Niacin Protects against Butyrate-Induced Apoptosis in Rumen Epithelial Cells
Niacin Protects against Butyrate-Induced Apoptosis in Rumen Epithelial Cells
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烟酸可防止丁酸盐诱导的瘤胃上皮细胞凋亡
DOI：
10.1155/2019/2179738
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发表时间：
2019-10-13
影响因子：
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通讯作者：
Ouyang, Kehui
中科院分区：
文献类型：
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作者：
Luo, Dan;Peng, Zhipeng;Ouyang, Kehui
研究了丁酸和丁酸+烟酸对绵羊瘤胃上皮细胞凋亡的影响及其机制。将细胞暴露于丁酸盐(0-140 mM)中6h，低浓度(20 MM)丁酸可提高细胞活力，促进细胞生长，而高浓度(40-140 mM)则抑制细胞增殖。将细胞与120 mM丁酸和烟酸(0-100 mM)共培养6h，加入烟酸可减轻20-80 mM烟酸对细胞的损伤，促进细胞增殖，其中以40 mM的效果最好。较高浓度的烟酸(100 MM)会导致细胞存活率降低。随后的实验证实，与未经处理的对照相比，120 mM丁酸盐增加了细胞内ROS的产生，降低了细胞内的总抗氧化能力(T-AOC)。与120 mM丁酸相比，40 mM烟酸显著降低细胞内ROS含量，增加细胞内T-AOC。流式细胞仪分析显示，120 mM丁酸处理组细胞凋亡率较未处理对照组增加17.8%，120 mM丁酸+40 mM烟酸处理组较未处理对照组和丁酸处理组分别降低28.6%和39.4%。120 mM丁酸处理组与未处理组比较，caspase-9、P53基因表达增强，Bcl2、Bax表达降低，Bcl2/Bax比值降低。与丁酸组比较，120 mM丁酸盐+40 mM烟酸可下调caspase-3和P53的表达，上调Bc l-2和Bax的表达，但对Bc l-2/Bax比值无影响。因此，高浓度的丁酸可能通过增加氧化应激和诱导caspase-9和p53的表达来诱导瘤胃上皮细胞的凋亡。烟酸联合治疗通过减少细胞内ROS的产生和DNA损伤，下调caspase-3和P53的表达，从而调节凋亡相关基因的表达，从而保护瘤胃上皮细胞免受丁酸诱导的细胞凋亡。
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 (40-140mM) inhibited proliferation. Cells were then cocultured with 120mM butyrate and niacin (0-100 mM) for 6 h. Niacin addition attenuated butyrate-induced cellular damage and promoted proliferation at 20-80 mM; 40mM presented the optimal effect. Higher concentrations (100 mM) of niacin resulted in low cell viability. Subsequent experiments confirmed that 120mM butyrate increased intracellular reactive oxygen species (ROS) production and reduced the intracellular total antioxidant capacity (T-AOC) versus the untreated control. Compared with 120mM butyrate, cotreatment with 40 mM niacin significantly reduced the intracellular ROS content and increased the intracellular T-AOC. Flow cytometry analysis revealed that 120mM butyrate increased the proportion of apoptotic cells by 17.8% versus the untreated control, and 120mM butyrate+40mM 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 120mM 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.