P物质通过抑制MES23.5细胞中神经激肽-1受体的凋亡来防止1-甲基-4-苯基吡啶鎓诱导的细胞毒性。,Molecular Medicine Reports

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P物质通过抑制MES23.5细胞中神经激肽-1受体的凋亡来防止1-甲基-4-苯基吡啶鎓诱导的细胞毒性。
Molecular Medicine Reports ( IF 3.4 ) Pub Date : 2015-10-27 , DOI: 10.3892/mmr.2015.4464
Shuang-Yan Wang ₁ , Lei Chen ₁ , Yan Xue ₁ , Yu-Jun Xia ₂

Affiliation

[Sar9，Met（O2）11]称为物质P（SP），是神经激肽-1（NK-1）受体的有效和选择性激动剂，神经激肽-1（NK-1）受体是合成肽，结构与SP类似。SP是由神经激肽受体（即中枢神经系统中的SP受体）介导的重要神经递质或神经调节剂。SP引起的兴奋作用可能被神经激肽-1受体拮抗剂（如SR140333B）选择性抑制。已经提出帕金森氏病（PD）主要是由营养性肽能神经递质（可能是SP）的丧失引起的，其可能导致神经元变性。在以前的研究中，1-甲基-4-苯基吡啶鎓（MPP +）经常用于建立PD的动物或细胞模型。在本研究中，为了进一步研究SP对PD的影响，MPP +被用来研究SP的有希望的抗凋亡作用，并研究MES23.5多巴胺能细胞系中病理的潜在机制。结果表明，用SP处理可防止MPP +触发的细胞凋亡。SP处理还减少了MPP +触发的Ca2 +内流，caspase-3反应性，活性氧的产生和线粒体膜电位的降低。MPP +处理还诱导c-Jun N-末端激酶和p38丝裂原活化蛋白激酶的磷酸化。此外，用SP处理可抑制MES23.5细胞中MPP +触发的神经毒性。但是，在SR140333B + SP + MPP +处理的MES23.5细胞系中未观察到变化。总之，SP可以通过抑制NK-1受体的凋亡来保护细胞免受MPP +诱导的细胞毒性作用。

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Substance P prevents 1-methyl-4-phenylpyridinium-induced cytotoxicity through inhibition of apoptosis via neurokinin-1 receptors in MES23.5 cells.

[Sar9, Met(O2)11] termed Substance P (SP), is an effective and selective agonist for the neurokinin‑1 (NK‑1) receptors, which are synthetic peptides, similar in structure to SP. SP is an important neurotransmitter or neuromodulator mediated by neurokinin receptors, namely the SP receptor in the central nervous system. The excitatory effects induced by SP may be selectively inhibited by a neurokinin‑1 receptor antagonist, such as SR140333B. It has been proposed that Parkinson's disease (PD) is primarily caused by the loss of trophic peptidergic neurotransmitter, possibly SP, which may lead to the degeneration of neurons. In previous studies, 1‑methyl‑4‑phenylpyridinium (MPP+) has been frequently utilized to establish animal or cell models of PD. In the present study, to further investigate the effects of SP in PD, MPP+ was employed to investigate the promising anti‑apoptotic effects of SP, and examine the underlying mechanisms of the pathology in the MES23.5 dopaminergic cell line. The results indicated that MPP+‑triggered apoptosis was prevented by treatment with SP. SP treatment also decreased the MPP+‑triggered Ca2+ influx, caspase‑3 re‑activity, reactive oxygen species production and mitochondrial membrane potential decrease. Treatment with MPP+ also induced phosphorylation of c‑Jun N‑terminal kinase and p38 mitogen‑activated protein kinase. In addition, treatment with SP inhibited the MPP+‑triggered neurotoxicity in MES23.5 cells. However, no changes were observed in SR140333B+SP+MPP+‑treated MES23.5 cell lines. In conclusion, SP could protect the cells from MPP+‑induced cytotoxicity by inhibiting the apoptosis via NK-1 receptors.

更新日期：2019-11-01

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