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前列腺素E1可提高大鼠95%肝切除术后的存活率。

Prostaglandin E1 improves survival rate after 95% hepatectomy in rats.

作者信息

Togo Shinji, Chen Haochuan, Takahashi Takuji, Kubota Toru, Matsuo Kenichi, Morioka Daisuke, Watanabe Kazuteru, Yamamoto Harumi, Nagashima Yoji, Shimada Hiroshi

机构信息

Department of Gastroenterological Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

出版信息

J Surg Res. 2008 May 1;146(1):66-72. doi: 10.1016/j.jss.2007.05.003. Epub 2007 Jun 27.

Abstract

BACKGROUND/AIM: Prostaglandin E1 (PGE1) has a wide-ranging effect on cytoprotection. Overproduction of heat shock protein 70 (HSP70) in the liver protects hepatocytes under various pathologic conditions. In this study, we examined the effect of a nontoxic HSP-inducer, PGE1, on acute liver failure after 95% hepatectomy in rats.

METHODS

PGE1 or vehicle was intravenously administered to rats 30 min before and during hepatectomy.

RESULTS

Nine of 30 rats pretreated with PGE1 survived, whereas all 20 rats pretreated with vehicle died within 96 h after operation. During the 24-h postoperative period, PGE1 significantly suppressed the release of alanine aminotransferase and elevation of hyaluronic acid. Histological examination showed that the vacuolized hepatocytes and round hepatocytes with pyknotic nuclei are frequently seen in rats pretreated with vehicle, whereas active regeneration is seen in rats pretreated with PGE1. During the first 24 h after surgery, HSP70 induction was absent in the residual livers of vehicle-treated rats. In contrast, PGE1 stimulated the HSP accumulation within 24 h, and viable hepatocytes contained abundant HSP70 in their nuclei.

CONCLUSION

Our results suggest that PGE1 may prevent acute liver failure after massive hepatectomy, at least in part, by enhancing HSP70 production in the residual liver.

摘要

背景/目的:前列腺素E1(PGE1)对细胞保护具有广泛作用。肝脏中热休克蛋白70(HSP70)的过度产生可在各种病理条件下保护肝细胞。在本研究中,我们检测了无毒的热休克蛋白诱导剂PGE1对大鼠95%肝切除术后急性肝衰竭的影响。

方法

在肝切除术前30分钟及手术过程中,对大鼠静脉注射PGE1或赋形剂。

结果

30只接受PGE1预处理的大鼠中有9只存活,而20只接受赋形剂预处理的大鼠在术后96小时内全部死亡。术后24小时内,PGE1显著抑制丙氨酸转氨酶的释放和透明质酸的升高。组织学检查显示,接受赋形剂预处理的大鼠中经常可见空泡化肝细胞和核固缩的圆形肝细胞,而接受PGE1预处理的大鼠中可见活跃的再生。在手术后的最初24小时内,接受赋形剂处理的大鼠残余肝脏中未出现HSP70诱导。相反,PGE1在24小时内刺激了HSP的积累,存活的肝细胞在其细胞核中含有丰富的HSP70。

结论

我们的结果表明,PGE1可能至少部分通过增强残余肝脏中HSP70的产生来预防大规模肝切除术后的急性肝衰竭。

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