Involvement of ERK1/2 pathway in neuroprotective effects of pyrroloquinoline quinine against rotenone-induced SH-SY5Y cell injury
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- 作者：Q. Zhanga ; c ; &dagger ; ; J. Zhanga ; b ; &dagger ; ; C. Jianga ; J. Qina ; b ; K. Keb ; F. Dinga ; c ; dingfei@ntu.edu.cn" class="auth_mail
- 关键词：3-NP ; 3-nitropropionic acid ; CoQ10 ; coenzyme Q10 ; DCFH-DA ; 2&prime ; 7&prime ; -dichlorofluorescin diacetate ; DMEM ; Dulbecco&rsquo ; s modified eagle&rsquo ; s medium ; DPI ; diphenyleneiodonium chloride ; ETC ; electron transport chain ; FBS ; fetal bovine serum ; FCCP ; p-trifluoromethoxyphenylhydrazone ; GSH ; glutathione ; MDA ; malondialdehyde ; NaN3 ; sodium azide ; PBS ; phosphate-buffered saline ; PD ; Parkinson&rsquo ; s disease ; PQQ ; pyrroloquinoline quinone ; qRT-PCR ; quantitative real-time reverse transcription
- 刊名：Neuroscience
- 出版年：13 June 2014
- 年：2014
- 卷：270
- 期：Complete
- 页码：183-191
- 全文大小：2237 K
文摘
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PQQ inhibited ROS production induced by ETC complex I and III inhibitors.
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Pretreatment with PQQ protected SH-SY5Y cells against rotenone injury.
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PQQ reduced ROS production and maintained mitochondrial function after rotenone injury.
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ERK1/2 signaling pathway was involved in neuroprotective effects of PQQ.