中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2015年
5期
900-905
,共6页
灯盏花素%糖尿病视网膜病%血管内皮生长因子
燈盞花素%糖尿病視網膜病%血管內皮生長因子
등잔화소%당뇨병시망막병%혈관내피생장인자
Scutellarin%Diabetic retinopathy%Vascular endothelial growth factors
目的:观察灯盏花素对高糖环境下人视网膜色素上皮细胞株ARPE-19中VEGF、VEGFR2和p-ERK蛋白的表达及对2型糖尿病大鼠视网膜VEGF表达的影响。方法:培养ARPE-19细胞,分为对照组、灯盏花素组、高糖组和高糖+灯盏花素组,ELISA检测VEGF的分泌水平,Western blot检测细胞VEGF、VEGFR2和p-ERK的蛋白水平;取正常大鼠,随机分为正常对照组、灯盏花素组、糖尿病模型组和糖尿病灯盏花素治疗组,16周后取各组大鼠眼球,观察大鼠视网膜的病理变化并评分,免疫组化观察VEGF的表达情况。结果:(1)细胞实验结果显示,灯盏花素组VEGF、VEGFR2和p-ERK的蛋白水平与正常对照组比较均减低( P<0.05);高糖组细胞上述蛋白水平与正常对照组比较均增加(P<0.05);高糖+灯盏花素组上述蛋白水平与高糖组比较表达均减少(P<0.05);(2)大鼠视网膜病理学评分显示糖尿病组与正常对照组、糖尿病灯盏花素治疗组相比差异显著,灯盏花素组与正常对照组相比差异无统计学意义。糖尿病大鼠与正常对照组、灯盏花素组相比,视网膜VEGF的表达增加;糖尿病灯盏花素治疗组中VEGF的表达较糖尿病组有所降低( P<0.05)。结论:灯盏花素可以降低ARPE-19细胞VEGF、VEGFR2和p-ERK的蛋白表达水平,抑制糖尿病大鼠视网膜VEGF的表达,提示灯盏花素可能通过降低糖尿病大鼠视网膜细胞和组织中VEGF的表达,缓解其糖尿病视网膜病变进程。
目的:觀察燈盞花素對高糖環境下人視網膜色素上皮細胞株ARPE-19中VEGF、VEGFR2和p-ERK蛋白的錶達及對2型糖尿病大鼠視網膜VEGF錶達的影響。方法:培養ARPE-19細胞,分為對照組、燈盞花素組、高糖組和高糖+燈盞花素組,ELISA檢測VEGF的分泌水平,Western blot檢測細胞VEGF、VEGFR2和p-ERK的蛋白水平;取正常大鼠,隨機分為正常對照組、燈盞花素組、糖尿病模型組和糖尿病燈盞花素治療組,16週後取各組大鼠眼毬,觀察大鼠視網膜的病理變化併評分,免疫組化觀察VEGF的錶達情況。結果:(1)細胞實驗結果顯示,燈盞花素組VEGF、VEGFR2和p-ERK的蛋白水平與正常對照組比較均減低( P<0.05);高糖組細胞上述蛋白水平與正常對照組比較均增加(P<0.05);高糖+燈盞花素組上述蛋白水平與高糖組比較錶達均減少(P<0.05);(2)大鼠視網膜病理學評分顯示糖尿病組與正常對照組、糖尿病燈盞花素治療組相比差異顯著,燈盞花素組與正常對照組相比差異無統計學意義。糖尿病大鼠與正常對照組、燈盞花素組相比,視網膜VEGF的錶達增加;糖尿病燈盞花素治療組中VEGF的錶達較糖尿病組有所降低( P<0.05)。結論:燈盞花素可以降低ARPE-19細胞VEGF、VEGFR2和p-ERK的蛋白錶達水平,抑製糖尿病大鼠視網膜VEGF的錶達,提示燈盞花素可能通過降低糖尿病大鼠視網膜細胞和組織中VEGF的錶達,緩解其糖尿病視網膜病變進程。
목적:관찰등잔화소대고당배경하인시망막색소상피세포주ARPE-19중VEGF、VEGFR2화p-ERK단백적표체급대2형당뇨병대서시망막VEGF표체적영향。방법:배양ARPE-19세포,분위대조조、등잔화소조、고당조화고당+등잔화소조,ELISA검측VEGF적분비수평,Western blot검측세포VEGF、VEGFR2화p-ERK적단백수평;취정상대서,수궤분위정상대조조、등잔화소조、당뇨병모형조화당뇨병등잔화소치료조,16주후취각조대서안구,관찰대서시망막적병리변화병평분,면역조화관찰VEGF적표체정황。결과:(1)세포실험결과현시,등잔화소조VEGF、VEGFR2화p-ERK적단백수평여정상대조조비교균감저( P<0.05);고당조세포상술단백수평여정상대조조비교균증가(P<0.05);고당+등잔화소조상술단백수평여고당조비교표체균감소(P<0.05);(2)대서시망막병이학평분현시당뇨병조여정상대조조、당뇨병등잔화소치료조상비차이현저,등잔화소조여정상대조조상비차이무통계학의의。당뇨병대서여정상대조조、등잔화소조상비,시망막VEGF적표체증가;당뇨병등잔화소치료조중VEGF적표체교당뇨병조유소강저( P<0.05)。결론:등잔화소가이강저ARPE-19세포VEGF、VEGFR2화p-ERK적단백표체수평,억제당뇨병대서시망막VEGF적표체,제시등잔화소가능통과강저당뇨병대서시망막세포화조직중VEGF적표체,완해기당뇨병시망막병변진정。
AIM:To evaluate the influence of scutellarin on the expression of vascular endothelial growth factor ( VEGF) in high glucose-treated human retinal pigment epithelial cell line ARPE-19 and to observe the effects of scutellarin on the protein expression of VEGF, p-ERK and VEGFR2 in the retinas of type II diabetic rats.METHODS: Cultured ARPE-19 cells were divided into normal control group, scutellarin group, high glucose group and high glucose+scutellarin group.The protein levels of VEGF, p-ERK and VEGFR2 were measured by Western blot.The VEGF release in ARPE-19 cells was detected by ELISA.Normal rats were randomly divided into normal control group and scutellarin group.Diabetic rat model was established by feeding with high-fat diet and injecting with streptozocin, and randomly divided into diabetes group and diabetes treated with scutellarin group.After 16 weeks, the eyes were removed.The morphological changes of the retinas were observed under light microscope with HE staining, and histopathological score was recorded.The expres-sion of VEGF in the retinas was observed by the method of immunohistochemistry.RESULTS:Compared with normal con-trol group, the protein levels of VEGF, p-ERK and VEGFR2 in the ARPE-19 cells decreased in scutellarin group, but in-creased in high glucose group.The histopathological score of the retinas showed significant difference among diabetes group, diabetes treated with scutellarin group and normal control group, and no significant difference between normal con-trol group and scutellarin group was observed.The expression of VEGF increased in diabetic group and was significantly higher than that in scutellarin treatment group (P<0.05).CONCLUSION:Scutellarin inhibits the increased protein le-vels of VEGF, p-ERK and VEGFR2 in ARPE-19 cells, and decreases the expression of VEGF in the retinas of diabetic rats.The suppression of the diabetic retinopathy development by scutellarin may be partly involved in the ERK/MAPK pathway.