国际中医中药杂志
國際中醫中藥雜誌
국제중의중약잡지
International Journal of Traditional Chinese Medicine
2015年
10期
909-913
,共5页
番茄红素%糖尿病,2型%氧化性应激%大鼠
番茄紅素%糖尿病,2型%氧化性應激%大鼠
번가홍소%당뇨병,2형%양화성응격%대서
Lycopene%Diabetes mellitus%type 2%Oxidative stress%Rats
目的 探讨番茄红素对2型糖尿病大鼠肝脏氧化应激损伤的保护作用.方法 将80只大鼠按随机数字表法分为正常对照组,模型组,番茄红素低、高剂量组各20只.除正常对照组外,其余各组大鼠通过高脂高糖饮食和腹腔注射链脲佐菌素(STZ)制备2型糖尿病大鼠模型.造模成功后,番茄红素低、高剂量组分别灌胃番茄红素溶液10、20 mg/kg,正常对照组及模型组灌胃等体积生理盐水.连续给药4周,1次/d.分别于给药前和给药后2、4周测定各组大鼠空腹血糖水平.4周后,测定各组大鼠体质量和肝脏指数;检测血清中谷氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、碱性磷酸酶(ALP)、总抗氧化能力(T-AOC)水平;测定肝组织中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)、丙二醛(MDA)水平;采用苏木精-尹红(HE)染色观察肝脏组织病理改变.结果 与模型组比较,番茄红素高、低剂量组大鼠血清中ALT[(714.8±291.5)U/L、(862.7±348.1)U/L比(1 007.6±375.7)U/L]、AST[(75.2±18.6)U/L、(87.6±20.3)U/L 比(99.3±21.5)U/L]、肝组织 MDA[(5.56±1.02)U/L、(5.83± 0.98)U/L 比(6.37 ± 1.18)U/L]均降低(P<0.05 或 P<0.01);番茄红素高剂量组大鼠血糖水平[(16.6 ± 1.1)mmol/L 比(17.9±1.2)mmol/L]、肝脏指数[(26.2±5.3)‰比(30.4±5.8)‰]降低,体质量[(281.5± 24.8)g 比(252.3 ± 23.5)g]增加,血清中 ALP[(135.2 ± 30.8)U/L 比(167.4 ± 32.5)U/L]活性降低、T-AOC[(10.8±2.8)U/L比(8.7±2.4)U/L]水平升高,肝组织中SOD[(10.8±2.3)U/mg比(9.1±2.3)U/mg]、GSH-Px[(16.1±3.4)U/mg 比(14.3±3.5)U/mg]、CAT[(3.16±1.08)U/mg 比(2.63±0.90)U/mg]升高(P<0.05或P<0.01).结论 番茄红素对2型糖尿病大鼠肝脏组织氧化应激损伤具有保护作用.
目的 探討番茄紅素對2型糖尿病大鼠肝髒氧化應激損傷的保護作用.方法 將80隻大鼠按隨機數字錶法分為正常對照組,模型組,番茄紅素低、高劑量組各20隻.除正常對照組外,其餘各組大鼠通過高脂高糖飲食和腹腔註射鏈脲佐菌素(STZ)製備2型糖尿病大鼠模型.造模成功後,番茄紅素低、高劑量組分彆灌胃番茄紅素溶液10、20 mg/kg,正常對照組及模型組灌胃等體積生理鹽水.連續給藥4週,1次/d.分彆于給藥前和給藥後2、4週測定各組大鼠空腹血糖水平.4週後,測定各組大鼠體質量和肝髒指數;檢測血清中穀氨痠轉氨酶(ALT)、天鼕氨痠轉氨酶(AST)、堿性燐痠酶(ALP)、總抗氧化能力(T-AOC)水平;測定肝組織中超氧化物歧化酶(SOD)、穀胱甘肽過氧化物酶(GSH-Px)、過氧化氫酶(CAT)、丙二醛(MDA)水平;採用囌木精-尹紅(HE)染色觀察肝髒組織病理改變.結果 與模型組比較,番茄紅素高、低劑量組大鼠血清中ALT[(714.8±291.5)U/L、(862.7±348.1)U/L比(1 007.6±375.7)U/L]、AST[(75.2±18.6)U/L、(87.6±20.3)U/L 比(99.3±21.5)U/L]、肝組織 MDA[(5.56±1.02)U/L、(5.83± 0.98)U/L 比(6.37 ± 1.18)U/L]均降低(P<0.05 或 P<0.01);番茄紅素高劑量組大鼠血糖水平[(16.6 ± 1.1)mmol/L 比(17.9±1.2)mmol/L]、肝髒指數[(26.2±5.3)‰比(30.4±5.8)‰]降低,體質量[(281.5± 24.8)g 比(252.3 ± 23.5)g]增加,血清中 ALP[(135.2 ± 30.8)U/L 比(167.4 ± 32.5)U/L]活性降低、T-AOC[(10.8±2.8)U/L比(8.7±2.4)U/L]水平升高,肝組織中SOD[(10.8±2.3)U/mg比(9.1±2.3)U/mg]、GSH-Px[(16.1±3.4)U/mg 比(14.3±3.5)U/mg]、CAT[(3.16±1.08)U/mg 比(2.63±0.90)U/mg]升高(P<0.05或P<0.01).結論 番茄紅素對2型糖尿病大鼠肝髒組織氧化應激損傷具有保護作用.
목적 탐토번가홍소대2형당뇨병대서간장양화응격손상적보호작용.방법 장80지대서안수궤수자표법분위정상대조조,모형조,번가홍소저、고제량조각20지.제정상대조조외,기여각조대서통과고지고당음식화복강주사련뇨좌균소(STZ)제비2형당뇨병대서모형.조모성공후,번가홍소저、고제량조분별관위번가홍소용액10、20 mg/kg,정상대조조급모형조관위등체적생리염수.련속급약4주,1차/d.분별우급약전화급약후2、4주측정각조대서공복혈당수평.4주후,측정각조대서체질량화간장지수;검측혈청중곡안산전안매(ALT)、천동안산전안매(AST)、감성린산매(ALP)、총항양화능력(T-AOC)수평;측정간조직중초양화물기화매(SOD)、곡광감태과양화물매(GSH-Px)、과양화경매(CAT)、병이철(MDA)수평;채용소목정-윤홍(HE)염색관찰간장조직병리개변.결과 여모형조비교,번가홍소고、저제량조대서혈청중ALT[(714.8±291.5)U/L、(862.7±348.1)U/L비(1 007.6±375.7)U/L]、AST[(75.2±18.6)U/L、(87.6±20.3)U/L 비(99.3±21.5)U/L]、간조직 MDA[(5.56±1.02)U/L、(5.83± 0.98)U/L 비(6.37 ± 1.18)U/L]균강저(P<0.05 혹 P<0.01);번가홍소고제량조대서혈당수평[(16.6 ± 1.1)mmol/L 비(17.9±1.2)mmol/L]、간장지수[(26.2±5.3)‰비(30.4±5.8)‰]강저,체질량[(281.5± 24.8)g 비(252.3 ± 23.5)g]증가,혈청중 ALP[(135.2 ± 30.8)U/L 비(167.4 ± 32.5)U/L]활성강저、T-AOC[(10.8±2.8)U/L비(8.7±2.4)U/L]수평승고,간조직중SOD[(10.8±2.3)U/mg비(9.1±2.3)U/mg]、GSH-Px[(16.1±3.4)U/mg 비(14.3±3.5)U/mg]、CAT[(3.16±1.08)U/mg 비(2.63±0.90)U/mg]승고(P<0.05혹P<0.01).결론 번가홍소대2형당뇨병대서간장조직양화응격손상구유보호작용.
Objective To investigate the protective effects of Lycopene (LP) on hepatic oxidative stress injury in type 2 diabetic rats.Methods The diabetic rat models were setup by intraperitoneal injecting STZ (60 mg/kg). 60 models were selected and randomly divided into three groups: diabetes model control group, LP 10 and 20 mg/kg treated groups, with 20 experimental animals in each group. While, selected another 20 normal same-aged rats as normal control group. The drug was given by intragastric administration for 4 weeks, once a day. Before the drug was given and after 2, 4 weeks, the level of blood sugar was determined. Four weeks later, the body weight and hepatic index were detected; the activity of ALT, AST, ALP and the level of T-AOC in serum were determined; the activity of SOD, GSH-Px, CAT and the content of MDA in hepatic tissue were determined; and the hepatic tissue histopathological changes was observed by HE staining.Results Compared with the diabetes model group, the activity of ALT in serum of LP 10, 20 mg/kg treated groups was significantly decreased (714.8±291.5 U/L, 862.7±348.1 U/Lvs. 1 007.6±375.7 U/L); AST was significantly decreased (75.2±18.6 U/L, 87.6±20.3 U/L vs. 99.3±21.5 U/L); and the content of MDA in hepatic tissue was significantly decreased (5.56±1.02 U/L, 5.83±0.98 U/L vs. 6.37±1.18 U/L); the blood sugar level of LP 20 mg/kg treated group was significantly decreased(16.6±1.1 mmol/L vs. 17.9±1.2 mmol/L), the body weight was significantly increased(281.5±24.8 g vs. 252.3±23.5g) and the hepatic index was significantly decreased (26.2±5.3 ‰vs. 30.4±5.8‰), the activity of ALP in serum was significantly decreased (135.2±30.8 U/L vs. 167.4±32.5 U/L) and the level of T-AOC was significantly increased (10.8±2.8 U/L vs. 8.7±2.4 U/L), the activity of SOD in hepatic tissue was significantly increased(10.8±2.3 U/mgvs. 9.1±2.3 U/mg), GSH-Px was significantly increased (16.1±3.4 U/mgvs. 14.3±3.5 U/mg), CAT was significantly increased (3.16± 1.08 U/mgvs. 2.63±0.90 U/mg).Conclusion LP had dose-dependent protective effect for hepatic oxidative stress injury in type 2 diabetic rats.
