International Journal of Pediatric Otorhinolaryngology
Effect of ginkgo biloba extract on recovery after facial nerve crush injury in the rat
Introduction
Peripheral nerve injury is a commonly encountered clinical problem, and it often results in long-term functional deficits. Injury to the facial nerve is a devastating complication of facial and temporal bone trauma. Depending on the magnitude of the injury, patients may present with a spectrum of symptoms ranging from mild, transient facial paresis to permanent facial paralysis with extensive cosmetic deformities and functional limitations
A crush injury induces a pathological change of the endoneurial microvessles in the peripheral nerves, which induce the decreases in both the nerve blood flow and endoneurial oxygen tension, resulting in endoneurial ischemia or hypoxia [1]. Crush gives a cause of oxidative stress, such as lipid peroxidant to the neurovascular cells by generating free radicals [2], [3]. Spontaneous regeneration, through the distal nerve stump with good functional return, can be expected after crush injury of peripheral nerve [4]. This type of nerve injury is with treated pharmacological agents, instead of surgery. Many pharmacological agents have shown successful results in an experimental crush injury of the peripheral nerve [5], [6], [7], [8], [9]. Ginkgo biloba extract (GBE) has an effect for peripheral vascular disease and cerebral insufficiency, and it has strong pharmacological effects, including antioxidant activity, which protects the vascular endothelial cell damage from oxidative injury by scavenging free radicals [10], [11] and vasoregulating activity [12], [13]. Its neuroprotective effect has been reported [14], [15]. GBE protected disturbed slow axonal transport and pathological alterations of peripheral nerve with abnormal endoneurial microvasculature [14]. GBE promoted seeding efficiency of Schwann cells in a tissue engineered polymer conduit. Addition of GBE in Schwann cells-seeded conduit could increase the total number of myelinated axons in nerve regeneration and improve peripheral nerve functional recovery [15]. To date, therapeutic effect of the GBE on peripheral nerve crush injury of rats has been rarely reported [16], [17]. Moreover, neuroprotective effect on the facial nerve crush injury has not been reported. The present study was evaluated whether or not GBE enhances the functional recovery on the facial nerve crush injury in rats.
Section snippets
Animals
All animal experiments were performed in accordance with the local ethical committee at the Research Center for Resistant Cells, Chosun University. Experiments were carried out on 10 adult Sprague-Dawley rats, weighing 250–300 g. Rats were anesthetized by the intraperitoneal injection of Zolletil® (a 1:1 combination of tiletamine and zolazepam, Virbac, Carros, France) and xylazine hydrochloride.
Surgical procedures
A postauricular incision was made at the left side. Under an operating microscope, the main trunk of
Results
There were no intraoperative complications. Fig. 1 demonstrates the effects of GBE on the timing of the onset and full recovery of the vibrissae function. The return of the quivering vibrissae movements was significantly earlier in the course of time compared to that of the control group. A significant improvement was observed in the return to full function by postoperative 2nd week in the experimental group (P < 0.05). The recovery of threshold and the conduction velocity postoperative 4th weeks
Discussion
The healing process after the nerve injury is reduced mainly of its free oxygen radicals, rather than neuroinflammation and edema [21]. Antioxidant materials contribute nerve regeneration, via free oxygen radicals scavenging effect. Antioxidant enzymes, such as superoxide dismutase and catalase, are found in mammalian organisms, and the purpose is to protect the cells from toxic effects of the free radicals. Free radicals induced traumatic cell damage is a basic mechanism for cell deaths. This
Conclusion
From this result, intraperitoneal injection of GBE has been found effective in the promotion of nerve regeneration in an experimental facial nerve crush rat model. Further studies, including morphological and molecular analyses are necessary to clarify the mechanisms of GBE on the facial nerve crush.
Acknowledgements
This study was supported by research fund from a National Research Foundation (NRF) grant funded from the Korea government (MEST) through the Research Center for Resistant Cells (R13-2003-009).
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