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钙离子通道阻滞剂、细胞外钙离子及磷脂酶A2抑制剂对叔丁基过氧化氢诱导的大鼠肝切片脂质过氧化及毒性的影响。

Effect of Ca2+ channel blockers, external Ca2+ and phospholipase A2 inhibitors on t-butylhydroperoxide-induced lipid peroxidation and toxicity in rat liver slices.

作者信息

Heo J, Kim G H, Lee K S, Go W U, Ju H J, Park S K, Song C S, Song G A, Cho M, Yang U S, Moon H K, Kim Y K

机构信息

Department of Internal Medicine and Physiology, College of Medicine, Pusan National University, Korea.

出版信息

Korean J Intern Med. 1997 Jun;12(2):193-200. doi: 10.3904/kjim.1997.12.2.193.

DOI:10.3904/kjim.1997.12.2.193
PMID:9439155
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4531990/
Abstract

OBJECTIVES

This study was undertaken to examine the effect of oxidant on lipid peroxidation and lethal cell injury in rat liver slices.

METHODS

t-Butylhydroperoxide (t-BHP) was employed as a model of an oxidant. The lipid peroxidation and lethal cell injury were estimated by measuring the formation of malondialdehyde (MDA) and lactate dehydrogenase (LDH) release, respectively.

RESULTS

t-BHP increased lipid peroxidation and LDH release in a dose-dependent manner over concentrations of 0.5-10 mM. t-BHP-induced lipid peroxidation was completely prevented by an antioxidant, N,N-diphenyl-p-phenylenediamine (DPPD), but LDH release was partially decreased. Both t-BHP-induced lipid peroxidation and LDH release were significantly protected by iron chelator, deferoxamine, sulfhydryl reducing agent, dithiothreitol and glutathione. Ca2+ channel blockers, verapamil, diltiazem and nifedipine exerted a significant protective effect against t-BHP-induced lipid peroxidation and LDH release. By contrast, addition of external Ca2+ chelator, ethylene glycol bis(b-aminoethyl ether)-N,N-tetraacetic acid (EGTA) did not alter t-BHP-induced lipid peroxidation, whereas t-BHP-induced lethal cell injury was significantly prevented. Phospholipase A2 (PLA2) inhibitors, mepacrine and butacaine produced a partial protective effect.

CONCLUSIONS

These results suggest that t-BHP induces cell injury by lipid peroxidation-dependent and -independent mechanisms which can be partially prevented by Ca2+ channel blockers and PLA2 inhibitors.

摘要

目的

本研究旨在探讨氧化剂对大鼠肝切片脂质过氧化和致死性细胞损伤的影响。

方法

以叔丁基过氧化氢（t-BHP）作为氧化剂模型。分别通过测量丙二醛（MDA）的形成和乳酸脱氢酶（LDH）的释放来评估脂质过氧化和致死性细胞损伤。

结果

在0.5 - 10 mM的浓度范围内，t-BHP以剂量依赖性方式增加脂质过氧化和LDH释放。抗氧化剂N，N-二苯基对苯二胺（DPPD）可完全抑制t-BHP诱导的脂质过氧化，但只能部分降低LDH释放。铁螯合剂去铁胺、巯基还原剂二硫苏糖醇和谷胱甘肽对t-BHP诱导的脂质过氧化和LDH释放均有显著的保护作用。钙通道阻滞剂维拉帕米、地尔硫䓬和硝苯地平对t-BHP诱导的脂质过氧化和LDH释放具有显著的保护作用。相比之下，添加细胞外钙螯合剂乙二醇双（β-氨基乙基醚）-N，N-四乙酸（EGTA）不会改变t-BHP诱导的脂质过氧化，而t-BHP诱导的致死性细胞损伤则得到显著预防。磷脂酶A2（PLA2）抑制剂美帕林和布他卡因产生部分保护作用。

结论

这些结果表明，t-BHP通过脂质过氧化依赖性和非依赖性机制诱导细胞损伤，钙通道阻滞剂和PLA2抑制剂可部分预防这些损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec5/4531990/3ec58550bd7e/kjim-12-2-193-11f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec5/4531990/8ef6bec9ce5b/kjim-12-2-193-11f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec5/4531990/0b3358b9b3aa/kjim-12-2-193-11f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec5/4531990/823f652d9997/kjim-12-2-193-11f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec5/4531990/cbf73a988d69/kjim-12-2-193-11f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec5/4531990/9e750c81f3eb/kjim-12-2-193-11f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec5/4531990/a9a9a73ae206/kjim-12-2-193-11f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec5/4531990/994318277732/kjim-12-2-193-11f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec5/4531990/e62244b3ad0f/kjim-12-2-193-11f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec5/4531990/3ec58550bd7e/kjim-12-2-193-11f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec5/4531990/8ef6bec9ce5b/kjim-12-2-193-11f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec5/4531990/0b3358b9b3aa/kjim-12-2-193-11f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec5/4531990/823f652d9997/kjim-12-2-193-11f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec5/4531990/cbf73a988d69/kjim-12-2-193-11f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec5/4531990/9e750c81f3eb/kjim-12-2-193-11f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec5/4531990/a9a9a73ae206/kjim-12-2-193-11f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec5/4531990/994318277732/kjim-12-2-193-11f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec5/4531990/e62244b3ad0f/kjim-12-2-193-11f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ec5/4531990/3ec58550bd7e/kjim-12-2-193-11f9.jpg

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本文引用的文献

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J Pharmacol Exp Ther. 1993 Apr;265(1):392-400.
2
Cyclosporin and carnitine prevent the anoxic death of cultured hepatocytes by inhibiting the mitochondrial permeability transition.环孢素和肉碱通过抑制线粒体通透性转换来防止培养的肝细胞缺氧死亡。
J Biol Chem. 1993 Jul 5;268(19):13791-8.
3
Ca2+ uptake, fatty acid, and LDH release during proximal tubule hypoxia: effects of mepacrine and dibucaine.
Am J Physiol. 1994 Feb;266(2 Pt 2):F196-201. doi: 10.1152/ajprenal.1994.266.2.F196.
4
Effects of Ca2+ channel blockers, low Ca2+ medium and glycine on cell Ca2+ and injury in anoxic rabbit proximal tubules.
Kidney Int. 1994 Jul;46(1):223-9. doi: 10.1038/ki.1994.263.
5
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FASEB J. 1995 Feb;9(2):219-28. doi: 10.1096/fasebj.9.2.7781924.
6
Protective effect of various calcium antagonists against an experimentally induced calcium overload in isolated hepatocytes.
Biochem Pharmacol. 1993 Dec 3;46(11):1937-44. doi: 10.1016/0006-2952(93)90634-9.
7
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8
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