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Iptakalim ameliorates MPP^+^‐induced astrocyte mitochondrial dysfunction by increasing mitochondrial complex activity besides opening mitoK~ATP~ channels by Shu Zhang; Jian‐Hua Ding; Fang Zhou; Zhi‐Yuan Wang; Xi‐Qiao Zhou; Gang Hu is a Neuroscience article available to read on EtoBox.

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## Abstract In addition to the established role of the mitochondrion in energy metabolism, regulation of cell death has been regarded as a major function of this organelle. Our previous studies have demonstrated that iptakalim (IPT), a novel ATP‐sensitive potassium channel (K~ATP~ channel) opener, protects against 1‐methyl‐4‐phenyl‐pyridinium ion (MPP^+^)–induced astrocyte apoptosis via mitochondria and mitogen‐activated protein kinase signal pathways. The present study aimed to investigate whether IPT can protect astrocyte mitochondria against MPP^+^‐induced mitochondrial dysfunction. We showed that treatment with IPT could ameliorate the inhibitory effect of MPP^+^ on mitochondrial respiration and ATP production by using mitochondrial complex I–supported substrates. IPT could also inhibit the increased production of mitochondrial reactive oxygen species (ROS) and the release of cytochrome __c__ from mitochondria induced by MPP^+^. However, mitochondrial ATP‐sensitive potassium (mitoK~ATP~) channel blocker 5‐hydroxydecanoate (5‐HD) could partly abolish all of the above effects of IPT. Because mitochondrial complex dysfunction impairs mitochondrial respiration and ATP production, a

Who reads Iptakalim ameliorates MPP^+^‐induced astrocyte mitochondrial dysfunction by increasing mitochondrial complex activity besides opening mitoK~ATP~ channels?

Author

Shu Zhang; Jian‐Hua Ding; Fang Zhou; Zhi‐Yuan Wang; Xi‐Qiao Zhou; Gang Hu

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley (ISSN 0360-4012)

Published

2008

Language

EN

Field

Neuroscience (Life Sciences)