| 白术多糖对环磷酰胺致雏鸡肝脏细胞凋亡中线粒体通路的影响 |
| |
| 引用本文： | 付晶,赵丹,林桐,田允波.白术多糖对环磷酰胺致雏鸡肝脏细胞凋亡中线粒体通路的影响[J].东北农业大学学报,2019,50(4):63-70. |
| |
| 作者姓名： | 付晶 赵丹 林桐 田允波 |
| |
| 作者单位： | 东北农业大学动物科学技术学院,哈尔滨150030;仲恺农业工程学院动物科技学院,广东省水禽健康养殖重点实验室,广州510225;东北农业大学动物科学技术学院,哈尔滨,150030;仲恺农业工程学院动物科技学院,广东省水禽健康养殖重点实验室,广州510225 |
| |
| 基金项目： | 留学归国基金;广东省科技计划;中国-白俄罗斯政府间科技交流项目;广东省现代产业技术体系项目 |
| |
| 摘 要： | 试验旨在从线粒体介导的细胞凋亡通路,探讨白术多糖(PAMK)对环磷酰胺(CTX)诱导的雏鸡肝脏损伤的影响。试验选取1日龄岭南黄鸡240羽,随机分成4组:对照(Control)、环磷酰胺(CTX)、白术多糖(PAMK)以及白术多糖环磷酰胺联合组(PAMK+CTX)。试验结束后,采集雏鸡肝脏组织,用于形态学观察及线粒体介导的细胞凋亡通路相关基因mRNA表达量和蛋白表达水平检测。光镜结果显示,环磷酰胺诱导雏鸡肝脏组织细胞形态结构不完整、肝细胞索排列紊乱、空泡化。电镜结果显示,环磷酰胺可导致雏鸡肝脏组织细胞线粒体明显受损,并发生细胞凋亡。从分子水平探讨线粒体介导的细胞凋亡通路结果显示,环磷酰胺可导致雏鸡肝脏组织中促凋亡基因Caspase-3、Caspase-8、Caspase-9、Bax和p53 mRNA表达量显著升高(P0.05),抑凋亡基因Bcl-2mRNA表达量显著降低(P0.05)。白术多糖环磷酰胺联合组雏鸡肝脏组织中Caspase-3、Caspase-8、Bax的mRNA表达量显著降低(P0.05),Bcl-2 mRNA表达量显著升高(P0.05)。此外,白术多糖环磷酰胺联合组雏鸡肝脏组织中Caspase-3蛋白表达水平显著降低(P0.05),Bcl-2蛋白表达水平显著升高(P0.05)。研究结果表明,环磷酰胺可诱导雏鸡肝细胞凋亡,白术多糖可通过调节线粒体通路相关基因表达抵抗环磷酰胺诱导雏鸡肝细胞凋亡,对雏鸡肝脏产生保护作用。
|
| 关 键 词： | 白术多糖 环磷酰胺 肝损伤 凋亡 线粒体通路 |
Effect of PAMK on apoptosis through mitochondrial pathway in chicken liver induced by CTX |
| |
| Institution: | ,School of Animal Sciences and Technology, Northeast Agricultural University,School of Animal Science and Technology, Zhongkai University of Agricultural and Engineering,Guangdong Province Key Laboratory of Waterfowl Healthy Breeding |
| |
| Abstract: | This trial was conducted to evaluate the effects of polysaccharide of atractylodes macrochala koidz(PAMK) on cyclophosphamide(CTX)-induced liver damage in chicks from mitochondriamediated apoptotic pathway. A total of 240 one-day-old Lingnan yel ow chicks were randomly divided into four groups control, CTX, PAMK and PAMK+CTX. At the end of the experiment, chick liver tissues were col ected for morphological observation and m RNA and protein expression of genes associated with mitochondrial pathwaymediated apoptosis. CTX induced irregularities in liver cel morphology of chicks and the hepatocyte cords were disorderly arranged and vacuolatedusing light microscope. CTX caused obvious damage to chickliver cel mitochondria and apoptosisusing electron microscope. Further studies on mitochondrial pathway-mediated apoptosis at the molecular level showed that treatment with CTX significantly increased(P<0.05) the m RNA expression of pro-apoptotic genes(Caspase-3, Caspase-8, Caspase-9, Bax, p53) and significantly decreased(P<0.05) the m RNA expression of Bcl-2 in liver. Further studies on mitochondrial pathway-mediated apoptosis at the molecular level showed that treatment with CTX significantly increased(P<0.05) the m RNA expression of pro-apoptotic genes(Caspase-3, Caspase-8, Caspase-9, Bax, p53) and significantly decreased(P<0.05) the m RNA expression of Bcl-2 in liver. However, compared with the CTX group, treatment with PAMK + CTX significantly decreased(P<0.05) the m RNA expression of pro-apoptotic genes(Caspase-3, Caspase-8, Bax)and significantly increased(P<0.05) the m RNA expression of Bcl-2 in liver. In addition, treatment with PAMK+CTX significantly decreased(P<0.05) the protein expression of Caspase-3 and significantly increased(P<0.05)the protein expression of Bcl-2 in liver. It indicated that CTX induced apoptosis in chickliver, PAMK resisted the apoptosis of chick liver induced by CTX through regulating the expression of mitochondrial pathway-related genes and protected liver of chicks. |
| |
| Keywords: | polysaccharide of atractylodes macrochala koidz cyclophosphamide liver injury apoptosis mitochondrial pathway |
| 本文献已被 CNKI 万方数据 等数据库收录！ |
|
