食品研究与开发
食品研究與開髮
식품연구여개발
FOOD RESEARCH AND CEVELOPMENT
2015年
15期
13-15
,共3页
曾泰%马磊%王伟%廖国玲
曾泰%馬磊%王偉%廖國玲
증태%마뢰%왕위%료국령
枸杞黄酮%血管内皮细胞%过氧化氢
枸杞黃酮%血管內皮細胞%過氧化氫
구기황동%혈관내피세포%과양화경
medlar flavonoids%umbilical vein endothelial cells%H2O2
研究枸杞黄酮对过氧化氢（H2O2）损伤血管内皮细胞的保护作用。以体外培养的人脐静脉内皮细胞（HUVEC）为实验对象，H2O2建立HUVEC的损伤模型。试验分正常对照组、过氧化氢损伤组、阳性对照组（VitC）、干预组（枸杞黄酮100、200、400 mg/L预处理）。用MTT法观察枸杞黄酮对H2O2损伤的血管内皮细胞活性的影响，测定内皮细胞中脂质过氧化物丙二醛（MDA）的含量及超氧化物歧化酶（SOD）的活性，分析其保护作用机制。MTT结果表明H2O2损伤后内皮细胞生长抑制率（IR）为38.8%；100、200、400 mg/L枸杞黄酮干预组IR分别为34.0%、30.7%、25.5%，IR显著降低，且与枸杞黄酮浓度呈相关（P<0.01）；干预组中H2O2损伤内皮细胞的MDA生成减少，SOD活力增加，与枸杞黄酮浓度呈相关（P<0.01）。枸杞黄酮的干预对H2O2所致内皮细胞的损伤有保护作用，且随枸杞黄酮浓度的增加，保护作用更强。其机制可能与枸杞黄酮抑制H2O2所致内皮细胞的脂质过氧化以及增强其抗氧化作用有关。
研究枸杞黃酮對過氧化氫（H2O2）損傷血管內皮細胞的保護作用。以體外培養的人臍靜脈內皮細胞（HUVEC）為實驗對象，H2O2建立HUVEC的損傷模型。試驗分正常對照組、過氧化氫損傷組、暘性對照組（VitC）、榦預組（枸杞黃酮100、200、400 mg/L預處理）。用MTT法觀察枸杞黃酮對H2O2損傷的血管內皮細胞活性的影響，測定內皮細胞中脂質過氧化物丙二醛（MDA）的含量及超氧化物歧化酶（SOD）的活性，分析其保護作用機製。MTT結果錶明H2O2損傷後內皮細胞生長抑製率（IR）為38.8%；100、200、400 mg/L枸杞黃酮榦預組IR分彆為34.0%、30.7%、25.5%，IR顯著降低，且與枸杞黃酮濃度呈相關（P<0.01）；榦預組中H2O2損傷內皮細胞的MDA生成減少，SOD活力增加，與枸杞黃酮濃度呈相關（P<0.01）。枸杞黃酮的榦預對H2O2所緻內皮細胞的損傷有保護作用，且隨枸杞黃酮濃度的增加，保護作用更彊。其機製可能與枸杞黃酮抑製H2O2所緻內皮細胞的脂質過氧化以及增彊其抗氧化作用有關。
연구구기황동대과양화경（H2O2）손상혈관내피세포적보호작용。이체외배양적인제정맥내피세포（HUVEC）위실험대상，H2O2건립HUVEC적손상모형。시험분정상대조조、과양화경손상조、양성대조조（VitC）、간예조（구기황동100、200、400 mg/L예처리）。용MTT법관찰구기황동대H2O2손상적혈관내피세포활성적영향，측정내피세포중지질과양화물병이철（MDA）적함량급초양화물기화매（SOD）적활성，분석기보호작용궤제。MTT결과표명H2O2손상후내피세포생장억제솔（IR）위38.8%；100、200、400 mg/L구기황동간예조IR분별위34.0%、30.7%、25.5%，IR현저강저，차여구기황동농도정상관（P<0.01）；간예조중H2O2손상내피세포적MDA생성감소，SOD활력증가，여구기황동농도정상관（P<0.01）。구기황동적간예대H2O2소치내피세포적손상유보호작용，차수구기황동농도적증가，보호작용경강。기궤제가능여구기황동억제H2O2소치내피세포적지질과양화이급증강기항양화작용유관。
To investigate the protective effect of medlar flavonoids on the injury of vascular endothelial cells (VEC) induced by hydrogen peroxide. The endothelial cells strain from human umbilical vein (HUVEC) was cultured and a model of VEC injured by hydrogen peroxide (H2O2) was established. This study was conducted as follows: normal control group, H2O2-injury group (1 000 μmol/L), VitC control group, medlar flavonoids protective groups (100,200,400 mg/L). Cell viability was tested by using MTT. The levels of malondialdehyde (MDA), superoxide dismutase (SOD)were measured with corresponding kits. and analysis its possible mechanisms. MTT result demonstrated that the inhibition ratio of HUVEC was 38.8%under hydrogen peroxide , but the inhibition ratio of medlar flavonoids protective groups were 34.0%,30.7%,25.5%,which were lower than H2O2-injury group .Medlar flavonoids could inhibit the hydrogen peroxide induced VEC reduction , reduced inhibition ratio ,the MDA production, and the activity of SOD was increased under hydrogen peroxide. And showed does-dependent manner. These results demonstrated that medlar flavonoids can protect the VECs from H2O2-induced injury, With the increase of the concentration of medlar flavone, stronger protective effect. The possible mechanism may refer to the its effect of anti-lipid peroxidation and SOD activity enhancing.
