کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2596676 1132542 2009 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Arachidonic acid-induced apoptosis of human neuroblastoma SK-N-SH cells is mediated through mitochondrial alteration elicited by ROS and Ca2+-evoked activation of p38α MAPK and JNK1
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم محیط زیست بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
Arachidonic acid-induced apoptosis of human neuroblastoma SK-N-SH cells is mediated through mitochondrial alteration elicited by ROS and Ca2+-evoked activation of p38α MAPK and JNK1
چکیده انگلیسی

Arachidonic acid (AA)-induced apoptosis of human neuroblastoma SK-N-SH cells was characteristic of elevation of intracellular Ca2+ concentration ([Ca2+]i), ROS generation, activation of 38 MAPK and JNK and loss of mitochondrial membrane potential (ΔΨm). Subsequent modulation of Bcl-2 family members and cytochrome c release accompanied with activation of caspase-9 and -3 were involved in the death of SK-N-SH cells. BAPTA-AM (Ca2+ chelator) pretreatment rescued viability of AA-treated cells through abolishing phosphorylation of p38 MAPK and JNK, ΔΨm loss and ROS generation. N-Acetylcysteine (ROS scavenger) pretreatment reduced the dissipation of ΔΨm, but insignificantly affected AA-induced p38 MAPK and JNK activation. SB202190 (p38 MAPK inhibitor) and SP600125 (JNK inhibitor) attenuated mitochondrial depolarization, degradation of Bcl-2/Bcl-xL, and mitochondrial translocation of Bax. Transfection of specific siRNA proved that p38α MAPK and JNK1 were involved in modulating Bcl-2 family proteins. Taken together, our data suggest that the cytotoxicity of AA toward SK-N-SH cells is mediated through mitochondria-dependent death pathway, eliciting by AA-induced ROS generation and Ca2+-evoked activation of p38α MAPK and JNK1.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology - Volume 262, Issue 3, 21 August 2009, Pages 199–206
نویسندگان
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