Bondan E F, Lallo M A, Trigueiro A H, Ribeiro C P, Sinhorini I L, Graça D L
Mestrado em Ciências da Reabilitação Neuromotora, Universidade Bandeirante de São Paulo, São Paulo, SP, Brasil.
Braz J Med Biol Res. 2006 May;39(5):637-46. doi: 10.1590/s0100-879x2006000500011. Epub 2006 Apr 20.
Schwann cell disturbance followed by segmental demyelination in the peripheral nervous system occurs in diabetic patients. Since Schwann cell and oligodendrocyte remyelination in the central nervous system is a well-known event in the ethidium bromide (EB) demyelinating model, the aim of this investigation was to determine the behavior of both cell types after local EB injection into the brainstem of streptozotocin diabetic rats. Adult male Wistar rats received a single intravenous injection of streptozotocin (50 mg/kg) and were submitted 10 days later to a single injection of 10 microL 0.1% (w/v) EB or 0.9% saline solution into the cisterna pontis. Ten microliters of 0.1% EB was also injected into non-diabetic rats. The animals were anesthetized and perfused through the heart 7 to 31 days after EB or saline injection and brainstem sections were collected and processed for light and transmission electron microscopy. The final balance of myelin repair in diabetic and non-diabetic rats at 31 days was compared using a semi-quantitative method. Diabetic rats presented delayed macrophage activity and lesser remyelination compared to non-diabetic rats. Although oligodendrocytes were the major remyelinating cells in the brainstem, Schwann cells invaded EB-induced lesions, first appearing at 11 days in non-diabetic rats and by 15 days in diabetic rats. Results indicate that short-term streptozotocin-induced diabetes hindered both oligodendrocyte and Schwann cell remyelination (mean remyelination scores of 2.57 +/- 0.77 for oligodendrocytes and 0.67 +/- 0.5 for Schwann cells) compared to non-diabetic rats (3.27 +/- 0.85 and 1.38 +/- 0.81, respectively).
糖尿病患者的外周神经系统会出现雪旺细胞紊乱，随后发生节段性脱髓鞘。由于在溴化乙锭（EB）脱髓鞘模型中，中枢神经系统中的雪旺细胞和少突胶质细胞的髓鞘再生是一个众所周知的现象，本研究的目的是确定在链脲佐菌素诱导的糖尿病大鼠脑干局部注射EB后这两种细胞类型的行为。成年雄性Wistar大鼠接受单次静脉注射链脲佐菌素（50 mg/kg），10天后在脑桥池单次注射10 μL 0.1%（w/v）EB或0.9%盐溶液。也将10 μL 0.1% EB注射到非糖尿病大鼠体内。在注射EB或盐水后7至31天，将动物麻醉并经心脏灌注，收集脑干切片并进行光镜和透射电镜处理。使用半定量方法比较糖尿病大鼠和非糖尿病大鼠在31天时髓鞘修复的最终平衡情况。与非糖尿病大鼠相比，糖尿病大鼠的巨噬细胞活性延迟，髓鞘再生较少。尽管少突胶质细胞是脑干中主要的髓鞘再生细胞，但雪旺细胞侵入了EB诱导的损伤区域，在非糖尿病大鼠中最早在11天出现，在糖尿病大鼠中在15天出现。结果表明，与非糖尿病大鼠（少突胶质细胞平均髓鞘再生评分为3.27±0.85，雪旺细胞为1.38±0.81）相比，短期链脲佐菌素诱导的糖尿病阻碍了少突胶质细胞和雪旺细胞的髓鞘再生（少突胶质细胞平均髓鞘再生评分为2.57±0.77，雪旺细胞为0.67±0.5）。
