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二氢吡啶类钙通道拮抗剂盐酸地尔硫卓对 MPP(+)诱导的大鼠纹状体羟自由基生成及溶血磷脂酰胆碱增强效应的保护作用。

Protective effect of diltiazem, a L-type calcium channel antagonist, on lysophosphatidylcholine-enhanced hydroxyl radical generation by MPP(+) in rat striatum.

机构信息

Yokkaichi Nursing and Medical Care University, 1200 Kayo-cho, Yokkaichi-shi, Mie 512-8045, Japan.

出版信息

Clin Biochem. 2013 Jan;46(1-2):164-6. doi: 10.1016/j.clinbiochem.2012.09.004. Epub 2012 Sep 19.

Abstract

BACKGROUND

The interaction between the PKC and oxygen free radicals.

OBJECTIVE AND METHODS

The present study examined the effects of lysophosphatidylcholine (LPC), an endogenous amphophilic lipid metabolite, on 1-methyl-4-phenylpyridinium ion (MPP(+))-induced hydroxyl radical (()OH) generation in rat striatum. LPC (50 μM) increased ()OH formation by MPP(+). Further, the effect of diltiazem, a L-type Ca(2+) channel antagonist, on MPP(+) (5mM)-induced ()OH generation was studied.

RESULTS

Diltiazem (100 μM) significantly suppressed LPC and MPP(+)-induced ()OH generation. The results indicate ()OH generation, and diltiazem may have preventive effect on MPP(+)-induced ()OH generation.

CONCLUSION

These results demonstrated that diltiazem suppressed LPC-induced generation of free radical through blockage of Ca(2+) channel in the rat striatum.

摘要

背景

蛋白激酶 C 与氧自由基的相互作用。

目的和方法

本研究探讨了内源性两亲性脂质代谢产物溶血磷脂酰胆碱(LPC)对 1-甲基-4-苯基吡啶鎓离子(MPP+)诱导的大鼠纹状体羟自由基(OH)生成的影响。LPC(50μM)增加 MPP+诱导的 OH 生成。此外,还研究了 L 型钙通道拮抗剂地尔硫卓对 MPP+(5mM)诱导的 OH 生成的影响。

结果

地尔硫卓(100μM)显著抑制了 LPC 和 MPP+诱导的 OH 生成。结果表明,地尔硫卓可能通过阻断大鼠纹状体中的钙通道,对 MPP+诱导的 OH 生成具有预防作用。

结论

这些结果表明,地尔硫卓通过阻断钙通道抑制 LPC 诱导的自由基生成。

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