ubiquinone and vinpocetine

This research was designed to ascertain the effect and mechanism of vinpocetine (VIN) and coenzyme Q10 (CoQ10) combination on cognitive impairment induced by ionizing radiation (IR).. Cognitive impairment in mice was induced by 9-Gy IR, and they were intraperitoneally injected with VIN, CoQ10, or VIN + CoQ10. Then novel object recognition and Morris water maze tests were used to detect cognitive function. The number of hippocampal neurons and BrdU. IR reduced novel object discrimination index, the time for platform crossing, and the time spent in platform quadrant, in addition to neuron loss, downregulated levels of mitochondrial respiratory complex I, ATP, and MMP, aggravated oxidative stress injury, increased expression of LC3 II/I, Beclin1, PINK1, and parkin, and decreased P62 expression. VIN or CoQ10 treatment mitigated cognitive dysfunction, neurons loss, mitochondrial damage, and oxidative stress injury, and enhanced mitophagy in hippocampal neurons. VIN and CoQ10 combination further protected against IR-induced cognitive dysfunction than VIN or CoQ10 alone.. VIN combined with CoQ10 improved neuron damage, promoted mitophagy, and ameliorated cognitive impairment in IR mice.

Topics: Adenosine Triphosphate; Animals; Cognitive Dysfunction; Electron Transport Complex I; Mice; Mitophagy; Radiation, Ionizing; Ubiquinone; Vinca Alkaloids

Alzheimer's disease is a neurodegenerative disorder characterized by a progressive decline of cognitive abilities as well as bone loss. Physical and mental activities maintain cognitive functions as well as increase bone mass by inhibiting bone resorption. VIN and CoQ10 are neuroprotective drugs that possess anti-inflammatory and antioxidant properties.. To study the effect of PH&M on enhancing the neuroprotective role of VIN and CoQ10 combination during induction of AD model in rats besides their role against bone mass loss associated with AD model.. Six groups of rats were received saline, AlCl. VIN and CoQ10 combination together with PH&M significantly attenuated the neurodegeneration induced by AlCl. Neuroprotective drugs together with PH&M have a more protective effect against AD and bone loss rather than PH&M alone.

Topics: Alzheimer Disease; Animals; Behavior, Animal; Bone Remodeling; Brain; Cognition; Combined Modality Therapy; Male; Neuroprotective Agents; Rats; Rats, Sprague-Dawley; Swimming; Ubiquinone; Vinca Alkaloids; Vitamins

Chlorpyrifos (CP) is an organophosphorus pesticide that induces oxidative stress through the production of free radicals and depletes intracellular antioxidant reserves. In this study, the efficacy of three antioxidants (melatonin, coenzyme Q10 (CoQ10), and vinpocetine) on alleviation of toxic effects of CP was evaluated.. Cytotoxicity of CP, in the presence or absence of effective doses of melatonin, CoQ10, and vinpocetine, was determined in human peripheral blood lymphocytes after 72-h exposure. The levels of acetylcholinesterase (AChE) activity along with tumor necrosis factor α (TNF-α), as inflammatory index, were measured. Further, the viability and oxidative stress markers including cellular mitochondrial activity, cell death modes (apoptosis vs. necrosis), total antioxidant power (TAP), total thiol molecules (TTM), lipid peroxidation (LPO), and myeloperoxidase (MPO) activity were measured.. CoQ10 and also the combination of the three antioxidants were the most notable in opposing toxicity of CP and led to increasing TAP and TTM; improvement of AChE activity; and lowering LPO, MPO, TNF-α, and apoptosis compared to CP alone.. CP toxicity overwhelms the intracellular antioxidant defense mechanisms. Exogenous supplementation with antioxidants, such as the ones we have investigated, seems to be effective in the prevention of cytotoxicity of CP.

Topics: Antioxidants; Cell Culture Techniques; Cells, Cultured; Chlorpyrifos; Environmental Pollutants; Free Radicals; Humans; Lymphocytes; Melatonin; Oxidative Stress; Ubiquinone; Vinca Alkaloids

Effects of OM-853 on behavioral responses in the forced swim test were studied. OM-853 significantly reduced the duration of immobility without any change in the exploratory activity. Imipramine also reduced the duration of immobility, but idebenone did not. On the other hand, vinpocetine enhanced the duration with a suppressive effect on ambulation. The anti-immobility effect of OM-853 was reversed by pretreatment with haloperidol. These results demonstrate that the effect of OM-853 on the swim test is different from that of idebenone and vinpocetine. Furthermore, the present results suggest that OM-853 may exert its anti-immobility activity through facilitated transmission of the dopaminergic and/or adrenergic systems.

Topics: Animals; Behavior, Animal; Benzoquinones; Haloperidol; Imipramine; Immobilization; Male; Motor Activity; Phosphodiesterase Inhibitors; Rats; Rats, Wistar; Swimming; Ubiquinone; Vinca Alkaloids

The effects of idebenone and vinpocetine which reportedly prevent impairment of learning and memory were studied in vitro, on the long-term potentiation of the population spike in the pyramidal layer of CA3 region of slices of hippocampus in the guinea pig. Idebenone (10(-9) M-10(-6) M) or vinpocetine (10(-7) M-10(-6) M) significantly augmented long-term potentiation in the mossy fibre-CA3 pyramidal cell system, without any significant changes in population spikes in the absence of tetanic stimulation. These results suggest that both drugs have direct actions on the hippocampal neurones to augment long-term potentiation at fairly small concentrations. Further, when the two drugs were applied together, the augmenting effects were additive.

Topics: 2-Amino-5-phosphonovalerate; Animals; Anticonvulsants; Benzoquinones; Electric Stimulation; Guinea Pigs; Hippocampus; In Vitro Techniques; Male; Pyramidal Tracts; Quinones; Receptors, N-Methyl-D-Aspartate; Receptors, Neurotransmitter; Time Factors; Ubiquinone; Valine; Vinca Alkaloids

The effects of idebenone and various nootropic drugs on lipid peroxidation in rat brain homogenate were examined. Idebenone inhibited lipoperoxide (LPO) production in brain homogenate in a concentration-dependent manner, with an IC50 of 38 microM. The inhibition was strongly enhanced (about 100-fold) by adding succinate, a substrate in the mitochondrial respiration. The optimal concentration of succinate was 0.5 mM. Inhibition of lipid peroxidation in brain homogenate by various nootropic drugs in the presence or absence of succinate was then examined. Drugs added to the brain homogenate at 100 microM in the absence of succinate inhibited LPO production in the order: idebenone greater than vinpocetine greater than bifemelane greater than indeloxazine greater than calcium hopantenate. However, when the drugs were added at 1 microM in the presence of succinate, only idebenone demonstrated inhibition. These results suggest that although almost all of the drugs tested inhibit lipid peroxidation in brain homogenate, only idebenone is activated by succinate, the other drugs being insensitive to this compound.

Topics: Animals; Benzhydryl Compounds; Benzoquinones; Brain; Depression, Chemical; Dose-Response Relationship, Drug; gamma-Aminobutyric Acid; In Vitro Techniques; Lipid Peroxides; Male; Morpholines; Pantothenic Acid; Quinones; Rats; Rats, Inbred Strains; Succinates; Ubiquinone; Vinca Alkaloids