中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2013年
11期
1359-1361
,共3页
何万友%王汉兵%杨承祥%贺简%杨子文%赵伟成
何萬友%王漢兵%楊承祥%賀簡%楊子文%趙偉成
하만우%왕한병%양승상%하간%양자문%조위성
受体作用蛋白丝氨酸苏氨酸激酶类%糖尿病神经病变
受體作用蛋白絲氨痠囌氨痠激酶類%糖尿病神經病變
수체작용단백사안산소안산격매류%당뇨병신경병변
Receptor-interacting protein serine-threonine kinases%Diabetic neuropathies
目的 评价脊髓mTOR在大鼠糖尿病神经痛形成中的作用.方法 健康成年雄性SD大鼠60只,2月龄,体重180~220 g,随机取45只大鼠,腹腔注射链脲霉素(STZ)60 mg/kg,3d后尾静脉血糖> 16.7 mmol/L确定糖尿病造模成功.余下15只大鼠腹腔注射等量的枸橼酸-枸橼酸钠缓冲液作为正常对照组(C组).于造模前、造模后3、6、9、12、15、18、21 d时采用von Frey纤维丝测定右后足机械性痛阀.糖尿病大鼠造模后21 d时机械性痛阈较基础值下降>50%时纳入糖尿病神经痛组(DP组),而机械性痛阈较基础值下降<25%时纳入糖尿病非神经痛组(NP组).于造模后21 d,处死大鼠,取脊髓腰膨大组织,采用Western blot法测定脊髓mTOR与磷酸化mTOR(p-mTOR)的表达水平.结果 与C组比较,DP组和NP组脊髓mTOR表达上调(P<0.05),DP组脊髓p-mTOR表达上调,NP组脊髓p-mTOR表达差异无统计学意义(P>0.05).与NP组比较,DP组p-mTOR表达上调(P<0.05),mTOR表达差异无统计学意义(P>0.05).结论 脊髓mTOR活化参与大鼠糖尿病神经痛的形成.
目的 評價脊髓mTOR在大鼠糖尿病神經痛形成中的作用.方法 健康成年雄性SD大鼠60隻,2月齡,體重180~220 g,隨機取45隻大鼠,腹腔註射鏈脲黴素(STZ)60 mg/kg,3d後尾靜脈血糖> 16.7 mmol/L確定糖尿病造模成功.餘下15隻大鼠腹腔註射等量的枸櫞痠-枸櫞痠鈉緩遲液作為正常對照組(C組).于造模前、造模後3、6、9、12、15、18、21 d時採用von Frey纖維絲測定右後足機械性痛閥.糖尿病大鼠造模後21 d時機械性痛閾較基礎值下降>50%時納入糖尿病神經痛組(DP組),而機械性痛閾較基礎值下降<25%時納入糖尿病非神經痛組(NP組).于造模後21 d,處死大鼠,取脊髓腰膨大組織,採用Western blot法測定脊髓mTOR與燐痠化mTOR(p-mTOR)的錶達水平.結果 與C組比較,DP組和NP組脊髓mTOR錶達上調(P<0.05),DP組脊髓p-mTOR錶達上調,NP組脊髓p-mTOR錶達差異無統計學意義(P>0.05).與NP組比較,DP組p-mTOR錶達上調(P<0.05),mTOR錶達差異無統計學意義(P>0.05).結論 脊髓mTOR活化參與大鼠糖尿病神經痛的形成.
목적 평개척수mTOR재대서당뇨병신경통형성중적작용.방법 건강성년웅성SD대서60지,2월령,체중180~220 g,수궤취45지대서,복강주사련뇨매소(STZ)60 mg/kg,3d후미정맥혈당> 16.7 mmol/L학정당뇨병조모성공.여하15지대서복강주사등량적구연산-구연산납완충액작위정상대조조(C조).우조모전、조모후3、6、9、12、15、18、21 d시채용von Frey섬유사측정우후족궤계성통벌.당뇨병대서조모후21 d시궤계성통역교기출치하강>50%시납입당뇨병신경통조(DP조),이궤계성통역교기출치하강<25%시납입당뇨병비신경통조(NP조).우조모후21 d,처사대서,취척수요팽대조직,채용Western blot법측정척수mTOR여린산화mTOR(p-mTOR)적표체수평.결과 여C조비교,DP조화NP조척수mTOR표체상조(P<0.05),DP조척수p-mTOR표체상조,NP조척수p-mTOR표체차이무통계학의의(P>0.05).여NP조비교,DP조p-mTOR표체상조(P<0.05),mTOR표체차이무통계학의의(P>0.05).결론 척수mTOR활화삼여대서당뇨병신경통적형성.
Objective To evaluate the role of mTOR in spinal cord in the development of diabetic neuropathic pain in rats.Methods Sixty adult male Sprague-Dawley rats,aged 2 months,weighing 180-220 g,were used in the study.Forty-five rats among them were chosen randomly and diabetes mellitus was induced by intraperitoneal streptozotocin (STZ) 60 mg/kg and confirmed by blood glucose > 16.7 mmol/L on day 3 after STZ injection.The left 15 rats received intraperitoneal injection of the equal volume of citric acid-sodium citrate buffer and served as normal control group (group C).Paw withdrawal threshold to von Frey filament stimulation was measured in the right hind paw before STZ injection and on 3,6,9,12,15,18,and 21 days after STZ injection.The diabetic rats with mechanical pain threshold decreasing by more than 50% of the baseline were allocated to diabetic neuropathic pain group (group DP),and by less than 25 % of the baseline were allocated to diabetic non-neuropathic pain group (group NP).The rats were sacrificed at 21 days after STZ injection,and their lumbar enlargements of the spinal cord were removed for determination of the expression of mTOR and phosphorylated mTOR (p-mTOR) by Western blot.Results The expression of mTOR was significantly up-regulated in DP and NP groups when compared with group C (P < 0.05),the expression of p-mTOR was up-regulated in DP group,and no significant change was found in the expression of p-mTOR in group NP (P > 0.05).Compared with group NP,the expression of p-mTOR was significantly up-regulated (P < 0.05),and no significant change was found in the expression of mTOR in group DP (P > 0.05).Conclusion Activation of mTOR in the spinal cord is involved in the development of diabetic neuropathic pain in rats.