The role of apitoxin in alleviating propionic acid-induced neurobehavioral impairments in rat pups: The expression pattern of Reelin gene.

The efficacy of apitoxin (bee venom; BV) in ameliorating propionic acid (PPA) -induced neurobehavioral impacts was studied. Sixty rat pups were enrolled in a split litter design to six groups: a control group, a PPA-treated group, a BV-treated group, a BV/PPA protective group, a PPA/BV therapeutic group, and a BV/PPA/BV protective and therapeutic group. Exploratory, social, locomotor, and repetitive/stereotype-like activities were assessed and prosocial, empathy, and acquired behavior were evaluated.

The possible counteractive effect of gold nanoparticles against streptozotocin-induced type 1 diabetes in young male albino rats.

The current study was performed to study the effect of biologically synthesised gold nanoparticles (AuNPs) to control hyperglycaemic conditions in streptozotocin (STZ)-induced diabetic mice. In this study, the rats were divided into four groups: Group I normal control rats (non-diabetic, untreated); Group II diabetes-induced rats used as diabetic controls DC (diabetic, untreated). Group III diabetes-induced rats treated with AuNPs DT; Group IV normal rats treated with AuNPs NT.

Apitoxin protects rat pups brain from propionic acid-induced oxidative stress: The expression pattern of Bcl-2 and Caspase-3 apoptotic genes.

The primary aim of this study was to determine the potential modulatory role of the apitoxin (bee venom; BV) against propionic acid (PPA)-induced neurotoxicity. The biochemical responses to PPA exposure in rat pups were assayed, including changes in the antioxidant barrier systems and lipid peroxidation and protein oxidation biomarkers in the brain tissue. DNA damage was measured by single-cell gel electrophoresis and differences in Bcl-2 and Caspase-3 mRNA expression were assessed using real-time PCR.

Pancreatic response to gold nanoparticles includes decrease of oxidative stress and inflammation in autistic diabetic model.

Background: Gold nanoparticles (AuNPs) have a wide range of applications in various fields. This study provides an understanding of the modulatory effects of AuNPs on an antioxidant system in male Wistar diabetic rats with autism spectrum disorder (ASD). Normal littermates fed by control mothers were injected with citrate buffer alone and served as normal, untreated controls controlin this study.

Possible ameliorative effect of breastfeeding and the uptake of human colostrum against coeliac disease in autistic rats.

Aim: To examine the possible ameliorative effect of breastfeeding and the uptake of human colostrum against coeliac disease in autistic rats.

Methods: Female rats were fed a standard diet and received a single intraperitoneal injection of 600 mg/kg sodium valproate on day 12.5 after conception.

Evaluation of the possible protective role of quercetin on letrozole-induced testicular injury in male albino rats.

Background: The purpose of this study was to appraise the possible adverse effects of quercetin against the aromatase inhibitor letrozole-induced developmental toxicity potential in male Wistar rats.

Methods: Control male albino rats were received vehicles used for flavonoids and vehicle used for letrozole. The rats in the first experimental group received letrozole at 0.

Gold nanoparticles induce apoptosis in MCF-7 human breast cancer cells.

Background: Gold nanoparticles have recently been investigated with respect to biocompatibility according to their interactions with cells. The purpose of this study was to examine cytotoxicity and apoptosis induction by well-characterized gold nanoparticles in human breast epithelial MCF-7 cells.

Methods: Apoptosis was assessed by TUNEL, cytotoxicity by MTT assay and caspase 3, 9, p53, Bax and Bcl expression by real-time PCR assays.

The protection role of heat shock protein 70 (HSP-70) in the testes of cadmium-exposed rats.

Cadmium (Cd) is an environmental carcinogenic pollutant known to inactivate several proteins involved in DNA repair systems while at the same time creating an oxidative stress that can result in additional DNA lesions. The testis and the lung are the target organs for cadmium carcinogenesis. Increased production of oxidants in vivo can cause damage to intracellular macromolecules such as DNA, proteins and lipids, which in turn lead to oxidative injury.