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Niacin Protects against Butyrate-Induced Apoptosis in Rumen Epithelial Cells
Joint Authors
Ouyang, Kehui
Luo, Dan
Peng, Zhipeng
Yang, Le
Qu, Mingren
Xiong, Xiaowen
Xu, Lanjiao
Zhao, Xianghui
Pan, Ke
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2019, Issue 2019 (31 Dec. 2019), pp.1-8, 8 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2019-10-13
Country of Publication
Egypt
No. of Pages
8
Main Subjects
Abstract EN
The effects and underlying mechanisms of butyrate and butyrate+niacin on apoptosis in sheep rumen epithelial cells were investigated.
Cells were exposed to butyrate (0–140 mM) for 6 h.
A low concentration (20 mM) of butyrate increased cell viability and promoted growth whereas high concentrations (40–140 mM) inhibited proliferation.
Cells were then cocultured with 120 mM butyrate and niacin (0–100 mM) for 6 h.
Niacin addition attenuated butyrate-induced cellular damage and promoted proliferation at 20–80 mM; 40 mM presented the optimal effect.
Higher concentrations (100 mM) of niacin resulted in low cell viability.
Subsequent experiments confirmed that 120 mM butyrate increased intracellular reactive oxygen species (ROS) production and reduced the intracellular total antioxidant capacity (T-AOC) versus the untreated control.
Compared with 120 mM butyrate, cotreatment with 40 mM niacin significantly reduced the intracellular ROS content and increased the intracellular T-AOC.
Flow cytometry analysis revealed that 120 mM butyrate increased the proportion of apoptotic cells by 17.8% versus the untreated control, and 120 mM butyrate+40 mM niacin treatment reduced the proportion of apoptotic cells by 28.6% and 39.4% versus the untreated control and butyrate treatment, respectively.
Treatment with 120 mM butyrate increased caspase-9 and p53 mRNA levels and decreased the expression of Bcl-2 and Bax, and the Bcl-2/Bax ratio versus the untreated control.
Treatment with 120 mM butyrate+40 mM niacin downregulated the expression of caspase-3 and p53 and increased the expression of Bcl-2 and Bax versus butyrate treatment alone but had no effect on the Bcl-2/Bax ratio.
Thus, high concentrations of butyrate may induce rumen epithelial cell apoptosis by increasing oxidative stress and inducing caspase-9 and p53 expression.
Cotreatment with niacin regulates apoptosis-related gene expression by reducing intracellular ROS production and DNA damage and downregulating caspase-3 and p53 expressions to protect rumen epithelial cells against butyrate-induced apoptosis.
American Psychological Association (APA)
Luo, Dan& Peng, Zhipeng& Yang, Le& Qu, Mingren& Xiong, Xiaowen& Xu, Lanjiao…[et al.]. 2019. Niacin Protects against Butyrate-Induced Apoptosis in Rumen Epithelial Cells. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-8.
https://search.emarefa.net/detail/BIM-1202537
Modern Language Association (MLA)
Luo, Dan…[et al.]. Niacin Protects against Butyrate-Induced Apoptosis in Rumen Epithelial Cells. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-8.
https://search.emarefa.net/detail/BIM-1202537
American Medical Association (AMA)
Luo, Dan& Peng, Zhipeng& Yang, Le& Qu, Mingren& Xiong, Xiaowen& Xu, Lanjiao…[et al.]. Niacin Protects against Butyrate-Induced Apoptosis in Rumen Epithelial Cells. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-8.
https://search.emarefa.net/detail/BIM-1202537
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1202537