大鼠肝脏缺血再灌注过程中热休克蛋白的表达研究

Study of the expression of hepatic heat shock protein 72 (HSP 72) in a rat model of hepatic ischemia and reperfusion by portal blood occlusion

目的 用肝组织内合成的热休克蛋白７２（ Ｈｅａｔｓｈｏｃｋ ｐｒｏｔｅｉｎ７２ ， Ｈ Ｓ Ｐ７２） 为指标，探讨门静脉缺血再灌注对肝脏的损害作用。 方法 Ｗｉｓｔａｒ 系雄性大鼠，随机分成两组： 甲组： 肝门阻断（ Ｐｒｉｎｇｌｅ 法）１５ 分钟； 乙组：先在右颈内静脉与盲肠静脉之间做一分流以消除门静脉淤血，然后阻断肝门血流１５ 分钟。术后１ 、３ 、４８ 小时检测血清生化酶 Ｇ Ｏ Ｔ、 Ｇ Ｐ Ｔ、 Ｌ Ｄ Ｈ 水平（ Ｉ Ｕ／ Ｌ） 及肝组织 Ａ Ｔ Ｐ 浓度（μｍｏｌ／ｇ） 。术后４８ 小时用 Ｗｅｓｔｅｒｎ ｂｌｏｔｔｉｎｇ 法测定肝组织内 Ｈ Ｓ Ｐ７２ 水平。 结果 甲组肝组织内 Ｈ Ｓ Ｐ７２的表达显著增强，而乙组仅有微弱表达。血清与肝组织生化测定，在术后１ 小时与３ 小时各指标均可见甲组有损害较重的倾向，但两组间差异无显著意义（ Ｐ＞ ００５） 。如 Ｇ Ｐ Ｔ 在术后１ 小时甲、乙组分别为：（４８６０ ±２０１５） Ｉ Ｕ／ Ｌ 与（４２３０ ±１４６０） Ｉ Ｕ／ Ｌ， Ａ Ｔ Ｐ 分别为（１４９ ±０６９） μｍｏｌ／ｇ 与（１６０ ±０５５） μｍｏｌ／ｇ。至术后４８ 小时，两组各生化指标均趋于恢复。 结论 淤滞的门静脉血流再灌注对缺血肝脏有明?

Objective In this study,the induction of heat shock protein 72 (HSP 72) in liver tissue were examined as a marker of hepatic injury during hepatic ischemic reperfusion process by portal blood occlusion in a rat model.Methods Male Wistar rats were allocated to two groups:In group A,total hepatic ischemia with portal congestion was induced by Pringle′s maneuver for 15 minutes.In group B,extracorporeal portosystemic shunt from the cecal vein to the external jugular vein was performed to avoid splanchnic congestion during Pringle′s maneuver for 15 minutes.For the detection of HSP 72 in the liver tissue at 48 hours after reperfusion,Western blotting analysis was carried out.At the points of 1,3,48 hours after reperfusion,biochemical parameters (GOT,GPT,LDH) in the blood and ATP in the liver tissue were evaluated.Results The accumulation of HSP 72 in group A was remarkably higher than that in group B.As for biochemical parameters,there were no significant differences between two groups ( P >0 05).Conclusions The reperfusion of the congested portal blood has harmful impacts on the ischemic liver tissue to result in HSP72 synthesis after short term hepatic inflow occlusion.