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
9期
812-816
,共5页
红景天苷%糖尿病%脑组织%氧化性应激
紅景天苷%糖尿病%腦組織%氧化性應激
홍경천감%당뇨병%뇌조직%양화성응격
Rhodioloside%Diabetes%Brain%Oxidative stress
目的 研究红景天苷对实验性糖尿病模型大鼠脑组织氧化应激的影响.方法 将大鼠按随机数字表法分为正常对照组,模型组,红景天苷高、中、低剂量组,阳性对照组,每组16只.除正常对照组外,其余各组大鼠采用高糖饮食后,一次性腹腔注射链脲佐菌素制备糖尿病大鼠模型.造模成功后,红景天苷高、中、低剂量组分别灌胃100、50、25 mg/kg红景天苷溶液;阳性对照组灌胃25 mg/kg盐酸二甲双胍溶液,正常对照组、模型组灌胃等体积生理盐水.各组均1次/d,连续给药12周后取材.分别于给药前,给药治疗第4、8、12周测定各组大鼠空腹血糖水平.给药12周后,测定各组大鼠体质量,测定血清中磷酸肌酸激酶(CPK)、乳酸脱氢酶(LDH)、总抗氧化能力(T-AOC);测定脑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-伊红(HE)染色观察脑组织病理学改变.结果 给药12周后,与模型组比较,红景天苷高剂量组大鼠空腹血糖[(16.0±0.9)mmol/L比(18.0±1.2)mmol/L]显著降低(P<0.01),血清中CPK[(240.7±62.3)U/L比 (312.5 ± 78.2)U/L] 、 LDH[(265.4±54.6)U/L 比 (346.3 ± 73.8)U/L] 水平升 高 (P < 0.01) , T-AOC[(10.8±2.8)U/L 比(8.7±2.4)U/L]水平降低(P<0.01),脑组织 SOD[(11.5±3.2)U/mg 比(8.1± 2.9)U/mg]、GSH-Px[(13.1±2.8)U/mg 比(11.4±2.5)U/mg]、CAT[(3.8±1.1)U/mg 比(2.6±0.8)U/mg]升高(P<0.01或P<0.05),MDA[(5.3±1.4)U/mg比(6.3±1.8)U/mg]水平降低(P<0.01).红景天苷治疗组大鼠脑组织病理形态学改变明显改善,以高剂量组最为显著.结论 红景天苷对实验性糖尿病大鼠脑组织具有剂量依赖性的保护作用,该作用可能与红景天苷改善抗氧化酶系统活性、抑制氧化应激损伤有关.
目的 研究紅景天苷對實驗性糖尿病模型大鼠腦組織氧化應激的影響.方法 將大鼠按隨機數字錶法分為正常對照組,模型組,紅景天苷高、中、低劑量組,暘性對照組,每組16隻.除正常對照組外,其餘各組大鼠採用高糖飲食後,一次性腹腔註射鏈脲佐菌素製備糖尿病大鼠模型.造模成功後,紅景天苷高、中、低劑量組分彆灌胃100、50、25 mg/kg紅景天苷溶液;暘性對照組灌胃25 mg/kg鹽痠二甲雙胍溶液,正常對照組、模型組灌胃等體積生理鹽水.各組均1次/d,連續給藥12週後取材.分彆于給藥前,給藥治療第4、8、12週測定各組大鼠空腹血糖水平.給藥12週後,測定各組大鼠體質量,測定血清中燐痠肌痠激酶(CPK)、乳痠脫氫酶(LDH)、總抗氧化能力(T-AOC);測定腦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-伊紅(HE)染色觀察腦組織病理學改變.結果 給藥12週後,與模型組比較,紅景天苷高劑量組大鼠空腹血糖[(16.0±0.9)mmol/L比(18.0±1.2)mmol/L]顯著降低(P<0.01),血清中CPK[(240.7±62.3)U/L比 (312.5 ± 78.2)U/L] 、 LDH[(265.4±54.6)U/L 比 (346.3 ± 73.8)U/L] 水平升 高 (P < 0.01) , T-AOC[(10.8±2.8)U/L 比(8.7±2.4)U/L]水平降低(P<0.01),腦組織 SOD[(11.5±3.2)U/mg 比(8.1± 2.9)U/mg]、GSH-Px[(13.1±2.8)U/mg 比(11.4±2.5)U/mg]、CAT[(3.8±1.1)U/mg 比(2.6±0.8)U/mg]升高(P<0.01或P<0.05),MDA[(5.3±1.4)U/mg比(6.3±1.8)U/mg]水平降低(P<0.01).紅景天苷治療組大鼠腦組織病理形態學改變明顯改善,以高劑量組最為顯著.結論 紅景天苷對實驗性糖尿病大鼠腦組織具有劑量依賴性的保護作用,該作用可能與紅景天苷改善抗氧化酶繫統活性、抑製氧化應激損傷有關.
목적 연구홍경천감대실험성당뇨병모형대서뇌조직양화응격적영향.방법 장대서안수궤수자표법분위정상대조조,모형조,홍경천감고、중、저제량조,양성대조조,매조16지.제정상대조조외,기여각조대서채용고당음식후,일차성복강주사련뇨좌균소제비당뇨병대서모형.조모성공후,홍경천감고、중、저제량조분별관위100、50、25 mg/kg홍경천감용액;양성대조조관위25 mg/kg염산이갑쌍고용액,정상대조조、모형조관위등체적생리염수.각조균1차/d,련속급약12주후취재.분별우급약전,급약치료제4、8、12주측정각조대서공복혈당수평.급약12주후,측정각조대서체질량,측정혈청중린산기산격매(CPK)、유산탈경매(LDH)、총항양화능력(T-AOC);측정뇌조직중초양화물기화매(SOD)、곡광감태과양화물매(GSH-Px)、과양화경매(CAT)、병이철(MDA)수평;채용소목정-이홍(HE)염색관찰뇌조직병이학개변.결과 급약12주후,여모형조비교,홍경천감고제량조대서공복혈당[(16.0±0.9)mmol/L비(18.0±1.2)mmol/L]현저강저(P<0.01),혈청중CPK[(240.7±62.3)U/L비 (312.5 ± 78.2)U/L] 、 LDH[(265.4±54.6)U/L 비 (346.3 ± 73.8)U/L] 수평승 고 (P < 0.01) , T-AOC[(10.8±2.8)U/L 비(8.7±2.4)U/L]수평강저(P<0.01),뇌조직 SOD[(11.5±3.2)U/mg 비(8.1± 2.9)U/mg]、GSH-Px[(13.1±2.8)U/mg 비(11.4±2.5)U/mg]、CAT[(3.8±1.1)U/mg 비(2.6±0.8)U/mg]승고(P<0.01혹P<0.05),MDA[(5.3±1.4)U/mg비(6.3±1.8)U/mg]수평강저(P<0.01).홍경천감치료조대서뇌조직병리형태학개변명현개선,이고제량조최위현저.결론 홍경천감대실험성당뇨병대서뇌조직구유제량의뢰성적보호작용,해작용가능여홍경천감개선항양화매계통활성、억제양화응격손상유관.
Objective To investigate the protection of Rhodioloside on brain tissue in diabetic rats. Methods The rats were randomly divided into six groups: a normal control group, a model control group, a Rhodioloside high, medium and low dose group, and a positive control group(n=16). Except normal control group, the diabetic models were set up by intraperitoneal injecting STZ(60 mg/kg). And then, the Rhodioloside high, medium, low dose group were respectively given Rhodioloside solution(100、50、25 mg/kg) by intragastrical administration(ig), the positive control group was given metformin hydrochloride(25 mg/kg) by ig, the normal control group and positive control group were given normal saline(NS). Before the drug was given and 4, 8, 12 weeks after, the level of blood sugar was determined. And 12 weeks later, the body weight was detected; the activity of CPK, LDH and the level of T-AOC in serum were determined; the activity of SOD, GSH-Px, CAT and the content of MDA in brain tissue were determined; and the histopathological changes of the brain tissue was observed by HE staining.Results Compared with the model control group, the level of blood sugar (16.0 ± 0.9 mmol/Lvs. 18.0 ± 1.2 mmol/L) in Rhodioloside high dose group was significantly decreased (P<0.01), the activity of CPK(240.7 ± 62.3 U/Lvs. 312.5 ± 78.2 U/L) and LDH (265.4 ± 54.6 U/Lvs. 346.3 ± 73.8 U/L) in serum were significantly decreased (P<0.01), the level of T-AOC (10.8 ± 2.8 U/Lvs. 8.7 ± 2.4U/L) was significantly increased (P<0.01); the activity of SOD(11.5 ± 3.2 U/mgvs. 8.1 ± 2.9 U/mg), GSH-Px(13.1 ± 2.8 U/mgvs. 11.4 ± 2.5 U/mg), CAT(3.8 ± 1.1 U/mgvs. 2.6 ± 0.8 U/mg) in brain tissue were significantly increased (P<0.05,P<0.01), and the content of MDA (5.3 ± 1.4 U/mgvs. 6.3 ± 1.8 U/mg) in brain tissue were significantly decreased (P<0.01), which were better than Rhodioloside low dose group; but compared with positive control group, the difference was not significant (P>0.05). The brain histopathological changes of Sal treated groups were significantly improved, while the treatment effect of Rhodioloside high dose group was the most significant.Conclusions Rhodioloside had dose-dependent protective effect on the brain tissue in diabetic rats, whose mechanism perhaps related to its effects on enhancing the activity of antioxidant enzymes, and reducing the damage of oxidative stress.
