scholarly journals Can regenerated nerve fibers return to normal size? A long-term post-traumatic study of the rat median nerve crush injury model

Microsurgery ◽  
2012 ◽  
Vol 32 (5) ◽  
pp. 383-387 ◽  
Author(s):  
Luisa Muratori ◽  
Giulia Ronchi ◽  
Stefania Raimondo ◽  
Maria G. Giacobini-Robecchi ◽  
Michele Fornaro ◽  
...  
Keyword(s):  
Median Nerve ◽  
Nerve Fibers ◽  
Crush Injury ◽  
Nerve Crush ◽  
Injury Model ◽  
Post Traumatic ◽  
Nerve Crush Injury

Dual Regeneration of Muscle and Nerve by Intramuscular Infusion of Mitochondria in a Nerve Crush Injury Model

Neurosurgery ◽  
2021 ◽  
Vol 89 (Supplement_2) ◽  
pp. S139-S139
Author(s):  
Meei-Ling Sheu ◽  
Chiung-Chyi Shen ◽  
Hsi-Kai Tsou ◽  
Meng Yin Yang ◽  
Hong-Lin Su ◽  
...  
Keyword(s):  
Crush Injury ◽  
Nerve Crush ◽  
Injury Model ◽  
Nerve Crush Injury

The promotion of peripheral nerve regeneration by chitooligosaccharides in the rat nerve crush injury model

2009 ◽  
Vol 454 (3) ◽  
pp. 239-243 ◽  
Author(s):  
Maorong Jiang ◽  
Xiaoming Zhuge ◽  
Yumin Yang ◽  
Xiaosong Gu ◽  
Fei Ding
Keyword(s):  
Peripheral Nerve ◽  
Nerve Regeneration ◽  
Peripheral Nerve Regeneration ◽  
Crush Injury ◽  
Nerve Crush ◽  
Injury Model ◽  
Rat Nerve ◽  
Nerve Crush Injury

scholarly journals Citrus Naringenin Increases Neuron Survival in Optic Nerve Crush Injury Model by Inhibiting JNK-JUN Pathway

2021 ◽  
Vol 23 (1) ◽  
pp. 385
Author(s):  
Jie Chen ◽  
Hui Li ◽  
Changming Yang ◽  
Yinjia He ◽  
Tatsuo Arai ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Nerve Injury ◽  
Ganglion Cells ◽  
Crush Injury ◽  
Optic Nerve Crush ◽  
Nerve Crush ◽  
Injury Model ◽  
Nerve Crush Injury

Traumatic nerve injury activates cell stress pathways, resulting in neuronal death and loss of vital neural functions. To date, there are no available neuroprotectants for the treatment of traumatic neural injuries. Here, we studied three important flavanones of citrus components, in vitro and in vivo, to reveal their roles in inhibiting the JNK (c-Jun N-terminal kinase)-JUN pathway and their neuroprotective effects in the optic nerve crush injury model, a kind of traumatic nerve injury in the central nervous system. Results showed that both neural injury in vivo and cell stress in vitro activated the JNK-JUN pathway and increased JUN phosphorylation. We also demonstrated that naringenin treatment completely inhibited stress-induced JUN phosphorylation in cultured cells, whereas nobiletin and hesperidin only partially inhibited JUN phosphorylation. Neuroprotection studies in optic nerve crush injury mouse models revealed that naringenin treatment increased the survival of retinal ganglion cells after traumatic optic nerve injury, while the other two components had no neuroprotective effect. The neuroprotection effect of naringenin was due to the inhibition of JUN phosphorylation in crush-injured retinal ganglion cells. Therefore, the citrus component naringenin provides neuroprotection through the inhibition of the JNK-JUN pathway by inhibiting JUN phosphorylation, indicating the potential application of citrus chemical components in the clinical therapy of traumatic optic nerve injuries.

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