Methanolic extracts of a selected Egyptian Vicia faba cultivar mitigate the oxidative/inflammatory burden and afford neuroprotection in a mouse model of Parkinson's disease.

Vicia faba L. is a legume from the family Fabaceae. Ancient Egyptians consumed fava beans thousands of years ago and they are still one of the most popular foods in Egypt. The current study examined the anti-Parkinson effect of 80% methanolic extracts of seeds or sprouts of the fava 'Sakha 3 'cultivar which has been selected based on the total phenol content among three cultivars tested. In addition, the extracts were characterized by reversed-phase high-performance liquid chromatography coupled with diode array detection and quadrupole-time-of-flight-mass spectrometry (RP-HPLC-DAD-QTOF-MS). Three doses (200, 400, and 600 mg/kg) of 80% methanol extracts of seeds or sprouts of the Sakha 3 cultivar were evaluated in rotenone-Parkinsonian mice from behavioral, biochemical, and histopathological aspects. The extract of fava sprouts (600 mg/kg dose) showed the most beneficial effect. It improved motor activity, enhanced striatal dopamine level, and decreased the striatal malondialdehyde, as well as the expression of the inflammatory markers, compared with the rotenone control group and groups receiving lower therapeutic doses of the extracts or L-Dopa. In addition, these findings were supported by a histopathological investigation which indicated that mice treated with the 600-mg/kg dose of the sprout extract showed a low number of degenerated neurons. The application of RP-HPLC-DAD-QTOF-MS and mass/mass spectroscopy enabled the metabolic profiling of the sprouts and seeds of the 'Sakha 3' cultivar. It is obvious that germination increased the amounts of phenolic acids, saponins, and aromatic amino acids, together with a dramatic increase in flavonoids. In conclusion, the 80% methanolic extract of sprouts of the fava "Sakha 3" cultivar may be a promising candidate for treating Parkinsonism if appropriate safety data are available.

Protective effect of metformin on rat diabetic retinopathy involves suppression of toll-like receptor 4/nuclear factor-k B expression and glutamate excitotoxicity.

Microvascular complications of diabetes mellitus are progressively significant reasons for mortality. Metformin (MET) is considered as the first-line therapy for type 2 diabetes patients, and may be especially beneficial in cases of diabetic retinopathy although the precise mechanisms of MET action are not fully elucidated. The current study was designed to inspect the antioxidant and modulatory actions of MET on DRET in streptozotocin-induced diabetic rats. The effect of MET on the toll-like receptor 4/nuclear factor kappa B (TLR4/NFkB), inflammatory burden and glutamate excitotoxicity was assessed. Twenty-four male rats were assigned to four experimental groups: (1) Vehicle group, (2) Diabetic control: developed diabetes by injection of streptozotocin (60 mg/kg, i.p.). (3&4) Diabetic + MET group: diabetic rats were left for 9 weeks without treatment and then received oral MET 100 and 200 mg/kg for 6 weeks. Retinal samples were utilized in biochemical, histological, immunohistochemical and electron microscopic studies. MET administration significantly decreased retinal level of insulin growth factor and significantly suppressed the diabetic induced increase of malondialdehyde, glutamate, tumor necrosis factor-α and vascular endothelial growth factor (VEGF). Further, MET decreased the retinal mRNA expression of NFkB, tumor necrosis factor-α and TLR4 in diabetic rats. The current findings shed the light on MET's efficacy as an adjuvant therapy to hinder the development of diabetic retinopathy, at least partly, via inhibition of oxidative stress-induced NFkB/TLR4 pathway and suppression of glutamate excitotoxicity.