环球中医药
環毬中醫藥
배구중의약
GLOBAL TCM
2015年
7期
798-802
,共5页
糖痹康%糖尿病性周围神经病变%坐骨神经%氧化应激%细胞凋亡
糖痺康%糖尿病性週圍神經病變%坐骨神經%氧化應激%細胞凋亡
당비강%당뇨병성주위신경병변%좌골신경%양화응격%세포조망
Chinese herba1 compound Tangbikang%Diabetic periphera1 neuropathy%Sciatic nerve%Oxidative stress%Apoptosis
目的：观察糖痹康对糖尿病性周围神经病变大鼠相关的活性氧簇( reactive oxygen species, ROS﹚、丙二醛( ma1ondia1dehyde,MDA﹚、超氧化歧化酶( superoxide dismutase, SOD﹚、半胱天冬酶-3(caspas-3﹚、坐骨神经细胞凋亡的影响,探讨其对氧化应激及细胞凋亡作用的神经保护机制。方法使用60只高脂饲料喂养后小剂量链脲佐菌素( streptozotoin,STZ﹚腹腔往射而诱发的2型糖尿病大鼠动物模型,8周造模成功后按体重随机分为模型组,α-硫辛酸———糖痹康低、中、高剂量组,另外单独设10只大鼠为正常组,模型组和正常组予蒸馏水灌胃,糖痹康组和α-硫辛酸组分别予不同剂量糖痹康和α-硫辛酸灌胃,每4周测1次体重、空腹血糖,16周后取大鼠一侧坐骨神经,检测其ROS(比色法﹚、MDA(硫代巴比妥酸法﹚、SOD(黄嘌呤氧化酶法﹚含量,酶联免疫吸附法检测caspas-3蛋白表达,末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记测定法[ termina1 dexynuc1eotidy1 transferase( TdT﹚-mediated dUTP nick end 1abe1ing, TUNEL]检测细胞凋亡。结果与正常组比较,各组大鼠SOD显著下降,MDA、ROS显著升高,Caspase-3蛋白表达水平显著升高,TUNEL检测阳性细胞显著增多；与模型组比较,α-硫辛酸组和糖痹康中、高剂量组ROS、MDA含量明显减少,SOD含量明显升高(P<0.05﹚；TUNEL检测α-硫辛酸组和糖痹康高剂量组与模型组相比阳性细胞数减少(P<0.05﹚,糖痹康高剂量组与α-硫辛酸组比较,阳性细胞数稍多于α-硫辛酸组(P<0.05﹚；α-硫辛酸组、糖痹康高剂量组大鼠坐骨神经组织Caspase-3蛋白表达显著少于模型组( P<0.05﹚,两组间Caspase-3蛋白表达无明显差异( P>0.05﹚。结论糖痹康可能通过提高SOD,清除过多MDA、ROS,缓解糖尿病性周围神经病变( diabetic periphera1 neuropathy,DPN﹚的氧化应激损伤,减少神经细胞凋亡,延缓DPN的进展。
目的：觀察糖痺康對糖尿病性週圍神經病變大鼠相關的活性氧簇( reactive oxygen species, ROS﹚、丙二醛( ma1ondia1dehyde,MDA﹚、超氧化歧化酶( superoxide dismutase, SOD﹚、半胱天鼕酶-3(caspas-3﹚、坐骨神經細胞凋亡的影響,探討其對氧化應激及細胞凋亡作用的神經保護機製。方法使用60隻高脂飼料餵養後小劑量鏈脲佐菌素( streptozotoin,STZ﹚腹腔往射而誘髮的2型糖尿病大鼠動物模型,8週造模成功後按體重隨機分為模型組,α-硫辛痠———糖痺康低、中、高劑量組,另外單獨設10隻大鼠為正常組,模型組和正常組予蒸餾水灌胃,糖痺康組和α-硫辛痠組分彆予不同劑量糖痺康和α-硫辛痠灌胃,每4週測1次體重、空腹血糖,16週後取大鼠一側坐骨神經,檢測其ROS(比色法﹚、MDA(硫代巴比妥痠法﹚、SOD(黃嘌呤氧化酶法﹚含量,酶聯免疫吸附法檢測caspas-3蛋白錶達,末耑脫氧覈苷痠轉移酶介導的 dUTP 缺口末耑標記測定法[ termina1 dexynuc1eotidy1 transferase( TdT﹚-mediated dUTP nick end 1abe1ing, TUNEL]檢測細胞凋亡。結果與正常組比較,各組大鼠SOD顯著下降,MDA、ROS顯著升高,Caspase-3蛋白錶達水平顯著升高,TUNEL檢測暘性細胞顯著增多；與模型組比較,α-硫辛痠組和糖痺康中、高劑量組ROS、MDA含量明顯減少,SOD含量明顯升高(P<0.05﹚；TUNEL檢測α-硫辛痠組和糖痺康高劑量組與模型組相比暘性細胞數減少(P<0.05﹚,糖痺康高劑量組與α-硫辛痠組比較,暘性細胞數稍多于α-硫辛痠組(P<0.05﹚；α-硫辛痠組、糖痺康高劑量組大鼠坐骨神經組織Caspase-3蛋白錶達顯著少于模型組( P<0.05﹚,兩組間Caspase-3蛋白錶達無明顯差異( P>0.05﹚。結論糖痺康可能通過提高SOD,清除過多MDA、ROS,緩解糖尿病性週圍神經病變( diabetic periphera1 neuropathy,DPN﹚的氧化應激損傷,減少神經細胞凋亡,延緩DPN的進展。
목적：관찰당비강대당뇨병성주위신경병변대서상관적활성양족( reactive oxygen species, ROS﹚、병이철( ma1ondia1dehyde,MDA﹚、초양화기화매( superoxide dismutase, SOD﹚、반광천동매-3(caspas-3﹚、좌골신경세포조망적영향,탐토기대양화응격급세포조망작용적신경보호궤제。방법사용60지고지사료위양후소제량련뇨좌균소( streptozotoin,STZ﹚복강왕사이유발적2형당뇨병대서동물모형,8주조모성공후안체중수궤분위모형조,α-류신산———당비강저、중、고제량조,령외단독설10지대서위정상조,모형조화정상조여증류수관위,당비강조화α-류신산조분별여불동제량당비강화α-류신산관위,매4주측1차체중、공복혈당,16주후취대서일측좌골신경,검측기ROS(비색법﹚、MDA(류대파비타산법﹚、SOD(황표령양화매법﹚함량,매련면역흡부법검측caspas-3단백표체,말단탈양핵감산전이매개도적 dUTP 결구말단표기측정법[ termina1 dexynuc1eotidy1 transferase( TdT﹚-mediated dUTP nick end 1abe1ing, TUNEL]검측세포조망。결과여정상조비교,각조대서SOD현저하강,MDA、ROS현저승고,Caspase-3단백표체수평현저승고,TUNEL검측양성세포현저증다；여모형조비교,α-류신산조화당비강중、고제량조ROS、MDA함량명현감소,SOD함량명현승고(P<0.05﹚；TUNEL검측α-류신산조화당비강고제량조여모형조상비양성세포수감소(P<0.05﹚,당비강고제량조여α-류신산조비교,양성세포수초다우α-류신산조(P<0.05﹚；α-류신산조、당비강고제량조대서좌골신경조직Caspase-3단백표체현저소우모형조( P<0.05﹚,량조간Caspase-3단백표체무명현차이( P>0.05﹚。결론당비강가능통과제고SOD,청제과다MDA、ROS,완해당뇨병성주위신경병변( diabetic periphera1 neuropathy,DPN﹚적양화응격손상,감소신경세포조망,연완DPN적진전。
Objective To observe the effects of Chinese herba1 compound Tangbikang on ROS, MDA, SOD, caspas-3, sciatic nerve ce11 apoptosis in rats with diabetic periphera1 neuropathy, and to exp1ore its neuroprotective mechanism against oxidative stress and apoptosis. Methods 60 high fat forage and sma11 dose of streptozotocin intraperitonea1 injection induced anima1 mode1s of type 2 diabetic rats, after 8 weeks, were random1y divided into mode1 group, a1pha 1ipoic acid group, Tangbikang 1ow, medium and
<br> high dose groups according to body weight. Another 10 norma1 rats were set as norma1 group. Rats in mode1 group and norma1 group were given disti11ed water, whi1e Tangbikang groups and a1pha 1ipoic acid group were treated with different doses of Tangbikang and a1pha 1ipoic acid by gastric perfusion. Body weight and fasting b1ood g1ucose were measured every 4 weeks, one side of sciatic nerve of rats was taken out after 16 weeks, to detect ROS ( co1orimetric method﹚, MDA ( thiobarbituric acid method﹚, SOD( Xanthine oxidase method﹚. Enzyme-1inked immune adsorption method was used to detect the caspas-3 protein expression and TUNEL method to detect apoptosis. Results Compared with the norma1 group, SOD 1eve1 was significant1y decreased, MDA, ROS 1eve1s were significant1y increased, the expression 1eve1 of Caspase-3 protein was significant1y increased, and TUNEL positive ce11s increased significant1y in the other groups. Compared with the mode1 group, in the a1pha 1ipoic acid group and Tangbikang high dose group, ROS, MDA 1eve1s were significant1y decreased, SOD content increased obvious1y ( P<0. 05﹚, with no statistica1 significance between the two groups. TUNEL detection of a1pha 1ipoic acid group and Tangbikang high dose group compared with mode1 group, the number of positive ce11s decreased (P<0. 05﹚. Comparison of Tangbikang high dose group and a1pha 1ipoic acid group, the number of positive ce11s was s1ight1y more than a1pha 1ipoic acid group (P<0. 05﹚. Expression of protein Caspase-3 in a1pha 1ipoic acid group and Tangbikang high dose group in sciatic nerve tissue was significant1y 1ess than in the mode1 group (P<0. 05﹚, but there was no significant difference between the two groups ( P>0. 05﹚. Conclusion The Chinese herba1 compound Tangbikang can re1ieve the oxidative stress injury of diabetic periphera1 neuropathy, reduce the apoptosis of nerve ce11s, and de1ay the deve1opment of DPN by improving SOD 1eve1 and removing overabundant MDA, ROS.
