Abstract
The evaluation of 2.3-diazepine influence on tissue respiration of the liver and its exocrine function in rats with a rotenone model of Parkinson’s disease
Highlights
Parkinson’s disease (PD) is a progressive neurodegenerative disorder, characterized by the selective loss of dopaminergic neurons in nigra pars compacta of the midbrain leading to a significant reduction in dopamine levels in the striatum [1]
Numerous studies suggest that an inhibition of mitochondrial complex I and a mitochondrial dysfunction leading to respiration disorder and energy deficit in the neurons might play an important role in neurodegeneration during progression of PD [3]
The present results revealed a significant decrease in rearing frequency and in locomotion frequency in ROT group as compared to the control group. 2.3-DP treatment improved behavioral performance of rats with PD (Fig. 1, 2)
Summary
Parkinson’s disease (PD) is a progressive neurodegenerative disorder, characterized by the selective loss of dopaminergic neurons in nigra pars compacta of the midbrain leading to a significant reduction in dopamine levels in the striatum [1]. Numerous studies suggest that an inhibition of mitochondrial complex I and a mitochondrial dysfunction leading to respiration disorder and energy deficit in the neurons might play an important role in neurodegeneration during progression of PD [3]. Dopamine agonists are the medicines that activate the dopamine receptor They mimic or copy the function of dopamine in the brain but cause several serious undesirable effects, including nausea, vomiting, hypotension, and, in the long run, motor complications [9]. In this context, the drugs with the ability to modulate mitochondrial dynamics, function and biogenesis may have important clinical applications in the future treatment of PD. The derivatives of triazolo [4.5-c] imidazo [1.2-c]
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