کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9428963 | 1297021 | 2005 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Diabetes: A potential enhancer of retinal injury in rat retinas
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موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
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چکیده انگلیسی
This study was performed to determine whether early diabetes accelerates retinal neuronal cell death and inhibits neurite regeneration. Five of ten rats were rendered diabetic with streptozotocin injection. After 3 weeks of diabetes, retinas were isolated and retinal explants were cultured in serum-free media. On day 6, the number of neurites was counted in retinal explants obtained from control and diabetic rat retinas. To identify neuronal cells undergoing apoptosis, retinas were fixed, cryosections prepared, and TdT-dUTP terminal nick-end labeling (TUNEL) was performed. Furthermore, the expression of Bax was determined in the retinas by immunohistochemistry and Western blot analysis. The number of TUNEL-positive cells in the ganglion cell layer of diabetic retinas was significantly increased (144.8 ± 33.6% of control, p < 0.01) compared to those in non-diabetic control rats. The number of regenerating neurites in the retinal explants of diabetic rats was significantly reduced (63.2 ± 25.1% of control, p < 0.05). In retinal neuronal cells of the diabetic retinas, proapoptotic Bax expression determined by immunohistochemistry and Western blot analysis showed a significant increase compared to the non-diabetic control retinas (158.1 ± 55.2% of control, p < 0.01; 161.6 ± 48.8% of control, p < 0.01, respectively). The findings indicate that diabetes upregulates Bax expression, accelerates retinal neuronal cell death, and inhibits neurite regeneration in rat retinas. Thus, it is likely that Bax dependent pathways may be activated in injured neuronal cells of the diabetic retinas.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 390, Issue 1, 16 December 2005, Pages 25-30
Journal: Neuroscience Letters - Volume 390, Issue 1, 16 December 2005, Pages 25-30
نویسندگان
Toshiyuki Oshitari, Sayon Roy,