BACKGROUND: Estrogen is neuroprotective, but long-term estrogen treatment can induce side effects such as breast carcinoma, endometrial cancer, and stroke. However, phytoestrogen is neuroprotective without these side effects. OBJECTIVE: To study the effects of Ginsenoside Rg1 on facial neurons and brain-derived neurotrophic factor (BDNF) expression in the facial nucleus in ovariectomized rats. DESIGN, TIME AND SETTING: The randomized, controlled animal experiments were performed at the Ultrasonic Institute, Second Affiliated Hospital, Chongqing Medical University, China, from September 2007 to September 2008. MATERIALS: Ginsenoside Rg1 (Sigma, USA), rabbit anti-rat BDNF, Bcl-2, Bax antibodies, biotin-labeled goat anti-rabbit IgG (Boster, China), and a TUNEL kit (Roche, Germany) were used in this study. METHODS: A total of 48 adult Sprague Dawley rats undergoing ovariectomy were randomly assigned into sham operation (n = 8), model (n = 20), and Ginsenoside Rg1 (n = 20) groups. Facial nerve damage was induced by bilateral clamping of the facial nerve trunk. The bilateral facial nerve trunk was exposed in the sham operation group, with no clamping. Rats in the Ginsenoside Rg1 group were intraperitoneally injected with 10 mg/kg per day Ginsenoside Rgl; other groups received 2 mL saline, once a day, for 14 days. MAIN OUTCOME MEASURES: Morphologic changes in neurons of the facial nucleus were observed following hematoxylin-eosin staining. Neuronal apoptosis was detected by TUNEL. Changes in ultrastructure of the facial nerve fibers were observed with a transmission electron microscope. Expression of BDNF, Bcl-2, and Bax protein was quantified by semiquantitative immunohistochemistry. RESULTS: At 3-14 days following facial nerve damage, Ginsenoside Rgl increased BDNF expression and the number of regenerated nerve fibers, and produced thicker myelin sheaths (P < 0.05). Ginsenoside Rgl also gradually increased BcI-2 protein expression and decreased Bax protein expression (P < 0.05). By day 7, apoptosis was observed in facial neurons, but Ginsenoside Rg1 reduced the number of apoptotic neurons. Sham animals did not show any changes in BDNF, Bcl-2, or Bax expression or facial neuron morphology. CONCLUSION: Ginsenoside Rgl can substantially inhibit facial neuronal apoptosis by increasing endogenous BDNF and Bcl-2 expression and by decreasing Bax expression in ovariectomized rats after facial nerve damage.
