α-硫辛酸、银杏叶提取物对波动高糖所致人视网膜色素上皮细胞损伤的作用
| 作者: |
1李立琴,
1张云良,
1郭淑芹,
1王翯,
2靳丽丽,
1董越华,
1辛欢欢,
1刘莉芳
1 保定市第一中心医院内分泌科，河北 保定 071000 2 保定市第一中心医院心血管心血管内五科，河北 保定 071000 |
| 通讯: |
张云良
Email: zhangyunliangnfm@sina.com |
| DOI: | 10.3978/j.issn.2095-6959.2017.09.005 |
摘要
研究α-硫辛酸(alpha lipoic acid，ALA)、银杏叶提取物(Gingko biloba，EGb761)对波动性高糖所致人视网膜色素上皮细胞(human retinal pigment epithelial，HRPE)氧化应激和炎性损伤的保护作用。方法：培养HRPE细胞株，取生长良好的对数期细胞用于实验，换用不同条件培养液，分10组进行试验。1)5.5 mmol/L葡萄糖对照组(N组)；2)33 mmol/L持续高糖组(H组)；3)5.5~33 mmol/L波动葡萄糖组(F组)；4)33 mmol/L渗透压对照组(P组)；5)ALA50干预组(ALA50组)：5.5~33 mmol/L波动葡萄糖组+50 μmol/L ALA；6)ALA100干预组(ALA100组)：5.5~33 mmol/L波动葡萄糖组+100 μmol/L ALA；7)ALA200干预组(ALA200组)：5.5~33 mmol/L波动葡萄糖组+200 μmol/L ALA；8)EGb7610.1干预组(EGb7610.1组)：5.5~33 mmol/L波动葡萄糖组+0.1 g/L EGb761；9)EGb7610.5干预组(EGb7610.5组)：5.5~33 mmol/L波动葡萄糖组+0.5 g/L EGb761；10)EGb7611.0干预组(EGb7611.0组)：5.5~33 mmol/L波动葡萄糖组+1.0 g/L EGb761。各组细胞培养72 h，72 h时检测各组HRPE细胞上清液中SOD，GSH，MDA，TNF-α与ICAM-1 的含量。采用SPSS18.0软件进行统计学分析。结果：与正常对照组相比，持续高糖组、波动性高糖组、ALA干预组(ALA50，ALA100，ALA200)、EGb761干预组(EGb7610.1，EGb7610.5，EGb7611.0)的SOD，GSH，MDA，TNF-α与ICAM-1含量差异有统计学意义(分别为FSOD=67.936，FGSH=71.363，FMDA=81.123，FTNF-α=70.684，FICAM-1=80.193；均P<0.05)；渗透压对照组与正常对照组相比各指标差异均无统计学意义(P>0.05)；波动性高糖组与持续性高糖组相比，SOD活性、GSH含量明显下降，MDA、ICAM-1与TNF-α的表达量明显升高(均P<0.05)。ALA干预组(ALA50，ALA100，ALA200)、EGb761干预组(EGb7610.1，EGb7610.5，EGb7611.0)与波动性高塘组相比，各组有统计学差异，且随药物剂量增加，SOD活性、GSH含量增加，MDA，ICAM-1与TNF-α的表达量下降，存在剂量相关性(均P<0.05)。结论：ALA，EGb761可能通过降低波动性高血糖对人HRPE所致氧化应激水平，减轻炎性反应，对波动性高血糖所导致的病理损伤有一定保护作用。
关键词：
血糖波动
α-硫辛酸
银杏叶提取物
氧化应激
炎性损伤
Effect of alpha lipoic acid and Gingko biloba extract on the damage of human retinal pigment epithelial induced by the intermittent high level of glucose
CorrespondingAuthor: ZHANG Yunliang Email: zhangyunliangnfm@sina.com
DOI: 10.3978/j.issn.2095-6959.2017.09.005
Abstract
To evaluate the protective effect of alpha lipoic acid (ALA) and Gingko biloba extract (EGb761) on the oxidative stress and inflammatory response induced by the intermittent high level of glucose in human retinal pigment epithelial (HRPE) cells. Methods: HRPE cells were randomly divided into different groups and were cultured for continuous 3 days. The ten experimental groups were followed as: the normal glucose group (group N), the sustained high glucose group (group H), the intermittent high glucose group (group F) and the high osmotic pressure group (group P), the intermittent high glucose group with various concentrations of ALA (group ALA50, ALA100, ALA200) and the intermittent high glucose group plus various concentrations of low, medium, and high concentrations of EGb761 groups (group EGb7610.1, EGb7610.5, EGb7611.0). The cells were all cultured for 72 h, then the level of SOD, GSH, MDA, TNF-α, and ICAM-1 were measured. The software SPSS 18.0 was used for statistically analysis. Results: Compared with the normal glucose group, the differences in the level of SOD, GSH, MDA, TNF-α, and ICAM-1 in the the sustained high glucose group, the intermittent high glucose group, the ALA-intervention group (group ALA50, ALA100, ALA200) and the EGb761-intervention group (group EGb7610.1, EGb7610.5, EGb7611.0) were all statistically significant (FSOD=67.936, FGSH=71.363, FMDA=81.123, FTNF-α=70.684, FICAM-1=80.193; all P<0.05), while the difference has no significance between the normal group and the high osmotic pressure group (P>0.05). Compared with the sustained high glucose group, SOD and GSH decreased significantly and MDA, ICAM-1 and TNF-α increased significantly in the intermittent high glucose group (P<0.05). Compared with the intermittent high glucose group, a notable decrease of ICAM-1, TNF-α, MDA and a dramatic increase in SOD and GSH varied with the concentration of drug in ALA (50, 100, 200 μmol/L) or EGb761 (0.1, 0.5, 1.0 g/L) group (P<0.05). Conclusion: ALA and EGb761 alleviate the oxidative stress and inflammatory response by increasing the intermittent high glucose, which may play a potential therapeutic role on the pathological injures induced by the intermittent high glucose.
Keywords：
intermittent high glucose
alpha lipoic acid
Gingko biloba
the oxidative stress
inflammatory response