کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9015367 | 1127168 | 2005 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Stimulation of 5-HT1A receptor with 8-OH-DPAT inhibits hydrogen peroxide-induced neurotoxicity in cultured rat cortical cells
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کلمات کلیدی
موضوعات مرتبط
علوم پزشکی و سلامت
داروسازی، سم شناسی و علوم دارویی
داروشناسی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Stimulation of 5-HT1A receptor with 8-OH-DPAT inhibits hydrogen peroxide-induced neurotoxicity in cultured rat cortical cells Stimulation of 5-HT1A receptor with 8-OH-DPAT inhibits hydrogen peroxide-induced neurotoxicity in cultured rat cortical cells](/preview/png/9015367.png)
چکیده انگلیسی
We investigated the effect of 8-hydroxy-2-(N,N-dipropylamino)tetralin (8-OH-DPAT), a specific 5-HT1A receptor agonist, on H2O2-induced neuronal cell death in cultured rat cortical cells. H2O2 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 μM significantly inhibited the H2O2 (100 μM)-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 μM) was completely blocked by the simultaneous treatment of 1-(2-methoxyphenyl)-4-[4-(2-phthalimideo)butyl]piperazine (NAN-190, 10 μM), a selective 5-HT1A receptor antagonist, but not in the presence of the dopamine receptor blocker spiperone (10 μM), indicating that the protective effect of 8-OH-DPAT was mediated via 5-HT1A receptors. In addition, 8-OH-DPAT inhibited the H2O2-induced elevation of glutamate release into the medium and cytosolic Ca2+ concentration ([Ca2+]c), generation of reactive oxygen species (ROS), and caspase-3 activity. These results suggest that the activation of 5-HT1A receptor with 8-OH-DPAT may ameliorate an oxydative stress-induced apoptosis of neuronal cell by interfering with the increase of [Ca2+]c, and then by inhibiting glutamate release, generation of ROS and caspase activity.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Pharmacological Research - Volume 51, Issue 3, March 2005, Pages 261-268
Journal: Pharmacological Research - Volume 51, Issue 3, March 2005, Pages 261-268
نویسندگان
Hyun Joo Lee, Ju Yeon Ban, Soon Ock Cho, Yeon Hee Seong,