中国全科医学
中國全科醫學
중국전과의학
CHINESE GENERAL PRACTICE
2015年
21期
2584-2588
,共5页
糖尿病神经病变%超氧化物歧化酶%丙二醛%温通活血乳膏
糖尿病神經病變%超氧化物歧化酶%丙二醛%溫通活血乳膏
당뇨병신경병변%초양화물기화매%병이철%온통활혈유고
Diabetic neuropathies%Superoxide dismutase%Malondialdehyde%Wen-tong-huo-xue cream
目的:探讨温通活血乳膏对糖尿病周围神经病变( DPN)大鼠氧化应激的作用机制。方法2013年5—9月,选用8周龄雄性SD大鼠50只。采用随机数字表法分为正常对照组10只和造模组40只;造模组大鼠饲养期间死去10只,将剩余大鼠采用随机数字表法分为模型组、硫辛酸组、温通活血乳膏组,各10只。制作DPN大鼠模型,硫辛酸组大鼠腹腔注射硫辛酸,温通活血乳膏组大鼠涂抹温通活血乳膏,正常对照组与模型组大鼠给予等量的基质。检测并比较各组大鼠甩尾时间、潜伏期及运动神经传导速度( MNCV)、血清及坐骨神经抗氧化指标〔超氧化物歧化酶( SOD)、丙二醛( MDA)水平〕,观察坐骨神经超微结构。结果模型组大鼠甩尾时间较正常对照组延长( P <0.05);硫辛酸组和温通活血乳膏组大鼠甩尾时间较模型组缩短(P<0.05)。模型组潜伏期较正常对照组延长(P<0.05);温通活血乳膏组潜伏期较模型组缩短(P<0.05)。模型组、硫辛酸组和温通活血乳膏组MNCV较正常对照组缩短(P<0.05);硫辛酸组和温通活血乳膏组MNCV较模型组延长(P<0.05)。模型组、硫辛酸组和温通活血乳膏组血清MDA较正常对照组升高(P<0.05)。模型组坐骨神经SOD、 MDA与正常对照组比较,差异有统计学意义(P<0.05)。硫辛酸组和温通活血乳膏组坐骨神经MDA较模型组降低( P<0.05)。模型组有髓神经纤维髓鞘增宽,板层结构破坏严重,神经严重脱髓鞘,细胞器空泡样变性;硫辛酸组、温通活血乳膏组大鼠有髓神经纤维髓鞘、板层结构、施万细胞结构变化较模型组减轻。结论温通活血乳膏局部用药可以改善MNCV,减轻周围神经结构和功能损伤,其作用机制可能是通过调节氧化还原间的失衡,从而达到治疗DPN的作用。
目的:探討溫通活血乳膏對糖尿病週圍神經病變( DPN)大鼠氧化應激的作用機製。方法2013年5—9月,選用8週齡雄性SD大鼠50隻。採用隨機數字錶法分為正常對照組10隻和造模組40隻;造模組大鼠飼養期間死去10隻,將剩餘大鼠採用隨機數字錶法分為模型組、硫辛痠組、溫通活血乳膏組,各10隻。製作DPN大鼠模型,硫辛痠組大鼠腹腔註射硫辛痠,溫通活血乳膏組大鼠塗抹溫通活血乳膏,正常對照組與模型組大鼠給予等量的基質。檢測併比較各組大鼠甩尾時間、潛伏期及運動神經傳導速度( MNCV)、血清及坐骨神經抗氧化指標〔超氧化物歧化酶( SOD)、丙二醛( MDA)水平〕,觀察坐骨神經超微結構。結果模型組大鼠甩尾時間較正常對照組延長( P <0.05);硫辛痠組和溫通活血乳膏組大鼠甩尾時間較模型組縮短(P<0.05)。模型組潛伏期較正常對照組延長(P<0.05);溫通活血乳膏組潛伏期較模型組縮短(P<0.05)。模型組、硫辛痠組和溫通活血乳膏組MNCV較正常對照組縮短(P<0.05);硫辛痠組和溫通活血乳膏組MNCV較模型組延長(P<0.05)。模型組、硫辛痠組和溫通活血乳膏組血清MDA較正常對照組升高(P<0.05)。模型組坐骨神經SOD、 MDA與正常對照組比較,差異有統計學意義(P<0.05)。硫辛痠組和溫通活血乳膏組坐骨神經MDA較模型組降低( P<0.05)。模型組有髓神經纖維髓鞘增寬,闆層結構破壞嚴重,神經嚴重脫髓鞘,細胞器空泡樣變性;硫辛痠組、溫通活血乳膏組大鼠有髓神經纖維髓鞘、闆層結構、施萬細胞結構變化較模型組減輕。結論溫通活血乳膏跼部用藥可以改善MNCV,減輕週圍神經結構和功能損傷,其作用機製可能是通過調節氧化還原間的失衡,從而達到治療DPN的作用。
목적:탐토온통활혈유고대당뇨병주위신경병변( DPN)대서양화응격적작용궤제。방법2013년5—9월,선용8주령웅성SD대서50지。채용수궤수자표법분위정상대조조10지화조모조40지;조모조대서사양기간사거10지,장잉여대서채용수궤수자표법분위모형조、류신산조、온통활혈유고조,각10지。제작DPN대서모형,류신산조대서복강주사류신산,온통활혈유고조대서도말온통활혈유고,정상대조조여모형조대서급여등량적기질。검측병비교각조대서솔미시간、잠복기급운동신경전도속도( MNCV)、혈청급좌골신경항양화지표〔초양화물기화매( SOD)、병이철( MDA)수평〕,관찰좌골신경초미결구。결과모형조대서솔미시간교정상대조조연장( P <0.05);류신산조화온통활혈유고조대서솔미시간교모형조축단(P<0.05)。모형조잠복기교정상대조조연장(P<0.05);온통활혈유고조잠복기교모형조축단(P<0.05)。모형조、류신산조화온통활혈유고조MNCV교정상대조조축단(P<0.05);류신산조화온통활혈유고조MNCV교모형조연장(P<0.05)。모형조、류신산조화온통활혈유고조혈청MDA교정상대조조승고(P<0.05)。모형조좌골신경SOD、 MDA여정상대조조비교,차이유통계학의의(P<0.05)。류신산조화온통활혈유고조좌골신경MDA교모형조강저( P<0.05)。모형조유수신경섬유수초증관,판층결구파배엄중,신경엄중탈수초,세포기공포양변성;류신산조、온통활혈유고조대서유수신경섬유수초、판층결구、시만세포결구변화교모형조감경。결론온통활혈유고국부용약가이개선MNCV,감경주위신경결구화공능손상,기작용궤제가능시통과조절양화환원간적실형,종이체도치료DPN적작용。
Objective To observe the mechanism of the effect of Wen-tong-huo-xue cream on oxidative stress among rats with diabetic peripheral neuropathy ( DPN) .Methods 50 male SD rats of 8 weeks old were selected as study subjects from May to September in 2013.The rats were divided into normal control group (n=10) and building model group (n=40) by random number table method.10 rats of building model group died during the study, and then the rest rats were equally divided into three groups: model group, lipoic acid group, and Wen-tong-huo-xue cream group by random number table method.Rats in lipoic acid group were injected intraperitoneally with lipoic acid, rats in Wen-tong-huo-xue cream group were bepainted with Wen-tong-huo-xue cream, rats in normal control group and model group were treated with the same amount of matrix.The tail flick latency, latency, motor nerve conduction velocity ( MNCV ) , levels of antioxidant markers〔superoxide dismutase ( SOD ) and methane dicarboxylic aldehyde ( MDA )〕 in serum and sciatic nerve were measured and compared among different groups of rats, the ultra microstructure of sciatic nerve was observed.Results The tail flick latency of rats in model group was significantly longer than that of rats in normal control group ( P<0.05 ); while the tail flick latency of rats in Wen-tong -huo-xue cream group and lipoic acid group was significantly shorter than that of rats in model group, respectively (P<0.05) .The latency of rats in model group was significantly longer than that of rats in normal control group (P<0.05); the latency of rats in Wen-tong-huo-xue cream group was significantly shorter than that of rats in model group (P<0.05) .MNCV of rats in model group, lipoic acid group, and Wen-tong-huo-xue group was significantly shorter than that of rats in normal control group, respectively ( all P<0.05 ); MNCV of rats in lipoic acid group and Wen-tong-huo-xue group was significantly longer than that of rats in model group, respectively ( P<0.05) .Serum level of MDA of rats in model group, lipoic acid group, and Wen-tong-huo-xue group was significantly higher than that of rats in normal control group, respectively ( P<0.05) .There were significant differences in levels of SOD and MDA in sciatic nerve between model group and normal control group ( P<0.05 ) .There was significant difference in sciatic nerve MDA level between lipoic acid group and model group (P<0.05), and there was significant difference in sciatic nerve MDA level between Wen-tong-huo-xue group and model group ( P<0.05 ) .Widened myelin sheath of spinal nerve, damaged lamellar structure, demyelination of nerves, and organelle vesicular degeneration were found among rats in model group; the structural changes of myelin sheath of spinal nerve, lamellar structure, and Schwann cells among rats in Wen -tong -huo -xue cream group and lipoic acid group were slighter than those among rats in model group.Conclusion Wen-tong-huo-xue cream can improve MNCV, alleviate the injury of peripheral nerve structure and function, and its mechanism might be related to adjusting the imbalance between oxidation and reduction, so as to achieve the goal of treating DPN.