Original Article

Growth-promoting activity of Hominis Placenta extract on regenerating sciatic nerve

Tae-beom Seo, In-sun Han, Jin-hwan Yoon, In-chan Seol, Yun-sik Kim, Hyun-kyung Jo, Joung-jo An, Kwon-eui Hong, Young-bae Seo, Dong-hee Kim, Seung-kiel Park, Deok-chun Yang, Uk Namgung

Abstract

Aim: Extract of Hominis Placenta (HP) has been used in oriental medicine as an
agent for improving physiological function. The present study was conducted to
investigate whether HP treatment in an experimental sciatic nerve injury animal
model produces growth-promoting effects on regenerating peripheral nerve fibers
after injury. Methods: After HP was injected into a sciatic nerve injury site, changes
in protein levels were analyzed in the regenerating nerve area by Western blotting
and immunofluorescence staining analyses. For quantitative assessment of axonal
regeneration, a retrograde tracing technique was used to identify the neuronal
cell bodies corresponding to regenerating axons, and the extent of neurite
outgrowth in cultured dorsal root ganglia (DRG) sensory neurons prepared from
animals that had experienced a sciatic nerve crush injury 7 d before neuron collection
was analyzed. Results: Induction levels of axonal growth-associated protein
(GAP-43) in the injured sciatic nerves were elevated by HP treatment. HP treatment
also upregulated cell division cycle 2 (Cdc2) protein levels in the distal
stump of the injured sciatic nerve. Induced Cdc2 protein was detected in Schwann
cells, suggesting that Cdc2 kinase activity may be involved in the growth-promoting
activity of regenerating axons via Schwann cell proliferation. Cell body measurement
by retrograde tracing indicated that HP treatment produced significant
increases in regenerating motor axons. Finally, HP treatment of cultured DRG
sensory neurons significantly increased neurite arborization and elongation.
Conclusion: HP promotes the regeneration of injured sciatic axons by upregulating
the synthesis of regeneration-related protein factors such as GAP-43 and Cdc2.
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