中华糖尿病杂志
中華糖尿病雜誌
중화당뇨병잡지
CHINES JOURNAL OF DLABETES MELLITUS
2009年
1期
43-46
,共4页
代喆%徐焱成%季振中%牛力
代喆%徐焱成%季振中%牛力
대철%서염성%계진중%우력
氧化性应激%脂联素%瘦素%抵抗素%内脏脂肪素
氧化性應激%脂聯素%瘦素%牴抗素%內髒脂肪素
양화성응격%지련소%수소%저항소%내장지방소
Oxidative stress%Adiponectin%Leptin%Resistin%Visfatin
目的 探讨氧化应激对于脂肪细胞因子脂联素、瘦素、抵抗素和内脏脂肪素表达和分泌的影响.方法 体外培养小鼠3T3-L1前脂肪细胞,并诱导其分化成熟.通过在高糖培养基中加入葡萄糖激酶制作氧化应激模型.分为4个试验组,分为四个试验组,A组:观察不同浓度的葡萄糖激酶对七述脂肪细胞因子的影响;B组:不同浓度的抗氧化应激物N乙酰半胱氨酸(NAC)拮抗氧化应激后,对脂肪细胞因子的作用;C组:NAC作用不同时间对抗氧化应激作用的影响;D组:观察氧化应激伴或不伴拮抗效应对脂肪细胞因子的影响.结果 (1)脂联素、瘦素、抵抗素和内脏脂肪素的表达随着葡萄糖激酶浓度的增加呈现浓度依赖性抑制,其中脂联素和瘦素的这种效应更为明显[葡萄糖激酶浓度25 U/L时,脂联素水平达(6.94±0.07)ng/L,瘦素水平达(0.64±0.11)ng/L,与空白对照组相比,均P<0.01];(2)随着NAC作用持续时间的延长,脂联素、瘦素、抵抗素和内脏脂肪素表达增加[NAC作用16 h,脂联素水平达(19.22±0.27)ng/L,瘦素水平达(2.95±0.22)ng/L,与空白对照组相比,均P<0.01];(3)在同一葡萄糖激酶浓度下(25 U/L),随着NAC浓度的增加,脂联素、瘦素、抵抗素和内脏脂肪素表达旱现浓度依赖性增加(与空白对照组相比,NAC 25 mmol/L组脂联素、瘦素、抵抗素和内脏脂肪素t值分别为6.88、6.96、4.52、3.15,均P<0.05);(4)与空白对照组相比,NAC作用组的脂联素、瘦素、抵抗素和内脏脂肪素表达明显增加,葡萄糖激酶作用组脂联素、瘦素、抵抗素和内脏脂肪素表达明显减少.结论 氧化应激对于脂肪细胞因子的表达有明显影响,对抗氧化应激可改善这种作用.此作用可能是氧化应激参与胰岛索抵抗和代谢功能紊乱的机制之一.
目的 探討氧化應激對于脂肪細胞因子脂聯素、瘦素、牴抗素和內髒脂肪素錶達和分泌的影響.方法 體外培養小鼠3T3-L1前脂肪細胞,併誘導其分化成熟.通過在高糖培養基中加入葡萄糖激酶製作氧化應激模型.分為4箇試驗組,分為四箇試驗組,A組:觀察不同濃度的葡萄糖激酶對七述脂肪細胞因子的影響;B組:不同濃度的抗氧化應激物N乙酰半胱氨痠(NAC)拮抗氧化應激後,對脂肪細胞因子的作用;C組:NAC作用不同時間對抗氧化應激作用的影響;D組:觀察氧化應激伴或不伴拮抗效應對脂肪細胞因子的影響.結果 (1)脂聯素、瘦素、牴抗素和內髒脂肪素的錶達隨著葡萄糖激酶濃度的增加呈現濃度依賴性抑製,其中脂聯素和瘦素的這種效應更為明顯[葡萄糖激酶濃度25 U/L時,脂聯素水平達(6.94±0.07)ng/L,瘦素水平達(0.64±0.11)ng/L,與空白對照組相比,均P<0.01];(2)隨著NAC作用持續時間的延長,脂聯素、瘦素、牴抗素和內髒脂肪素錶達增加[NAC作用16 h,脂聯素水平達(19.22±0.27)ng/L,瘦素水平達(2.95±0.22)ng/L,與空白對照組相比,均P<0.01];(3)在同一葡萄糖激酶濃度下(25 U/L),隨著NAC濃度的增加,脂聯素、瘦素、牴抗素和內髒脂肪素錶達旱現濃度依賴性增加(與空白對照組相比,NAC 25 mmol/L組脂聯素、瘦素、牴抗素和內髒脂肪素t值分彆為6.88、6.96、4.52、3.15,均P<0.05);(4)與空白對照組相比,NAC作用組的脂聯素、瘦素、牴抗素和內髒脂肪素錶達明顯增加,葡萄糖激酶作用組脂聯素、瘦素、牴抗素和內髒脂肪素錶達明顯減少.結論 氧化應激對于脂肪細胞因子的錶達有明顯影響,對抗氧化應激可改善這種作用.此作用可能是氧化應激參與胰島索牴抗和代謝功能紊亂的機製之一.
목적 탐토양화응격대우지방세포인자지련소、수소、저항소화내장지방소표체화분비적영향.방법 체외배양소서3T3-L1전지방세포,병유도기분화성숙.통과재고당배양기중가입포도당격매제작양화응격모형.분위4개시험조,분위사개시험조,A조:관찰불동농도적포도당격매대칠술지방세포인자적영향;B조:불동농도적항양화응격물N을선반광안산(NAC)길항양화응격후,대지방세포인자적작용;C조:NAC작용불동시간대항양화응격작용적영향;D조:관찰양화응격반혹불반길항효응대지방세포인자적영향.결과 (1)지련소、수소、저항소화내장지방소적표체수착포도당격매농도적증가정현농도의뢰성억제,기중지련소화수소적저충효응경위명현[포도당격매농도25 U/L시,지련소수평체(6.94±0.07)ng/L,수소수평체(0.64±0.11)ng/L,여공백대조조상비,균P<0.01];(2)수착NAC작용지속시간적연장,지련소、수소、저항소화내장지방소표체증가[NAC작용16 h,지련소수평체(19.22±0.27)ng/L,수소수평체(2.95±0.22)ng/L,여공백대조조상비,균P<0.01];(3)재동일포도당격매농도하(25 U/L),수착NAC농도적증가,지련소、수소、저항소화내장지방소표체한현농도의뢰성증가(여공백대조조상비,NAC 25 mmol/L조지련소、수소、저항소화내장지방소t치분별위6.88、6.96、4.52、3.15,균P<0.05);(4)여공백대조조상비,NAC작용조적지련소、수소、저항소화내장지방소표체명현증가,포도당격매작용조지련소、수소、저항소화내장지방소표체명현감소.결론 양화응격대우지방세포인자적표체유명현영향,대항양화응격가개선저충작용.차작용가능시양화응격삼여이도색저항화대사공능문란적궤제지일.
Objective To investigate the influence of oxidative stress on expression and secretion of adiponectin, leptin, resisitin and visfatin in adipocytes. Methods In vitro culture 3T3-L1 preadipocyte, induce the cell differentiation and maturity. Adding glucokinase into high-glucose culture media to make oxidative modeL The cultured cells were divided into four groups for experiment, Group A: the expression of adipanectin, leptin, resistin and visfatin were examined in different concentration of glucokinase; Group B: the expression of above mentioned 4 adipocytokines were examined after against oxidative stress in different concentration of N - acetyl eysteine(NAG) ; Group C : the effect of different time period of NAC against the oxidative stress; Group D: oxidative stress with or without antagonistic effect on the above 4 adipocytokines.Results (1) With the increase of glucokinase concentration, concentration-dependent inhibition of expression were observed with adiponectin, leptin, visfatin and resistin. Among these, adiponectin and ghcokinase concentration of 25 U/L, all P <0.01 compared with control). (2) With the extension of NAC incubation duration, the expression of adiponectin, leptin, resistin and visfatin were increased (adiponectin with control). (3) With the same concentration of glucose oxidase (25 U/L), concentration-dependent increase of adipokine expression were observed with the increase of NAC concentration(adiponectin t = 6.88, leptin t = 6.96, resistin t = 4.52, visfatin t = 3.15 with NAC concentration of 25 mmol/L, all P < 0.05) . (4) Compared with the blank control, the expression of adiponectin, leptin, visfatin and resistin in NAC group were increased significantly, the expression of the adipokines were decreased significantly in glucokinase group. Conclusions Oxidative stress has significant influence on adiponectin, leptin, resistin and visfatin expression in adipocytes. Anti-oxidative can improve this effect. The influence of oxidative stress on adipokines maybe one of the mechanisms of insulin resistance and metabolic dysfunction pathogenesis.