Evaluation of Fluoxetine Treatment on Facial Nerve Healing

Abstract

therapeutic effects. In this study, we investigated the effects of EGCG in inhibiting HGF induced tumor growth and invasion of oral cancer in vitro and in vivo. METHOD: We examined the effect of EGCG on HGF-induced cell proliferation, migration, invasion, induction of apoptosis, and modulation of HGF/c-Met signaling pathway in KB oral cancer cell line. We investigated the antitumor effect and the inhibition of c-Met expression by EGCG in a syngeneic mouse model (C3H/HeJ mice, SCC VII/SF cell line). RESULTS: HGF promoted cell proliferation, migration, invasion, and induction of MMP-2 and 9 in KB cells. EGCG significantly inhibited HGF-induced phosphorylation of Met as well as cell growth, invasion, and expression of MMP-2 and 9. EGCG blocked HGF-induced phosphorylation of c-Met as well as of the downstream kinases, AKT and ERK and inhibition of p-AKT and p-ERK by EGCG was associated with marked increases in the phosphorylation of p38, JNK, cleaved caspase-3, and PARP. In C3H/HeJ syngeneic mice, as an in vivo model, tumor growth was suppressed and apoptosis was increased by EGCG. CONCLUSION: Our results suggest that EGCG may be a potential therapeutic agent to inhibit HGF-induced tumor growth and invasion in oral cancer. Evaluation of Fluoxetine Treatment on Facial Nerve HealingHakan Cincik, MD (presenter); Mustafa Guens, MD; Salim Dogru, MD; Atila Gungor, MD; Engin Cekin, MD OBJECTIVE: BDNF (brain-derived neurotrophic factor), an important neurotrophic factor, accelerates healing of the nerve injury. Many studies have been showed antidepressant treatment induces BDNF levels. In our study, an experimental facial nerve crush injury in rats model was created, and effect of fluoxetine treatment on serum BDNF level and on facial nerve healing were investigated by EMG. METHOD: Thirty-eight rats were allocated for this study. Group E consisted of six rats, that did not have any injury or treatment. Rest of the rats were divided into four groups as each group had 8 rats. Temporary facial nerve crush injury was performed in Group A, B, C and D. Trunk of the facial nerve was temporarily injured by crushing with the standard vascular clamp for 40 minutes. Groups C, D and E were not treated with any drug. Fluoxetin (at a dose of 1 mg/kg/day) was injected intraperitoneally for 7 days in Group A, for 28 days in Group B. EMG evaluation of facial nerve was performed at 7th day in Groups A and C, at 28th day in Group B and D. Latencies and amplitudes of the groups were compared with each other. In addition, serum samples were taken from the groups for the measurement of BDNF level. RESULTS: When BDNF levels were compared between rats with facial nerve injury (Group A, B, C, D) and rats with no injury (Group E), statistically significant decrease of serum BDNF levels was noted, approximately 1 / 3 ratio. Statistical significantly increase of BDNF level was not seen in rats serum after fluoxetine treatment in Group A (7 days) and B (28 days). Fluoxetine did not effect statistical significantly latans value in EMG study of group B, ...