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[线粒体脂质过氧化对肝硬化大鼠肝脏部分切除术后肝再生的影响]

[Effects of mitochondrial lipoperoxidation on liver regeneration after partial hepatectomy of the cirrhotic rat liver].

作者信息

Kikuchi J, Ouchi K, Matsuno S

机构信息

Sendai Tokushukai Hospital, Japan.

出版信息

Nihon Geka Gakkai Zasshi. 1991 Feb;92(2):167-74.

PMID:2038291
Abstract

Lipoperoxide levels in mitochondrial fraction and mitochondrial respiratory activity during hepatic regeneration were studied serially in normal (N) and cirrhotic (C) rats following one-third (I) or two-third (II) partial hepatectomy. Recovery of liver weight after 14 days was about 90% in each group except C-II group, in which it was 71.3%. ATP synthetic activity (ATP-S) was always higher in N-II group than N-I which reached maximum on the first postoperative day (POD) and returned to the preoperative levels on the 14th POD. Lipoperoxide peak value of N-II group was obtained sooner than that of N-I group, in addition the peak value of N-II group was higher than that of the N-I group. ATP-S of C-II group reached maximum levels on the third POD and thereafter decreased progressively. In contrast, ATP-S of C-I group returned to preoperative level on the 14th POD. Peak lipoperoxide levels were obtained on the first POD in both groups, but that of C-II group was 1.6 times higher than that of C-I. Moreover, it was observed that inhibition of lipoperoxidation by alpha-tocopherol administration improved respiratory activity significantly. From these results it can be said that hepatectomy-induced lipoperoxidation in massive resection of the cirrhotic liver may inhibit activation of mitochondrial respiration and hepatic regeneration.

摘要

在正常(N)和肝硬化(C)大鼠中,分别进行三分之一(I)或三分之二(II)肝部分切除术后,连续研究肝再生过程中线粒体部分的脂过氧化物水平和线粒体呼吸活性。除C-II组外,每组术后14天肝脏重量恢复率约为90%,C-II组为71.3%。N-II组的ATP合成活性(ATP-S)始终高于N-I组,N-I组在术后第1天(POD)达到最大值,并在第14天POD恢复到术前水平。N-II组的脂过氧化物峰值比N-I组出现得更早,此外,N-II组的峰值高于N-I组。C-II组的ATP-S在第3天POD达到最高水平,此后逐渐下降。相比之下,C-I组的ATP-S在第14天POD恢复到术前水平。两组在第1天POD均达到脂过氧化物峰值水平,但C-II组是C-I组的1.6倍。此外,观察到给予α-生育酚抑制脂过氧化可显著改善呼吸活性。从这些结果可以看出,肝硬化肝脏大规模切除术中肝切除诱导的脂过氧化可能会抑制线粒体呼吸的激活和肝再生。

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