RÉSUMÉ
BACKGROUND:Cholecystokinin as an endogenous neuroprotective factor in the nervous system has garnered increasing attention. Findings from previous animal studies show that cholecystokinin can effectively promote the regeneration of the injured peripheral nerve. On this basis, further clinical trials wil be performed to observe whether local application of cholecystokinin at nerve anastomosis can promote peripheral nerve regeneration. METHODS/DESIGN:As a prospective randomized controled trial, this study wil enrol 100 patients with complete rupture of the peroneal nerve, who wil be randomly divided into two groups: after nerve suture and partial gelatin sponge infiltration at nerve anastomosis, the patients wil be treated with 8 nmol/kg cholecystokinin (treatment group) or saline (control group). At 6, 12, 24 weeks after treatment, common peroneal nerve conduction velocity and electromyography and nerve fiber morphology wil be detected; the clinical efficacy at the last folow-up wil be assessed; and al adverse events during the folow-up wil be recorded to assess the therapeutic efficacy and safety. DISCUSSION:In this study, cholecystokinin as an inducing agent for nerve growth factor synthesis wil be observed and studied, with a view to providing a new idea for seeking peripheral nerve therapy. ETHICAL APPROVAL: The study protocol was approved by the Medical Ethics Committee of the Affiliated Hospital of Putian University (approval No. 2014116). Written informed consent wil be obtained from patients before treatment.
RÉSUMÉ
BACKGROUND:Previous studies have found that cholecystokinin octapeptide (CCK-8) can promote the regeneration after sciatic nerve injury in rats, but the exact mechanism remains unclear. OBJECTIVE:To screen effective indicators and analyze the mechanism of CCK-8 promoting sciatic nerve regeneration from the perspective of nerve growth factor and nerve regeneration microenvironment. METHODS:Healthy Sprague-Dawley rats, for the preparation of unilateral sciatic nerve transection injury model, were randomly divided into two groups. In the CCK-8 group, the animal model received intraperitoneal injection of CCK-8 (8 nmol/kg) for consecutive 7 days, while the control group was injected with equal volume of normal saline. The nerve growth factor expression, inducible nitric oxide synthase in the spinal cord, serum superoxide dismutase activity and malondialdehyde concentration, as wel as apoptotic cel s in spinal cord were al detected. RESULTS AND CONCLUSION:In the CCK-8 group, nerve growth factor expression was higher than that in the control group (P<0.01), while inducible nitric oxide synthase and the number of apoptotic cel s were lower (P<0.01), serum superoxide dismutase activity was higher but malondialdehyde concentrations was lower (P<0.01, 0.05). The mechanisms of CCK-8 promoting sciatic nerve regeneration include protecting neurons, anti-apoptosis, inhibiting inflammatory response, anti-NO and anti-oxidation, reducing malondialdehyde, and al eviating free radical damage, as wel as stimulating nerve growth factor expression and release.
RÉSUMÉ
BACKGROUND:In the past 20 years, cholecystokinin in clinical application and nerve repair has been extensively studied. OBJECTIVE:To explore the role of cholecystokinin in nerve repair and its possible mechanism of action. METHODS:Relevant research results were retrospectively analyzed at the celland organ levels through retrieving recent literatures concerning the biological characteristics of cholecystokinin and its biological role in the nervous system. Then, we summarized the effect of cholecystokinin after nerve injury and its possible RESULTS AND CONCLUSION:Cholecystokinin and its receptors are widely distributed in the body, and under physiological and pathological conditions, their roles were complex and diverse. However, studies addressing the neuroprotective effect of cholecystokinin are not sufficient, most of which are limited to phenomenon observation. Neuroprotective mechanism of cholecystokinin is stil worthy of further studies, which can provide the basis for the clinical application.