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国际生理学与病理学期刊

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ISSN 打印: 2155-014X

ISSN 在线: 2155-0158

SJR: 0.116

Target Correction of Mitochondrial Dysfunction in Parkinson's Disease by Capicor

卷 9, 册 4, 2018, pp. 303-313
DOI: 10.1615/IntJPhysPathophys.v9.i4.30
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摘要

The effect of Capicor, containing Meldonium dihydrate and gamma-butirobetain dihydrate, on the mitochondrial dysfunction and oxidative stress development in patients with Parkinson's disease was studied. For this, the pro- and antioxidant balance of the blood plasma, the morphofunctional state of the platelet mitochondria, and changes in the Parkin gene expression in the leukocytes of patients with this disease were investigated before and after Capicor treatment. It has been shown that morphological signs of mitochondrial dysfunction are manifested in patients as destructive lesions of the mitochondrial structure (vacuolization, membrane lysis, and appearance of septate organelles). After treatment with Capicor, the destructive changes were reduced, and adaptive changes were observed as to the platelet mitochondrial apparatus (an increase in the mitochondrial number and area, the mitochondrial biogenesis intensification, a rise of autophagy and fusion of mitochondria). They were aimed at improving oxygen consumption by the tissues, which was manifested as an increase in the number of mitochondria 3.5 times, their average diameter by 26.7%, an increase in the area of mitochondria by 12%, transformation of mitochondrial cristae into more energy-intensive form, intensification of mitochondrial biogenesis, an increase in the level of autophagy and mitochondria fusion. In addition, the severity of oxidative stress was reduced, as evidenced by a decrease in the content of malondialdehyde by 35% and an increase in the activity of the antioxidant enzyme glutathione peroxidase by 14% in the blood plasma. Sharp increase (almost 20 times) in expression of the Parkin gene under the action of Capicor indicates an increase in proteasomal proteolysis of E3-ubiquitin-ligaza substrate with a possible decrease in the severity of neurodegeneration.

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