CAJ | 학술논문

研究采用酶联免疫吸附测定(Enzyme-linked immunosorbent assays,ELISA)技术,比较分析了转GH基因鲤鱼和对照鲤鱼在饥饿和饱食状态下血清生长激素水平的变化规律,并探讨其可能机制.实验结果表明,在投喂实验中,转基因鲤鱼和对照鲤鱼血清生长激素水平均无明显变化,但转基因鲤鱼血清生长激素远高于对照鲤鱼,分别为(142.0±4.9)ng/mL和(1.6±0.2)ng/mL,转基因鲤鱼体重增长速率显著高于对照鱼.在饥饿实验中,转基因鲤鱼的血清生长激素迅速下降,从(142.0±4.9)ng/mL降至(46.0±3.2)ng/mL,而后稳定在这一较低水平;对照鲤鱼血清生长激素持续卜升,从(1.6±0.2)ng/mL升至(10.9±1.4)ng/mL,体重负增长速率没有显著差异.研究结果提示,转GH基因鲤鱼血清生长激素的调控机制与对照鲤鱼的不同,其表达水平不受脑垂体反馈抑制调控机制的影响,而与重组GH基因中β-actin基因启动子的调控模式相关.
연구채용매련면역흡부측정(Enzyme-linked immunosorbent assays,ELISA)기술,비교분석료전GH기인리어화대조리어재기아화포식상태하혈청생장격소수평적변화규률,병탐토기가능궤제.실험결과표명,재투위실험중,전기인리어화대조리어혈청생장격소수평균무명현변화,단전기인리어혈청생장격소원고우대조리어,분별위(142.0±4.9)ng/mL화(1.6±0.2)ng/mL,전기인리어체중증장속솔현저고우대조어.재기아실험중,전기인리어적혈청생장격소신속하강,종(142.0±4.9)ng/mL강지(46.0±3.2)ng/mL,이후은정재저일교저수평;대조리어혈청생장격소지속복승,종(1.6±0.2)ng/mL승지(10.9±1.4)ng/mL,체중부증장속솔몰유현저차이.연구결과제시,전GH기인리어혈청생장격소적조공궤제여대조리어적불동,기표체수평불수뇌수체반궤억제조공궤제적영향,이여중조GH기인중β-actin기인계동자적조공모식상관.
This study comparatively analyzed the change regulation of serum growth hormone of transgenic fish and control under starvation and feeding condition by using the Enzyme-linked immunosorbent assays, ELISA technology, and discussed its possible mechanism. The result showed that there was no obviously change in serum growth hormone level of both transgenic fish and the control in feeding experiment, but serum growth hormone level of the former was extremely higher than the latter, which were (142.0±4.9)ng/mL and (1.6±0.2) ng/mL respectively, body weight growth rate of the former was also higher than the latter. In starvation experiment, the concentration of serum growth hormone in transgenic fish descended from (142.0±4.9) ng/mL to (46.0±3.2) ng/mL rapidly, and then kept at this lower level, while the concentration of serum growth hormone in the control rose up from (1.6±0.2) ng/mL to (10.9±1.4) ng/mL continuously, there was no significant difference in body weight minus growth rate between transgenic fish and the control. The study result revealed that the regulatory mechanism of serum growth hormone of transgenic common carp was different with that of the control, because its expression level was not impacted by pituitary feedback inhibition mechanism but related to the control mode of β-actin gene promoter in the transgene.