热休克蛋白90与门静脉高压大鼠的高动力循环有关。
Heat shock protein 90 is responsible for hyperdynamic circulation in portal hypertensive rats.
作者信息
Ai Jian-Hua, Yang Zhen, Qiu Fa-Zu, Zhu Tong
机构信息
Center for Hepatic Surgery, Tongi Hospital, Tongi Medical College, Huazhong Science and Technological University, Wuhan, Hubei Province, China.
出版信息
World J Gastroenterol. 2003 Nov;9(11):2544-7. doi: 10.3748/wjg.v9.i11.2544.
AIM
To examine the participation of HSP90 in portal hypertensive rat mesentery in vitro.
METHODS
Immunohistochemistry and Western-blot were used to examine the expression of HSP90 in mesenteric vasculature. HSP90 mRNA was detected by RT-PCR, and the role of HSP90 in hyperdynamic circulation was examined by in vitro mesenteric perfusion studies.
RESULTS
HSP90 was overexpressed in endothelium of mesentery vasculature in animals with experimental portal hypertension induced by partial portal vein ligation (PVL) compared with normal animals. Geldanamycin (GA), a special inhibitor of HSP90 signaling, attenuated ACh-dependent vasodilation but did not affect vasodilation in response to sodium nitroprusside in normal rats. In PVL animals, the perfused mesentery was hyporesponsive to vasoconstrictor methoxamine. GA significantly potentiated methoxamine-induced vasoconstrictor after PVL.
CONCLUSION
HSP90 plays a key role in NO-dependent hyperdynamic circulation in portal hypertension and provides a novel method for future treatment of portal hypertension.
目的
在体外研究热休克蛋白90（HSP90）在门静脉高压大鼠肠系膜中的作用。
方法
采用免疫组织化学和蛋白质印迹法检测肠系膜血管中HSP90的表达。通过逆转录聚合酶链反应（RT-PCR）检测HSP90 mRNA，并通过体外肠系膜灌注研究检测HSP90在高动力循环中的作用。
结果
与正常动物相比，部分门静脉结扎（PVL）诱导的实验性门静脉高压动物肠系膜血管内皮中HSP90表达上调。格尔德霉素（GA），一种HSP90信号通路的特异性抑制剂，减弱了正常大鼠中乙酰胆碱（ACh）依赖性血管舒张，但不影响硝普钠诱导的血管舒张。在PVL动物中，灌注的肠系膜对血管收缩剂甲氧明反应性降低。GA显著增强了PVL后甲氧明诱导的血管收缩。
结论
HSP90在门静脉高压中依赖一氧化氮（NO）的高动力循环中起关键作用，并为未来门静脉高压的治疗提供了一种新方法。
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