中华神经医学杂志
中華神經醫學雜誌
중화신경의학잡지
CHINESE JOURNAL OF NEUROMEDICINE
2013年
8期
779-782
,共4页
卫重娟%程焱%梁浩%陈英%孔晓冬%古今颖
衛重娟%程焱%樑浩%陳英%孔曉鼕%古今穎
위중연%정염%량호%진영%공효동%고금영
糖尿病周围神经病变%神经生长因子%神经肽%神经传导速度
糖尿病週圍神經病變%神經生長因子%神經肽%神經傳導速度
당뇨병주위신경병변%신경생장인자%신경태%신경전도속도
Diabetic neuropathy%Nerve growth factor%Neuropeptide%Nerve conduction velocity
目的 探讨神经生长因子对糖尿病周围神经病变大鼠神经肽和神经传导速度的影响. 方法 雄性Wistar大鼠35只按随机数字表法分为健康对照组(n=10)、糖尿病模型组(n=13)和神经生长因子治疗组(n=12),后两组用链脲佐菌素制成糖尿病周围神经病变大鼠模型,并给予神经生长因子治疗组神经生长因子治疗(40μg/kg).显微镜下观察并计算背根神经节中P物质、降钙素基因相关肽(CGRP)免疫阳性细胞率,检测运动神经传导速度(MNCV)和感觉神经传导速度(SNCV). 结果 糖尿病模型组大鼠背根神经节中P物质、CGRP免疫阳性细胞率(27.710%±3.471%;36.360%±12.027%)以及神经生长因子治疗组治疗前MNCV [(35.80±6.19) m/s]、SNCV[(39.62±6.69) m/s]与健康对照组[P物质:44.225%±8.213%;CGRP:47.400%±13.723%;MNCV:(55.83±10.30) m/s; SNCV:(47.02±7.52) m/s]相比显著下降,差异有统计学意义(P<0.05).经神经生长因子治疗后,P物质、CGRP免疫阳性细胞率(49.417%±6.753%;53.811%±7.125%)较糖尿病模型组显著增高,MNCV[(41.80±3.45) m/s]、SNCV[(42.92±6.69) m/s]均治疗前显著增高,差异有统计学意义(P<0.05). 结论 糖尿病周围神经病变大鼠可出现神经传导速度下降和神经生长因子相关神经肽P物质、CGRP缺乏,而神经生长因子可促进神经肽的表达并提高神经传导速度.
目的 探討神經生長因子對糖尿病週圍神經病變大鼠神經肽和神經傳導速度的影響. 方法 雄性Wistar大鼠35隻按隨機數字錶法分為健康對照組(n=10)、糖尿病模型組(n=13)和神經生長因子治療組(n=12),後兩組用鏈脲佐菌素製成糖尿病週圍神經病變大鼠模型,併給予神經生長因子治療組神經生長因子治療(40μg/kg).顯微鏡下觀察併計算揹根神經節中P物質、降鈣素基因相關肽(CGRP)免疫暘性細胞率,檢測運動神經傳導速度(MNCV)和感覺神經傳導速度(SNCV). 結果 糖尿病模型組大鼠揹根神經節中P物質、CGRP免疫暘性細胞率(27.710%±3.471%;36.360%±12.027%)以及神經生長因子治療組治療前MNCV [(35.80±6.19) m/s]、SNCV[(39.62±6.69) m/s]與健康對照組[P物質:44.225%±8.213%;CGRP:47.400%±13.723%;MNCV:(55.83±10.30) m/s; SNCV:(47.02±7.52) m/s]相比顯著下降,差異有統計學意義(P<0.05).經神經生長因子治療後,P物質、CGRP免疫暘性細胞率(49.417%±6.753%;53.811%±7.125%)較糖尿病模型組顯著增高,MNCV[(41.80±3.45) m/s]、SNCV[(42.92±6.69) m/s]均治療前顯著增高,差異有統計學意義(P<0.05). 結論 糖尿病週圍神經病變大鼠可齣現神經傳導速度下降和神經生長因子相關神經肽P物質、CGRP缺乏,而神經生長因子可促進神經肽的錶達併提高神經傳導速度.
목적 탐토신경생장인자대당뇨병주위신경병변대서신경태화신경전도속도적영향. 방법 웅성Wistar대서35지안수궤수자표법분위건강대조조(n=10)、당뇨병모형조(n=13)화신경생장인자치료조(n=12),후량조용련뇨좌균소제성당뇨병주위신경병변대서모형,병급여신경생장인자치료조신경생장인자치료(40μg/kg).현미경하관찰병계산배근신경절중P물질、강개소기인상관태(CGRP)면역양성세포솔,검측운동신경전도속도(MNCV)화감각신경전도속도(SNCV). 결과 당뇨병모형조대서배근신경절중P물질、CGRP면역양성세포솔(27.710%±3.471%;36.360%±12.027%)이급신경생장인자치료조치료전MNCV [(35.80±6.19) m/s]、SNCV[(39.62±6.69) m/s]여건강대조조[P물질:44.225%±8.213%;CGRP:47.400%±13.723%;MNCV:(55.83±10.30) m/s; SNCV:(47.02±7.52) m/s]상비현저하강,차이유통계학의의(P<0.05).경신경생장인자치료후,P물질、CGRP면역양성세포솔(49.417%±6.753%;53.811%±7.125%)교당뇨병모형조현저증고,MNCV[(41.80±3.45) m/s]、SNCV[(42.92±6.69) m/s]균치료전현저증고,차이유통계학의의(P<0.05). 결론 당뇨병주위신경병변대서가출현신경전도속도하강화신경생장인자상관신경태P물질、CGRP결핍,이신경생장인자가촉진신경태적표체병제고신경전도속도.
Objective To investigate the influence of nerve growth factor (NGF) in neuropeptides and nerve conduction velocity in rats with experimental diabetic peripheral neuropathy (DNP).Methods Thirty-five 6-week-old male Wistar rats,weighing 175-215 g,were chosen in our study and randomly divided into healthy control group (n=10),DNP model group (n=13) and NGF treatment group (n=12).Rats in the latter 2 group were induced with the interference of administered streptozotocin,and rats in the NGF treatment group were treated with NGF (40 μg/kg).The immunopositive cells percentages of substance P (SP) and calcitonin gene-related peptide (CGRP) in dorsal root ganglion (DRG) were observed and measured; the motor nerve conduction velocity (MNCV) and sensory nerve conduction velocity (SNCV) were measured and compared among the three groups.Results As compared with those in the healthy control group,the immunopositive cells percentages of SP (27.710%±3.471% vs 44.225%±8.213%) and CGRP (36.360%±12.027% vs 47.400%±13.723%) in the DRG of DNP model group were significantly decreased (P<0.05); as compared with those in the healthy control group,the MNCV[(35.80±6.19) m/s vs (55.83±10.30) m/s] and SNCV[(39.62±6.69) m/s vs (47.02 ±7.52) m/s)] of DNP model group were significantly decreased (P<0.05); however,obvious increase of SP (49.417%±6.753%) and CGRP (53.811%±7.125%),MNCV (41.80±3.45) m/s and SNCV (42.92±6.69 m/s) in the NGF treatment group was noted as compared with those in the DNP model group (P<0.05).Conclusion The nerve conduction velocity and NGF related neuropeptides (SP and CGRP) decrease in rats with DNP; treatment with NGF promotes the expression ofneuropeptides and increases the nerve conduction velocity.