国际中医中药杂志
國際中醫中藥雜誌
국제중의중약잡지
INTERNATIONAL JOURNAL OF TRIDITIONAL CHINESE MEDICINE
2011年
7期
597-600
,共4页
龙少华%李晓丹%于竹芹%帅莉%符鹏飞%郭云良%段德麟
龍少華%李曉丹%于竹芹%帥莉%符鵬飛%郭雲良%段德麟
룡소화%리효단%우죽근%수리%부붕비%곽운량%단덕린
海带%糖尿病%四氧嘧啶%氧化应激
海帶%糖尿病%四氧嘧啶%氧化應激
해대%당뇨병%사양밀정%양화응격
Laminaria japonica%Diabetes mellitus%Alloxan%Oxidative stress
目的 探讨海带对四氧嘧啶糖尿病(DM)大鼠血糖影响的机制.方法 成年健康雌性Wister大鼠60只,采用随机数字表法随机取10只作为正常对照组,其余50只腹腔注射四氧嘧啶建立高血糖大鼠模型.造模成功的40只按随机数字表法分为DM模型组、治疗A组(低剂量海带饲料,相当于2.5 g/kg·d-1体重)、治疗B组(中剂量海带粉饲料,相当于10 g/kg·d-1体重),治疗C组(高剂量海带粉饲料,相当于25 g/kg·d-1体重),每组各10只.检测大鼠空腹血糖(FBG)、血清胰岛素(Insulin)水平,观察胰岛细胞的形态结构,检测胰岛细胞超氧化物歧化酶(SOD)和诱导性一氧化氮合酶(iNOS)的表达.结果 治疗B组、C组大鼠血清FBG水平[分别为(9.37±1.70)mmol/L、(9,18±1165)mmol/L]较DM模型组[(12.63±1.67)mmol/L]显著降低(F=32.81,q=6.35～11.72,P<0.05),治疗A组、B组、C组血清Insulin水平吸光度值A[分别为(0.0378±0.0026)、(0.0378±0.0027)、(0.0367±0.0035)]均较DM模型组(0.04564±0.0057)升高(F=11.40,q=4.28～8.47,P<0.05),胰岛细胞组织结构病变减轻,治疗B组、C组大鼠胰岛细胞SOD表达较DM模型组明显增强(t=4.73～4.76,P<0.05),iNOS表达较DM模型组显著降低(t=4.81～5.30,P<0.05).结论 海带可通过增强抗氧化作用,促进胰岛细胞分泌功能恢复而降低血糖.
目的 探討海帶對四氧嘧啶糖尿病(DM)大鼠血糖影響的機製.方法 成年健康雌性Wister大鼠60隻,採用隨機數字錶法隨機取10隻作為正常對照組,其餘50隻腹腔註射四氧嘧啶建立高血糖大鼠模型.造模成功的40隻按隨機數字錶法分為DM模型組、治療A組(低劑量海帶飼料,相噹于2.5 g/kg·d-1體重)、治療B組(中劑量海帶粉飼料,相噹于10 g/kg·d-1體重),治療C組(高劑量海帶粉飼料,相噹于25 g/kg·d-1體重),每組各10隻.檢測大鼠空腹血糖(FBG)、血清胰島素(Insulin)水平,觀察胰島細胞的形態結構,檢測胰島細胞超氧化物歧化酶(SOD)和誘導性一氧化氮閤酶(iNOS)的錶達.結果 治療B組、C組大鼠血清FBG水平[分彆為(9.37±1.70)mmol/L、(9,18±1165)mmol/L]較DM模型組[(12.63±1.67)mmol/L]顯著降低(F=32.81,q=6.35～11.72,P<0.05),治療A組、B組、C組血清Insulin水平吸光度值A[分彆為(0.0378±0.0026)、(0.0378±0.0027)、(0.0367±0.0035)]均較DM模型組(0.04564±0.0057)升高(F=11.40,q=4.28～8.47,P<0.05),胰島細胞組織結構病變減輕,治療B組、C組大鼠胰島細胞SOD錶達較DM模型組明顯增彊(t=4.73～4.76,P<0.05),iNOS錶達較DM模型組顯著降低(t=4.81～5.30,P<0.05).結論 海帶可通過增彊抗氧化作用,促進胰島細胞分泌功能恢複而降低血糖.
목적 탐토해대대사양밀정당뇨병(DM)대서혈당영향적궤제.방법 성년건강자성Wister대서60지,채용수궤수자표법수궤취10지작위정상대조조,기여50지복강주사사양밀정건립고혈당대서모형.조모성공적40지안수궤수자표법분위DM모형조、치료A조(저제량해대사료,상당우2.5 g/kg·d-1체중)、치료B조(중제량해대분사료,상당우10 g/kg·d-1체중),치료C조(고제량해대분사료,상당우25 g/kg·d-1체중),매조각10지.검측대서공복혈당(FBG)、혈청이도소(Insulin)수평,관찰이도세포적형태결구,검측이도세포초양화물기화매(SOD)화유도성일양화담합매(iNOS)적표체.결과 치료B조、C조대서혈청FBG수평[분별위(9.37±1.70)mmol/L、(9,18±1165)mmol/L]교DM모형조[(12.63±1.67)mmol/L]현저강저(F=32.81,q=6.35～11.72,P<0.05),치료A조、B조、C조혈청Insulin수평흡광도치A[분별위(0.0378±0.0026)、(0.0378±0.0027)、(0.0367±0.0035)]균교DM모형조(0.04564±0.0057)승고(F=11.40,q=4.28～8.47,P<0.05),이도세포조직결구병변감경,치료B조、C조대서이도세포SOD표체교DM모형조명현증강(t=4.73～4.76,P<0.05),iNOS표체교DM모형조현저강저(t=4.81～5.30,P<0.05).결론 해대가통과증강항양화작용,촉진이도세포분비공능회복이강저혈당.
Objective To investigate the hypoglycemic effects of Laminaria japonica (L. japonica) on diabetic model induced by alloxan in rats. Methods Sixty healthy female rats were used to establish diabetic models by injecting alloxan peritoneally, and L.japonica was applied as raw materials for potential marine drugs.The levels of fasting blood glucose (FBG) were detected by automatic blood glucose device. Enzyme linkedimmunoabsorbant assay was applied to determine the insulin level in serum. The shape and structure of isletcells were observed with histopathological staining, and the expression of superoxide dismutase (SOD) and inducible nitric oxide synthase (iNOS) in islet cells were detected by immunohistochemical technique. Results After the treatment, the levels of FBG of L.japonica treated group B [(9.37±1.70) mmol/LandC (9.18±1.65 ) mmol/L, F= 32.81, q=6.35～11.72, P<0.05 ] reduced, while the serum levels of insulin in treated group A, Band C (0.0378±0.0026, 0.0378±0.0027, 0.0367±0.0035) increased(F= 11.40, q=4.28～8.47, P<0.05) significantly than those of diabetic model group (0.0456 ±0.0057) . The shape and structure of islet cells improved with the up-expressing SOD(t=4.73～4.76, P<0.05)and down-expressing iNOS (t=4.81～5.30, P<0.05) in L.japonica treated group B and C than those in diabetic model group. Conclusion L.japonica might decrease the serum level of FBG through promoting the islet cell recovery by an anti-oxide effect.
