EFFECT OF CAPICOR ON THE PARKINSON’S DISEASE PATHOGENIC LINKS
I.M. Mankovska1, K.V. Rosova1, O.O. Gonchar1, V.I. Nosar1, L.V. Bratus1, T.I. Drevitska1, I.D. Glazyrin1, N.V. Karasevich2, I.M. Karaban2
- O.O.Bogomoletz Institute of Physiology. National Academy
of Sciences of Ukraine, Kiev, Ukraine
- D.F. Chebotarev Institute of Gerontology National
Academy of Medical Sciences of Ukraine, Kiev, Ukraine
It was studied the influence of Capicor (containing Meldonium
dihydrate and gamma-butyrobetain dihydrate) on the
mitochondrial dysfunction and oxidative stress development
in humans with Parkinson’s disease. The aim of the present
work was to investigate the pro- and antioxidant balance of
blood plasma, the morphofunctional state of blood platelets
as well as the Parkin gene expression changes in blood
leukocytes of patients with Parkinson’s disease before and
after Capicor treatment. It was registered the morphological
sings of mitochondrial dysfunction (vacuolization, membrane
lysis, septiration) in patients with Parkinson’s disease. After
Capicor treatment, there was demonstrated a decrease in these
destructive changes as well as restructuring of the platelets
mitochondrial apparatus (an increase in the mitochondrial
number and area, the mitochondrial biogenesis intensification,
a rise of autophagy and fusion of mitochondria). These
changes are favoring the growth of the energy power of
mitochondria. Under the influence of Capicor, there was
demonstrated a reduction in oxidative stress expressiveness
(a decrease in blood malon dialdehyde content and a rise in
blood glutathione peroxidase activity). After Capicor treatment,
there was shown the significant increase in the Parkin
gene expression in leukocytes of patients with Parkinson’s
disease. This increase account for the intensification of the
E3-ubiquitin-ligase-substrates proteasomal degradation
which are thought to contribute to neuronal cell death.
Parkinson’s disease; mitochondria; oxidative stress; Parkin gene; Capicor
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