Feng Long
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Feng Long has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Hongyu Lei
College of Veterinary Medicine, Hunan Agricultural University, Changsha 410125, China
1 shared publication - Jianming Su
Department of Basic Veterinary Medicine, College of Veterinary Medicine, Hunan Agricultural University, Changsha, Hunan, China
1 shared publication - Lihua Zhou
Provincial Key Laboratory of Protein Engineering in Animal Vaccines College of Veterinary Medicin, Hunan Agricultural University, Changsha 410128, China
1 shared publication - Meiwen Tang
Provincial Key Laboratory of Protein Engineering in Animal Vaccines College of Veterinary Medicin, Hunan Agricultural University, Changsha 410128, China
1 shared publication - Qing Li
Provincial Key Laboratory of Protein Engineering in Animal Vaccines College of Veterinary Medicin, Hunan Agricultural University, Changsha 410128, China
1 shared publication - Qing Liu
Provincial Key Laboratory of Protein Engineering in Animal Vaccines College of Veterinary Medicin, Hunan Agricultural University, Changsha 410128, China
1 shared publication
Latest Publications
- Open Access
Effect of Fumonisin B1 on Proliferation and Apoptosis of Intestinal Porcine Epithelial Cells
Fumonisin B1 (FB1), which is a mycotoxin produced by Fusarium moniliforme and Fusarium rotarum, has a number of toxic effects in animals. Moldy feed containing FB1 can damage the intestine. In this study, we used intestinal porcine epithelial cells (IPEC-J2) as an in vitro model to explore the effects of FB1 on cell cycle and apoptosis. The results showed that IPEC-J2 cells treated with 10, 20, and 40 μg/mL FB1 for 48 h experienced different degrees of damage manifested as decreases in cell number and viability, as well as cell shrinkage and floating. In addition, FB1 reduced cell proliferation and the mRNA and protein expression of proliferating cell nuclear antigen (PCNA), cyclin-dependent kinase 2 (CDK2), CDK4, cyclinD1, and cyclinE1. FB1 blocked the cell cycle in the G1 phase. FB1 also induced mitochondrial pathway apoptosis, reduced mitochondrial membrane potential, and promoted mRNA and protein expression of Caspase3, Caspase9, and Bax. The findings suggest that FB1 can induce IPEC-J2 cell damage, block the cell cycle, and promote cell apoptosis.
Open AccessEffect of Fumonisin B1 on Proliferation and Apoptosis of Intestinal Porcine Epithelial Cells
Fumonisin B1 (FB1), which is a mycotoxin produced by Fusarium moniliforme and Fusarium rotarum, has a number of toxic effects in animals. Moldy feed containing FB1 can damage the intestine. In this study, we used intestinal porcine epithelial cells (IPEC-J2) as an in vitro model to explore the effects of FB1 on cell cycle and apoptosis. The results showed that IPEC-J2 cells treated with 10, 20, and 40 μg/mL FB1 for 48 h experienced different degrees of damage manifested as decreases in cell number and viability, as well as cell shrinkage and floating. In addition, FB1 reduced cell proliferation and the mRNA and protein expression of proliferating cell nuclear antigen (PCNA), cyclin-dependent kinase 2 (CDK2), CDK4, cyclinD1, and cyclinE1. FB1 blocked the cell cycle in the G1 phase. FB1 also induced mitochondrial pathway apoptosis, reduced mitochondrial membrane potential, and promoted mRNA and protein expression of Caspase3, Caspase9, and Bax. The findings suggest that FB1 can induce IPEC-J2 cell damage, block the cell cycle, and promote cell apoptosis.