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. 2021 Aug 9;12:703894. doi: 10.3389/fphar.2021.703894

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Copyright © 2021 Lai, Lin, Wu, Tsai and Tsai.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The actions of neuroprotective mechanism of CA on LID in in vivo and in vitro studies. (A) In in vivo study, _L-dopa stimulates DIR protein, and then activates the phosphorylation of DARPP-32 and ERK1/2, which elevates ΔFosB protein, leading to develop the LID in 6-OHDA-lesioned rats. Moreover, _L-dopa administration induced neuronal cell death through regulating ERK1/2-c-Jun pathway. However, CA alleviates these effects induced by _L-dopa. (B) In in vitro study, pretreatment of CA with SH-SY5Y cells attenuates _L-dopa-triggered apoptotic cell death mediated via increasing c-Jun ser73 activation and decreasing c-Jun ser63 activation by ERK1/2. Additionally, CA could be improved the development of LID is related to the induction of parkin protein, leading to prevent the ubiquitinated protein accumulation and D1R abnormal trafficking (gray line).