Cadmium (Cd) is wide-spread toxic metal that pollutes most of the vegetables, which eaten by numerous populations all over the world. The aim of the current work is to evaluate the protective and prophylactic effects of the antioxidant materials in the grape seed extract (GSE) on the hepatic intoxication induced by cadmium chloride toxic material in male Wistar rats. Male adult Wistar rats were divided into four groups. Control group fed on balanced diet and given drinking water. Group two (control positive) given CdCl2 in the dose of 0.44 mg/kg body weight (BW) by stomach tube daily. Group three given grape seed extract GSE in the dose of (100 mg/kg BW) daily by stomach tube. Finally, the fourth group gave mixture of (GSE and CdCl2) by stomach tube in the recommended dose. Blood and liver tissues were collected for further biochemical and histopathological studies. CdCl2 significantly increased the serum levels of malondialdehyde, ALT and AST. Cadmium administration decreased levels of antioxidants (Catalase, GSH-R and GSH-Px). The liver of the control positive groups which given CdCl2 showed degenerative changes in the form of vacuolar and hydropic degeneration. Congestion was evident in the central vein and proliferation of the kupffer cells. These hepatic biochemical and degenerative changes were ameliorated by the co addition of GSE.

Background: The wrong use of drugs results in disturbances in the immunity that affect human health. These drugs have side effects that may lead to death because of lake of immunity. Human beings need to use natural products to strength the immune system and avoid such side effects. Of these products is the onion that used to strength the immune system. This study was conducted to study the protective effect of onion extract on immune-suppressed rats and its impact on the expression level of cytokines, acute phase proteins and antioxidants compared to both control and immune suppressed groups. Materials and Methods: Forty rats were divided into four groups (10 per group) control group (CNT), immunesuppressed group (DEXA) injected with dexamethasone at a dose of 5 mg per kg intraperitoneally (IP) twice daily for 3 days, onion extract administered group (OE) given orally at a dose of 500 mg per kg for 4 weeks. Group 4 (y), was given onion extract for a week then immune-suppressed with DEXA for 3 days then continued with OE for 3 weeks. Serum and RNA were extracted for examining the biochemical and genetic changes. Results: Injection of dexamethasone decreased number of leukocytes with increase in the number of neutrophils and the decrease of all other types of white blood cells. Moreover, a decrease in antioxidant levels such as catalase, super oxide dismutase (SOD), and reduced glutathione (GSH) with an increase in the level malondialdehyde (MDA). In parallel, a decrease in serum levels of cytokines, such as TNF and IL-6, together with immunoglobulins (IgG and IgM), were reported in DEXA injected rats that were ameliorated by prior administration of OE. Gene expression analysis revealed that dexamethasone suppressed gene expression of antioxidants together with IL-1 and 8 while increased IL-10 mRNA expression. All of these changes have been normalized to the normal level by OE administration to DEXA injected rats. Conclusion: The present findings clearly emphasize the medical importance of onions as immune-stimulants at genetic and cellular levels, and that they are good for human health.

Neurological disorders, such as amyotrophic lateral sclerosis, Parkinson’s disease, and Alzheimer’s disease, are commonly associated with persistent neuro-inflammation, and there is an urgent need to discover new therapeutic agents that may target the various pathways involved in neurodegeneration. In this study, we investigated the therapeutic potential of folecitin, a flavonoid isolated from Hypericum oblongifolium, against lipopolysaccharide (LPS)-induced oxidative stress associated with neurodegeneration, amyloidogenic Aβ production pathway, and memory dysfunction in mice. LPS was administered i.p. at 250 µg/kg/day for 3 weeks, followed by the administration of folecitin at a dose of 30 mg/kg/day for the last two weeks. A Western blot technique was used to assess the expression of different proteins involved in oxidative stress, neurodegeneration, and neuronal synapse. Results indicated that folecitin significantly reduced LPS-induced apoptotic neurodegeneration, including the expression of BAX, Caspase-3, and PARP-1 proteins, inhibited BACE1, and the amyloidogenic Aβ production pathway. Folecitin improved both pre- and post-neuronal synapse, as well as memory dysfunction. Furthermore, folecitin significantly activated endogenous antioxidant proteins such as Nrf-2 and HO-1 via stimulating the phosphorylation of Akt proteins. These findings suggest that folecitin may be a suitable lead to design new drugs for neurotoxin-triggered neurodegenerative disorders.