further analysis revealed that BPFL exposure induced oxidative stress, mitochondrial membrane potential dysfunction and DNA damage accumulation. Transcriptome analysis and further real-time quantitative PCR and Western blot results showed that BPFL exposure induced endoplasmic reticulum stress and apoptosis. Supplementation with CA dramatically ameliorated these phenotypes in BPFL-exposed porcine SCs. Overall, the present research reveals the possible underlying mechanisms by which BPFL exposure induced impairments and CA supplementation protected against these impairments in porcine SCs.
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页数:13
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