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[AEDG和KE肽对体外培养的人松果体及胸腺细胞衰老过程中线粒体染色及L7A核糖体蛋白表达的影响。]

[The influence of AEDG and KE peptides on mitochondries stain and L7A ribosomes protein expression during human pineal gland and thymus cell senescence in vitro.].

作者信息

Ivko O M, Drobintseva A O, Leont'eva D O, Kvetnoy I M, Polyakova V O, Linkova N S

机构信息

Saint-Petersburg Institute of Bioregulation and Gerontology, 3 pr. Dynamo, St. Petersburg 197110, Russian Federation, e-mail:

Saint-Petersburg State Pediatric Medical University, 2 Litovskaya str., St. Petersburg 194100, Russian Federation.

出版信息

Adv Gerontol. 2020;33(4):741-747.

Abstract

It was verified new molecular targets of geroprotective activity of AEDG (epitalon) and KE (vilon) peptides by the method of confocal laser scanning microscopy. It was shown that the MitoTracker Red mitochondries staining decreased and L7A ribosomal protein synthesis compensatory increased during pineal and thymic cell senescence in vitro. AEDG peptide increases in 1,5 times the square of MitoTracker Red mitochondries staining and decreases on 22% the expression of ribosomal protein L7A in cultures of human pineal gland cells during its senescence. KE peptide increases in 1,5 times the square of MitoTracker Red mitochondries staining and decreases on 15% the expression of ribosomal protein L7A in cultures of human thymic cells during its senescence. The square of MitoTracker Red mitochondries staining decreases and the expression of L7A ribosomal protein compensatory increases during pineal gland and thymic cells senescence. We can suppose that AEDG and KE peptides have a tissue-specific effect that normalizes the functions of mitochondria and ribosomes of pinealocytes and thymocytes.

摘要

通过共聚焦激光扫描显微镜法验证了AEDG(依普黄酮)和KE(维隆)肽的老年保护活性的新分子靶点。结果表明,在体外松果体和胸腺细胞衰老过程中,MitoTracker Red线粒体染色减少,L7A核糖体蛋白合成代偿性增加。在人松果体细胞衰老培养过程中,AEDG肽使MitoTracker Red线粒体染色面积增加1.5倍,核糖体蛋白L7A的表达降低22%。在人胸腺细胞衰老培养过程中,KE肽使MitoTracker Red线粒体染色面积增加1.5倍,核糖体蛋白L7A的表达降低15%。在松果体和胸腺细胞衰老过程中,MitoTracker Red线粒体染色面积减少,L7A核糖体蛋白的表达代偿性增加。我们可以推测,AEDG和KE肽具有组织特异性作用,可使松果体细胞和胸腺细胞的线粒体和核糖体功能正常化。

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