Browsing by Author "Hu, Chiao-Ya"

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Extracellular signal-regulated kinase 1/2 is involved in a tamoxifen neuroprotective effect in a lateral fluid percussion injury rat model
(2014-06-01)
Tsai, Yin-Tzu
;
Wang, Che-Chuan
;
Leung, Pak-On
;
Lin, Kao-Chang
;
Chio, Chung-Ching
Background: The aim of the present study was to determine whether tamoxifen (TMX) causes attenuation of traumatic brain injury (TBI) induced by fluid percussion injury. Materials and methods: Immediately after the onset of fluid percussion TBI, anesthetized male Sprague-Dawley rats were divided into three major groups and intraperitoneally administered the vehicle solution (1 mL/kg), TMX (1 mg/kg), or TMX (1 mg/kg) plus the extracellular signal-regulated kinase 1/2 antagonist SL327 (30 mg/kg). Another group of rats were used as sham-operated controls. The functional outcomes, such as motor outcomes, were evaluated using an incline plane. The cellular infarction volume was evaluated by triphenyltetrazolium chloride staining. Neuronal loss, apoptosis, and p-ERK1/2 and Bcl2 expression in neuronal cortex cells were evaluated by immunofluorescence methods. All the parameters were assessed on day 4 after injury. Results: Compared with the sham-operated controls, the TBI-induced motor deficits and cerebral infarction after TBI were significantly attenuated by TMX therapy. The TBI-induced neuronal loss and apoptosis were also significantly reduced by TMX therapy. The numbers of Bcl2- and phospho-ERK1/2-positive neuronal cells in the ischemic cortex after TBI were significantly increased by TMX therapy. These TMX effects were significantly blocked by SL327 administration. Conclusions: Our results suggest that intravenous injection of TMX may ameliorate TBI in rats by increasing neuronal p-ERK1/2 expression, which might lead to an increase in neuronal Bcl2 expression and a decrease in neuronal apoptosis and cell infarction volume, and it might represent one mechanism by which functional recovery occurred. TMX may be a promising TBI treatment strategy. (C) 2014 Elsevier Inc. All rights reserved.
The neuronal protective effects of local brain cooling at the craniectomy site after lateral fluid percussion injury in a rat model
(2013-12-01)
Wang, Che-Chuan
;
Chen, Yuan-Shen
;
Lin, Bor-Shyh
;
Chio, Chung-Ching
;
Hu, Chiao-Ya
Background: The aim of the present study is to investigate whether local brain cooling at the craniectomy site causes attenuation of traumatic brain injury (TBI) induced by fluid percussion injury (FPI). Methods: Anesthetized male SpragueeDawley rats were divided into two major treatment groups. Immediately after the onset of fluid percussion TBI, a craniectomy window of 6 x 8 mm was made at the right parietal, and a cold water bag (0 x C-1 x degrees C or 5 x C-6 degrees C) was applied locally for 30 min. Additional groups of rats were used as craniectomy and craniectomy FPI controls. Physiological parameters, such as brain and colonic temperature, mean arterial pressure, and heart rate, were monitored during FPI. Functional motor outcomes were evaluated using the inclined plane test (maximal grasp angle). Cellular infarction volume was calculated using triphenyltetrazolium chloride staining. Apoptosis and neuronal markerepositive cells in the cortex were measured by immunofluorescence staining. All functional and morphologic parameters were assessed 72 h after injury. Results: Compared with the craniectomy + FPI control groups, the groups treated with 5 degrees C-6 degrees C local cold water therapy showed significant attenuation of the FPI-induced motor deficits, weight loss, and cerebral infarction but no effect on colonic temperature. The FPI-induced apoptosis and neuronal loss were also significantly reduced by local cooling. Conclusions: Our results suggest that local cooling with 5 degrees C-6 degrees C cold water therapy may ameliorate TBI in rats by reducing infarction volume, neuronal cell loss, and apoptosis, resulting in improved functional outcome. We propose that the use of local cooling at the craniectomy site after FPI might have clinical benefits in the future. (C) 2013 Elsevier Inc. All rights reserved.