Статья

Tannic Acid Induces the Mitochondrial Pathway of Apoptosis and S Phase Arrest in Porcine Intestinal IPEC-J2 Cells

Ji WangLaboratory of Animal Clinical Toxicology, Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Hunan Agricultural University, Changsha 410128, ChinaHaisi XiaoLaboratory of Animal Clinical Toxicology, Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Hunan Agricultural University, Changsha 410128, ChinaYuanyuan ZhuLaboratory of Animal Clinical Toxicology, Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Hunan Agricultural University, Changsha 410128, ChinaShuiping LiuLaboratory of Animal Clinical Toxicology, Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Hunan Agricultural University, Changsha 410128, ChinaZhihang YuanLaboratory of Animal Clinical Toxicology, Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Hunan Agricultural University, Changsha 410128, ChinaJing WuLaboratory of Animal Clinical Toxicology, Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Hunan Agricultural University, Changsha 410128, ChinaLixin WenHunan Collaborative Innovation Center of Animal Production Safety, Changsha 410128, China

2019en

ABI

Аннотация

The presence of tannic acid (TA), which is widely distributed in plants, limits the utilization of non-grain feed. Illustrating the toxicity mechanism of TA in animals is important for preventing poisoning and for clinical development of TA. The aim of the present study was to evaluate the toxic effects and possible action mechanism of TA in porcine intestinal IPEC-J2 cells, as well as cell proliferation, apoptosis, and cell cycle. We investigated the toxic effects of TA in IPEC-J2 cells combining the analysis of TA-induced apoptotic responses and effect on the cell cycle. The results revealed that TA is highly toxic to IPEC-J2 cells. The stress-inducible factors reactive oxygen species, malondialdehyde, and 8-hydroxy-2′-deoxyguanosine were increased in response to TA. Furthermore, TA suppressed mitochondrial membrane potential, reduced adenosine triphosphate production, and adversely affected B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein, caspase-9, caspase-3, cytochrome c, cyclin A, cyclin-dependent kinases, ataxia-telangiectasia mutated, and P53 expression in a dose-dependent manner. We suggest that TA induces the mitochondrial pathway of apoptosis and S phase arrest in IPEC-J2 cells.

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Идентификаторы

DOI: 10.3390/toxins11070397

Цитирования и источники

Цитирований: 2Использованных источников: 0

Показатели — AkademScholar