The Regulatory Effects of Lateral Hypothalamus Area GABA(B) Receptor on Gastric Ischemia-Reperfusion Injury in Rats.
The Regulatory Effects of Lateral Hypothalamus Area GABA(B) Receptor on Gastric Ischemia-Reperfusion Injury in Rats.
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下丘脑外侧区GABAB受体对大鼠胃缺血再灌注损伤的调节作用
DOI：
10.3389/fphys.2017.00722
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发表时间：
2017
影响因子：
4
通讯作者：
Du D
中科院分区：
文献类型：
--
作者：
Gao L;Zhao H;Zhu T;Liu Y;Hu L;Liu Z;Huang H;Chen F;Deng Z;Chu D;Du D
本研究旨在探讨GABAB受体在大鼠胃缺血再灌注损伤中的作用及其分子机制。下丘脑外侧区GABAB受体通过上调脑内GABA、GABABR的产生，下调P-GABABR，减轻胃缺血再灌注损伤。本研究为急性胃损伤的治疗提供了新的思路。胃缺血再灌注（GI-R）损伤进展在很大程度上与内脏大神经（GSN）的过度激活有关。本研究旨在探讨下丘脑外侧区（LHA）GABAB受体（GABABR）对GI-R损伤的保护作用。采用夹闭腹腔动脉30 min再灌注1 h的方法建立胃肠道缺血再灌注损伤模型。在立体定位坐标中确定FN和LHA的坐标，然后将L-Glu显微注射到FN中，将GABAB受体激动剂巴氯芬或GABAB受体拮抗剂CGP 35348显微注射到LHA中，最后制备GI-R模型。Western blot、PCR、RT-PCR检测LHA中GABABR、P-GABABR、NOX 2、NOX 4和SOD的表达。Western blot检测胃黏膜IL-1β、NOX 2、NXO 4的表达。我们发现，微量注射L-Glu到FN或GABAB受体激动剂（巴氯芬）到LHA减轻GI-R损伤。用GABAB受体拮抗剂CGP 35348预处理可逆转FN刺激或巴氯芬对LHA的保护作用。LHA内微量注射巴氯芬可明显降低胃粘膜炎症因子IL-1β、NOX 2和NOX 4的表达。结论：LHA内微量注射GABABR激动剂对GI R损伤的保护作用可能是通过上调LHA内GABA、GABABR的产生和下调P-GABABR而实现的。
The aim of the research was to determine the functional effects and molecular mechanisms of GABAB receptor on ischemia reperfusion-induced gastric injury in rats. The lateral hypothalamus area GABAB receptor attenuated the ischemia reperfusion-induced gastric injury by up-regulating the production of GABA, GABABR, and down-regulating P-GABABR in the brain. This work would provide a new therapeutic strategy for acute gastric injury. HIGHLIGHTS Gastric ischemia-reperfusion (GI-R) injury progression is largely associated with excessive activation of the greater splanchnic nerve (GSN). This study aims to investigate the protective effects of GABAB receptor (GABABR) in the lateral hypothalamic area (LHA) on GI-R injury. A model of GI-R injury was established by clamping the celiac artery for 30 min and then reperfusion for 1 h. The coordinate of FN and LHA was identified in Stereotaxic Coordinates and then the L-Glu was microinjected into FN, GABAB receptor agonist baclofen, or GABAB receptor antagonist CGP35348 was microinjected into the LHA, finally the GI-R model was prepared. The expression of GABABR, P-GABABR, NOX2, NOX4, and SOD in the LHA was detected by western blot, PCR, and RT-PCR. The expression of IL-1β, NOX2, and NXO4 in gastric mucosa was detected by western blot. We found that microinjection of L-Glu into the FN or GABAB receptor agonist (baclofen) into the LHA attenuated GI-R injury. Pretreatment with GABAB receptor antagonist CGP35348 reversed the protective effects of FN stimulation or baclofen into the LHA. Microinjection of baclofen into the LHA obviously reduced the expression of inflammatory factor IL-1β, NOX2, and NOX4 in the gastric mucosa. Conclusion: The protective effects of microinjection of GABABR agonist into LHA on GI-R injury in rats could be mediated by up-regulating the production of GABA, GABABR, and down-regulating P-GABABR in the LHA.
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