Dietary choline deficiency aggravated the intestinal apoptosis in association with the MAPK signalling pathways of juvenile grass carp (Ctenopharyngodon idella)
Dietary choline deficiency aggravated the intestinal apoptosis in association with the MAPK signalling pathways of juvenile grass carp (Ctenopharyngodon idella)
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日粮胆碱缺乏加剧了草鱼幼鱼（Ctenopharyngodon idella）肠道细胞凋亡，与 MAPK 信号通路相关
DOI：
10.1016/j.aquaculture.2020.736046
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发表时间：
2021-02
期刊：
影响因子：
4.5
通讯作者：
Xiaoqiu Zhou
中科院分区：
文献类型：
--
作者：
Zehong Yuan;Lin Feng;Weidan Jiang;Pei Wu;Yang Liu;Shengyao Kuang;Ling Tang;Xiaoqiu Zhou
为探讨饲料中胆碱对草鱼幼鱼肠道细胞凋亡的影响及其可能机制，在饲料中添加不同胆碱的饲料(142.2、407.4、821.6、1215.8、1589.3和1996.6 mg/kg−1)，共70天。结果表明，饲料中胆碱缺乏(1)降低了草鱼肠道中胆碱、磷脂酰胆碱、甜菜碱和乙酰胆碱(不在远端肠道[DI])的含量；下调了高亲和力胆碱转运蛋白CHT1(不在近端肠道[PI]和DI)、类胆碱转运蛋白CTL-1、CTL-2、CTL-4(不在DI中)和CTL-5等胆碱转运蛋白的mRNA丰度；(2)增加了DNA片段的程度。上调Caspase-3、−-8、-9的活性；下调Caspase-3、−-7、−-8(非DI)、−-9、Fas配体(Fas L)(非PI)、细胞色素蛋白(Cty C)的蛋白水平。饲料中胆碱缺乏还下调了草鱼肠道髓系细胞白血病-1(Mcl-1)(非PI)、B细胞淋巴瘤-2(Bcl-2)和凋亡抑制蛋白(IAP)的mRNA水平，提示胆碱抑制了鱼类肠道中的细胞凋亡：(3)P38MAPK和JNK(不在中肠[MI])的mRNA水平，以及PI中的p-p38MAPK和T-p38MAPK蛋白水平以及MI和DI中p-p38MAPK/T-p38MAPK的比例，表明胆碱缺乏加剧了鱼类肠道中的细胞凋亡，这与MAPK信号通路有关；综上所述，胆碱缺乏促进鱼类肠道细胞凋亡可能与MAPK信号通路有关。此外，计算出草鱼(9.28-108.97 mg/kg−1饲料)抗肠道细胞凋亡指标(caspase-8和capase-9活性)的胆碱需要量分别为(1162.13-1780.93)mg/kg饲料。
To investigate the effects and potential mechanisms of apoptosis in the intestines of juvenile grass carp (Ctenopharyngodon idella) for dietary choline, fish were fed different choline-containing diets (142.2, 407.4, 821.6, 1215.8, 1589.3, and 1996.6 mg kg−1) for 70 days. Results revealed that dietary choline deficiency (1) decreased the contents of choline, phosphatidylcholine, betaine, and acetylcholine (not in distal intestine [DI]) in grass crap intestines; down-regulated the mRNA abundances of choline transportations, such as high-affinity choline transporter CHT1 (not in proximal intestine[PI] and DI), choline transporter-like proteins such as CTL-1, CTL-2, CTL-4 (not in DI), and CTL-5 in grass crap intestines; (2) enhanced the degree of DNA fragments. Moreover, it up-regulated the activities of caspase-3, −8, and-9; reduced mRNA levels of caspase-3, −7, −8 (not in DI), and − 9, Fas ligand (FASL) (not in PI), and apoptotic protease activating factor-1(Apaf1), as well as the protein level of cytochromec(Cty c). Dietary choline deficiency also down-regulated myeloid cell leukemia-1 (Mcl-1) (not in PI), B-cell lymphoma-2 (Bcl-2), and the inhibitor of apoptosis protein (IAP) mRNA levels in grass carp intestines, suggesting that choline inhibited cell apoptosis in fish intestines; (3) increased p38MAPK and JNK(not in mid intestine [MI]) mRNA level, as well as p-p38MAPK and T-p38MAPK protein levels in the PI and the ratio of p-p38MAPK/T-p38MAPK in the MI and DI, indicating that choline deficiency aggravated cell apoptosis in association with the MAPK signalling pathway in fish intestines; In conclusion, choline insufficiency promotion of intestinal apoptosis might be related to MAPK signalling pathways in fish. Moreover, the requirements of choline for resist intestinal apoptosis indices (caspase-8 and capase-9 activities) of grass carp (9.28–108.97 g) were calculated to be (1162.13–1780.93) mg kg−1diet, respectively.
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影响因子：
4.5
作者：
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DOI：
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期刊：
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影响因子：
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