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首页> 外文期刊>Pharmacological research: The official journal of The Italian Pharmacological Society >Stimulation of 5-HT(1A) receptor with 8-OH-DPAT inhibits hydrogen peroxide-induced neurotoxicity in cultured rat cortical cells.
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Stimulation of 5-HT(1A) receptor with 8-OH-DPAT inhibits hydrogen peroxide-induced neurotoxicity in cultured rat cortical cells.

机译：用8-OH-DPAT刺激5-HT（1A）受体抑制培养的大鼠皮层细胞中过氧化氢诱导的神经毒性。

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摘要

We investigated the effect of 8-hydroxy-2-(N,N-dipropylamino)tetralin (8-OH-DPAT), a specific 5-HT(1A) receptor agonist, on H(2)O(2)-induced neuronal cell death in cultured rat cortical cells. H(2)O(2) produced a concentration-dependent reduction of cell viability, which was significantly reduced by (5R,10S)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-imine (MK-801), an N-methyl-d-aspartate (NMDA) receptor antagonist. Pretreatment of 8-OH-DPAT over the concentration range of 1-100 microM significantly inhibited the H(2)O(2) (100 microM)-induced neuronal cell death as assessed by a MTT assay and the number of apoptotic nuclei, evidenced by Hoechst 33342 staining. The protective effect of 8-OH-DPAT (100 microM) was completely blocked by the simultaneous treatment of 1-(2-methoxyphenyl)-4-[4-(2-phthalimideo)butyl]piperazine (NAN-190, 10muM), a selective 5-HT(1A) receptor antagonist, but not in the presence of the dopamine receptor blocker spiperone (10 microM), indicating that the protective effect of 8-OH-DPAT was mediated via 5-HT(1A) receptors. In addition, 8-OH-DPAT inhibited the H(2)O(2)-induced elevation of glutamate release into the medium and cytosolic Ca(2+) concentration ([Ca(2+)](c)), generation of reactive oxygen species (ROS), and caspase-3 activity. These results suggest that the activation of 5-HT(1A) receptor with 8-OH-DPAT may ameliorate an oxydative stress-induced apoptosis of neuronal cell by interfering with the increase of [Ca(2+)](c), and then by inhibiting glutamate release, generation of ROS and caspase activity.
机译：我们调查了特异的5-HT（1A）受体激动剂8-羟基-2-（N，N-二丙基氨基）四氢化萘（8-OH-DPAT）对H（2）O（2）诱导的神经元的影响培养的大鼠皮质细胞中的细胞死亡。 H（2）O（2）产生了浓度依赖性的细胞活力降低，其显着降低了（5R，10S）-（+）-5-甲基-10,11-二氢-5H-二苯并[a，d ] cyclohepten-5,10-imine（MK-801），一种N-甲基-d-天冬氨酸（NMDA）受体拮抗剂。通过MTT分析和凋亡核数目评估，预处理8-OH-DPAT的浓度范围在1-100 microM范围内可显着抑制H（2）O（2）（100 microM）诱导的神经元细胞死亡。由Hoechst 33342染色。同时处理1-（2-甲氧基苯基）-4- [4-（2-邻苯二甲酰亚胺基）丁基]哌嗪（NAN-190，10μM）可完全阻断8-OH-DPAT（100 microM）的保护作用，选择性5-HT（1A）受体拮抗剂，但不存在多巴胺受体阻滞剂spiperone（10 microM），表明8-OH-DPAT的保护作用是通过5-HT（1A）受体介导的。此外，8-OH-DPAT抑制H（2）O（2）诱导的谷氨酸释放到培养基和胞质Ca（2+）浓度（[Ca（2 +）]（c））的升高，活性氧（ROS）和caspase-3活性。这些结果表明，通过干扰[Ca（2 +）]（c）的增加，用8-OH-DPAT激活5-HT（1A）受体可以减轻氧化应激诱导的神经元细胞凋亡。通过抑制谷氨酸释放，ROS的产生和胱天蛋白酶活性。

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