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.

Combination of pomegranate extract and curcumin ameliorates thioacetamide-induced liver fibrosis in rats: impact on TGF-ß/Smad3 and NF-κB signaling pathways.

Protection against liver injury and its consequences is considered an essential issue to minimize the number of annual deaths caused by liver diseases. The present study was designed to evaluate the potential role of pomegranate extract (PE) and/or curcumin in the regression of thioacetamide (TAA)-induced liver fibrosis, focusing on their modulatory effects on Nrf2/HO-1, NF-κB, and TGF-ß/Smad3 signaling pathways. Liver fibrosis was induced in male Wistar rats by intraperitoneal injection of TAA (100 mg/kg) three times a week, for 8 weeks. To assess the protective effects of PE and/or curcumin against TAA-induced liver fibrosis, rats were treated on a daily basis with oral doses of PE (200 mg/kg) and/or curcumin (200 mg/kg) for 8 weeks. The results indicated that PE and/or curcumin attenuated TAA-induced liver fibrogenesis, as evidenced by a significant improvement in the liver function tests (AST, ALT, ALP, and albumin), oxidative stress biomarkers (MDA, SOD, and GSH), and inflammatory biomarkers (NF-ĸB, TNF-α, IL-1ß, iNOS, TGF-ß, and MPO), compared to TAA group. Moreover, treatment with PE and/or curcumin exerted a significant upregulation of Nrf2/HO-1 gene expressions along with significant downregulation of NF-ĸB, TGF-ß, and phospho-Smad3 protein expressions, as well as α-SMA and collagen-1 gene expressions. The histopathological examination has corroborated these findings. In conclusion, hepatoprotective activities of PE and/or curcumin could be linked to their abilities to modulate Nrf2/HO-1, NF-κB, and TGF-ß/Smad3 signaling pathways. It is worth noting that the combination of PE and curcumin exerted superior hepatoprotective effects against TAA-induced liver fibrosis, as compared to monotherapy.