Paclitaxel Inhibits Expression of Neuronal Nitric Oxide Synthase and Prevents Mitochondrial Dysfunction in Spinal Ventral Horn in Rats After C7 Spinal Root Avulsion
AIm: This study evaluated the neuroprotective effect of intrathecally infused paclitaxel in the prevention of motoneuron death and mitochondrial dysfunction following brachial plexus avulsion injury. Mat erIal and Methods: Brachial root avulsion injury was induced in Sprague-Dawley rats. The Pacli...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Turkish Neurosurgery, ITN
2015
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| Subjects: | |
| Online Access: | http://ir.unimas.my/id/eprint/10709/ http://ir.unimas.my/id/eprint/10709/1/Abdul%20Aziz.pdf |
| Summary: | AIm: This study evaluated the neuroprotective effect of intrathecally infused paclitaxel in the prevention of motoneuron death and
mitochondrial dysfunction following brachial plexus avulsion injury.
Mat erIal and Methods: Brachial root avulsion injury was induced in Sprague-Dawley rats. The Paclitaxel treatment group (n = 32) received
a 5-d intrathecal infusion of paclitaxel (256 ng/d) via a micro infusion pump, whereas the Control group (n = 32) received normal saline. The
cervical cord was harvested at survival times of 1, 2, 4, and 6 wk (n = 8 each). The number of surviving and nNOS-positive motoneurons at the
injury level in the ventral horn was determined with NADPH-d histochemistry. Mitochondrial function at this location was measured with CcO
histochemistry and densitometry. An independent t-test was applied to detect differences between the study groups at specific survival times.
Result s: The Paclitaxel treatment group showed a significant relative reduction in nNOS expression at 2, 4, and 6 wk, and significantly
improved mitochondrial function at 4 and 6 wk. Motoneuron survival was significantly increased at 2, 4, and 6 wk.
ConclusIon: Paclitaxel has a significant neuroprotective effect against spinal motoneuron degeneration following brachial plexus avulsion
injury, which involves inhibition of nNOS expression and prevention of mitochondrial dysfunction. |
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