中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2014年
4期
430-432
,共3页
黄晓雷%李晓芸%吴铭广%文亚杰%齐晓非%胡薇%李元涛
黃曉雷%李曉蕓%吳銘廣%文亞傑%齊曉非%鬍薇%李元濤
황효뢰%리효예%오명엄%문아걸%제효비%호미%리원도
氧化还原酶类%糖尿病%神经痛%脊髓
氧化還原酶類%糖尿病%神經痛%脊髓
양화환원매류%당뇨병%신경통%척수
Oxidoreductases%Diabetes mellitus%Neuralgia%Spinal cord
目的 评价脊髓烟酰胺腺嘌呤二核苷酸磷酸氧化酶(NADPH氧化酶)在大鼠糖尿病神经痛维持中的作用.方法 清洁级雄性SD大鼠,2月龄,体重180 ~ 220 g,采用腹腔注射1%链脲佐菌素(STZ)的方法制备糖尿病模型,注射STZ后72 h血糖>16.7 mmol/L的大鼠作为糖尿病大鼠.采用随机数字表法,将20只糖尿病大鼠分为2组(n=10):糖尿病神经痛组(DN组)和NADPH氧化酶特异性抑制剂香荚兰乙酮组(A组),另取10只大鼠为正常对照组(C组).A组于注射STZ后28 d腹腔注射香荚兰乙酮5 mg/kg,1次/d,连续7d.分别于注射STZ前(T1)、注射STZ后7、14、21、28、35 d(T2-6)时测定机械缩足反应阈(PWT).于T6时PWT测定结束后,处死大鼠,取L4,5节段脊髓组织,检测NADPH氧化酶亚基gp91phox和p47phox的表达、MDA含量及SOD活性.结果 与C组比较,DN组和A组T3-5时PWT降低,脊髓gp91phpx和p47phox的表达上调,MDA含量升高,SOD活性降低(P<0.05);与DN组比较,A组T6时PWT升高,脊髓gp91phox和p47phox的表达下调,MDA含量降低,SOD活性升高(P<0.05).结论 脊髓NADPH氧化酶参与了大鼠糖尿病神经痛的维持.
目的 評價脊髓煙酰胺腺嘌呤二覈苷痠燐痠氧化酶(NADPH氧化酶)在大鼠糖尿病神經痛維持中的作用.方法 清潔級雄性SD大鼠,2月齡,體重180 ~ 220 g,採用腹腔註射1%鏈脲佐菌素(STZ)的方法製備糖尿病模型,註射STZ後72 h血糖>16.7 mmol/L的大鼠作為糖尿病大鼠.採用隨機數字錶法,將20隻糖尿病大鼠分為2組(n=10):糖尿病神經痛組(DN組)和NADPH氧化酶特異性抑製劑香莢蘭乙酮組(A組),另取10隻大鼠為正常對照組(C組).A組于註射STZ後28 d腹腔註射香莢蘭乙酮5 mg/kg,1次/d,連續7d.分彆于註射STZ前(T1)、註射STZ後7、14、21、28、35 d(T2-6)時測定機械縮足反應閾(PWT).于T6時PWT測定結束後,處死大鼠,取L4,5節段脊髓組織,檢測NADPH氧化酶亞基gp91phox和p47phox的錶達、MDA含量及SOD活性.結果 與C組比較,DN組和A組T3-5時PWT降低,脊髓gp91phpx和p47phox的錶達上調,MDA含量升高,SOD活性降低(P<0.05);與DN組比較,A組T6時PWT升高,脊髓gp91phox和p47phox的錶達下調,MDA含量降低,SOD活性升高(P<0.05).結論 脊髓NADPH氧化酶參與瞭大鼠糖尿病神經痛的維持.
목적 평개척수연선알선표령이핵감산린산양화매(NADPH양화매)재대서당뇨병신경통유지중적작용.방법 청길급웅성SD대서,2월령,체중180 ~ 220 g,채용복강주사1%련뇨좌균소(STZ)적방법제비당뇨병모형,주사STZ후72 h혈당>16.7 mmol/L적대서작위당뇨병대서.채용수궤수자표법,장20지당뇨병대서분위2조(n=10):당뇨병신경통조(DN조)화NADPH양화매특이성억제제향협란을동조(A조),령취10지대서위정상대조조(C조).A조우주사STZ후28 d복강주사향협란을동5 mg/kg,1차/d,련속7d.분별우주사STZ전(T1)、주사STZ후7、14、21、28、35 d(T2-6)시측정궤계축족반응역(PWT).우T6시PWT측정결속후,처사대서,취L4,5절단척수조직,검측NADPH양화매아기gp91phox화p47phox적표체、MDA함량급SOD활성.결과 여C조비교,DN조화A조T3-5시PWT강저,척수gp91phpx화p47phox적표체상조,MDA함량승고,SOD활성강저(P<0.05);여DN조비교,A조T6시PWT승고,척수gp91phox화p47phox적표체하조,MDA함량강저,SOD활성승고(P<0.05).결론 척수NADPH양화매삼여료대서당뇨병신경통적유지.
Objective To evaluate the role of nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase) in the spinal cord in the maintenance of diabetic neuropathic pain in rats.Methods Pathogenfree male Sprague-Dawley rats,aged 2 months,weighing 180-220 g,were used in the study.Diabetes mellitus was induced by intraperitoneal streptozotocin (STZ) 60mg/kg and confirmed by blood glucose > 16.7 mmol/L at 72 h after STZ injection.Twenty diabetic rats were randomly allocated to diabetic neuropathic pain group (DN group,n =10) and apocynin (specific NADPH oxidase inhibitor) group (A group,n =10).Another 10 agematched normal rats served as control group (C group,n =10).Twenty-eight days after STZ injection,apyconin 5 mg/kg was injected intraperitoneally once a day for 7 consecutive days in A group.Paw withdrawal threshold to yon Frey filament stimulation (PWT) was measured before STZ injection (T1) and at 7,14,21,28 and 35 days after STZ injection (T2-6).The rats were sacrificed after PWT was measured at T6 and L4.5 segments of the spinal cord were removed for determination of NADPH oxidase subunits gp91phox and p47phox expression,MAD content and SOD activity.Results Compared with C group,PWT was significantly decreased at T3-5,gp91phox and p47phox expression was up-regulated,MAD content was increased,and SOD activity was decreased in DN and A groups.Compared with DN group,PWT was significantly increased at T6,gp91phox and p47phox expression was downregulated,MAD content was decreased,and SOD activity was increased in A group.Conclusion NADPH oxidase in the spinal cord is involved in the maintenance of diabetic neuropathic pain in rats.