伏隔核区Jak/Stat3抑制剂注射调控布氏田鼠的能量代谢
Nucleus Accumbens Microinjection Jak/Stat3 Inhibitor Regulate Energy Metabolism of Lasiopodomys brandtii

中文摘要： 目的 探究抑制布氏田鼠 Lasiopodomys brandtii伏隔核区leptin-Stat3（瘦素-Stat3）细胞信号通路对其能量代谢以及体质量的影响。 方法 在布氏田鼠伏隔核区定点注射Jak/Stat3抑制剂（WP1066）|使用TSE代谢笼系统检测布氏田鼠的基础代谢|并随时记录布氏田鼠的体质量。 结果 在伏隔核区定点注射Jak/Stat3抑制剂后，布氏田鼠伏隔核区P-Stat3表达量以及瘦素表达水平明显下降（ P<0.05），而血清瘦素浓度以及血糖浓度没有显著变化（ P>0.05）。TSE代谢笼实验检测发现，实验组布氏田鼠总能量消耗显著降低（ P<0.05）、呼吸交换率显著增加（ P<0.05）、总耗氧量显著降低（ P<0.05）、总自主运动量显著减弱（ P<0.05）、总饮水量显著增加（ P<0.05）、体质量显著增加（ P<0.05）。 结论 调控伏隔核区的leptin-Stat3信号通路能够调控基础代谢，进而在10 d内改变布氏田鼠体质量。
英文摘要： Objective To explore the effect of impaired leptin-Stat3 in nucleus accumbens on the metabolism and body mass of Lasiopodomys brandtii. Methods Inhibitor of Jak/Stat3 (WP1066) was injected into the nucleus accumbens of L. brandtii, and then the basic metabolism was tested by TSE metabolic cage system followed by monitoring the body mass. Results Jak/Stat3 could significantly decrease the levels of P-Stat3 and leptin in nucleus accumbens ( P<0.05). However, there was no significant difference in the levels of serum leptin and blood glucose ( P>0.05). The result of TSE metabolic cage system showed that the energy expenditure, cumulative O 2 consumption and cumulative locomotor activity decreased significantly, while the respiratory exchange rate and cumulative drink increased significantly in experimental group ( P<0.05). Moreover, the average body mass of experimental group increased significantly ( P<0.05). Conclusion Inhibition of leptin-Stat3 pathway in nucleus accumbens of L. brandtii can influence energy metabolism and body mass of L. brandtii in 10 days. 2018,37(1): 57-61 收稿日期：2017-08-24 DOI：10.11984/j.issn.1000-7083.20170258 分类号：Q95-33;Q955 基金项目：国家自然科学基金项目（31471790）；农业虫害鼠害综合治理研究国家重点实验室开放研究基金项目（Chinese IPM1615） 作者简介：闫立新,女,硕士研究生,主要从事行为神经学研究,E-mail:lixinyan1992@163.com *通讯作者：宋铭晶,E-mail:songmj@cnilas.org 参考文献： Banks WA. 2001. Enhanced leptin transport across the blood-brain barrier by alpha 1-adrenergic agents[J]. Brain Research, 899(1-2):209-217. Bouret SG, Draper SJ, Simerly RB. 2004. Trophic action of leptin on hypothalamic neurons that regulate feeding[J]. Science, 304(5667):108-110. Chekhranova MK, Karpova SK, Iatsyshina SB, et al. 2008. A new mutation c.422C>G (p.S141C) in homo-and heterozygous forms of the human leptin gene[J]. Bioorganicheskaia Khimiia, 34(6):854-856. Fatima W, Shahid A, Imran M, et al. 2011. Leptin deficiency and leptin gene mutations in obese children from Pakistan[J]. International Journal of Pediatric Obesity, 6(5-6):419-427. Fischer-Posovszky P, von Schnurbein J, Moepps B, et al. 2010. A new missense mutation in the leptin gene causes