Behavioral, Biochemical and Histopathological effects of Standardised Pomegranate extract with Vinpocetine, Propolis or Cocoa in a rat model of Parkinson's disease.

INTRODUCTION: Parkinsonism is a neurodegenerative disorder. Pomegranate (POM) has been previously shown to have a dopaminergic neuroprotective effect against parkinsonism. OBJECTIVE: The aim of the current study is to investigate the possible effect of POM in combination with each of vinpocetine, propolis, or cocoa in the treatment of parkinsonism disease even without being given as adjuvant to L-dopa . METHODS: Rats were divided into seven groups, one normal and six RT model groups. One of the RT groups (2.5 mg/kg/48 h/10 doses sc), for 20 days served as non-treated parkinsonism model, whereas the others were treated with either L-dopa (10 mg/kg, p.o./day) or with POM (150 mg/kg, p.o./day) together with each of the following; vinpocetine (VIN) (20 mg/kg, p.o./day), propolis (300 mg/kg, p.o./day), cocoa (24 mg/kg, p.o./day). Motor and cognitive performances were examined using four tests (catalepsy, swimming, Y-maze, open field). Striatal dopamine, norepinephrine, serotonin, GABA, glutamate, acetylcholinesterase, GSK-3ß, BDNF levels were assessed as well as MDA, SOD, TAC, IL-1ß, TNF-α, iNOs, and caspase-3. Also, histopathological examinations of different brain regions were determined. RESULTS: Treatment with L-dopa alone or with all POM combination groups alleviated the deficits in locomotor activities, cognition, neurotransmitter levels, acetylcholinesterase activity, oxidative stress, and inflammatory markers as well as caspase-3 expression induced by RT. CONCLUSION: Combinations of POM with each of VIN, propolis, or cocoa have a promising disease-modifying antiparkinsonian therapy even without being given as an adjuvant to L-dopa.

The influence of vinpocetine alone or in combination with Epigallocatechin-3-gallate, Coenzyme COQ10, Vitamin E and Selenium as a potential neuroprotective combination against aluminium-induced Alzheimer's disease in Wistar Albino Rats.

Alzheimer's disease (AD) is one of such diseases that represent the most prominent cause of dementia in elderly people. To explore the possible neuroprotective effect as well as mechanism of action of Vinpocetine either alone or in combination with EGCG, CoQ10, or VE & Se in ameliorating aluminum chloride-induced AD in rats. Rats were received AlCl3 (70 mg/kg) intraperitoneal daily dose for 30 days along with EGCG (10 mg/kg, I.P), CoQ10 (200 mg/kg, P.O), VE (100 mg/kg, P.O) & Se (1 mg/kg, P.O) as well as Vinpocetine (20 mg/kg, P.O) either alone or in combination. Results revealed that the combination of Vinpocetine with EGCG showed the best neuroprotection. This protection in the brain was indicated by the significant decrease in Aß and ACHE. The same pattern of results were shown in the levels of monoamines and BDNF. In addition, the combination of Vinpocetine with EGCG showed more pronounced anti-inflammatory (TNF-α, IL-1ß) and antioxidant (MDA, SOD, TAC) effects in comparison to other combinations. These results were confirmed using histopathological examinations as well as DNA fragmentation assays. Vinpocetine with EGCG showed pronounced protection on neurons against AD induced by AlCl3 in rats.

Natural antioxidants enhance the power of physical and mental activities versus risk factors inducing progression of Alzheimer's disease in rats.

BACKGROUND: Alzheimer's disease (AD) is a progressive neurodegenerative disease that is exacerbated by social isolation (SI) and protein malnutrition (PM). Antioxidants, physical and mental activities (Ph&M) can maintain cognitive functions and protect against dementia. OBJECTIVE: To investigate the impact of Epigallocatechin-3-gallate (EGCG), Vitamin E (VE), Vitamin C (VC), and Selenium (Se), in enhancing the potential effect of Ph&M versus SI&PM as risk factors in the progression of AD in rats. METHODS: Aluminum chloride (70 mg/kg, I.P for 5 weeks) was used to induce AD in rats that either normally fed or socially isolated and protein malnourished (SI&PM). Simultaneously, rats were weekly exposed to Ph&M either alone or in combination with EGCG (10 mg/kg, I.P), VC (400 mg/kg, P.O), VE (100 mg/kg, P.O), and Se (1 mg/kg, P.O). RESULTS: The combination protocol of EGCG, VE, VC, and Se together with Ph&M significantly increased brain monoamines, superoxide dismutase (SOD), total antioxidant capacity (TAC) and brain-derived neurotrophic factor (BDNF) in AD, SI&PM and SI&PM/AD groups. Additionally, this regimen significantly mitigated brain acetylcholine esterase (ACHE), ß-amyloid (Aß), Tau protein, ß-secretase, malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), and Interleukin 1ß (IL-1ß) as well as DNA fragmentation. These biochemical findings were supported by the histopathological examinations of brain tissue. CONCLUSION: The combination protocol of antioxidants with Ph&M activities mitigated SI&PM-induced progressive risk of AD.