The effects of supplementation of Withania coagulans and α-tocopherol acetate in diets containing oxidised oil on growth performance, immune response and antioxidant indices in broiler chickens.

This experiment was designed to study the effects of a hydroalcoholic fruit extract from Withania coagulans (WC) and α-tocopherol acetate (α-Toc) in diets containing oxidised oil on growth performance, immune response and antioxidant indices of broiler chickens. The experiment was arranged 2 × 3 × 2 factorial comprising the oxidised oil (0% and 2% diet), WC (0, 100 and 200 mg/kg diet) and α-Toc (0 and 200 mg/kg diet). A total of 600 1-day-old male broiler chickens of the Ross strain were randomly allocated to 12 treatments with 5 replicates of 10 birds each. On day 42, one bird from each replicate was sacrified to measure the lymphoid organ weights, intestinal morphometric characteristics, and malondialdehyde content in the thigh meat. Dietary inclusion of oxidised oil significantly reduced the body weight gain in birds receiving no dietary WC (p < 0.05). In contrast, dietary supplementation of WC at 100 mg/kg diet in birds fed with the diets lacking in WC and oxidised oil resulted in significant increase in body weight gain (p < 0.05). Dietary supplementation of WC significantly increased the total anti-sheep red blood cell titre (p < 0.01). The birds fed with the dietary oxidised oil revealed significantly higher values of malondialdehyde and lower glutathione peroxidase and superoxide dismutase activities (p < 0.05). Feeding diets containing WC resulted in a significant decrease in malondialdehyde content in thigh meat while conversely, increased the glutathione peroxidase and superoxide dismutase activities (p < 0.05). The findings indicated that the dietary inclusion of WC could be recommended as a potent alternative to synthetic compounds in order to improve broilers performance, immunity and meat quality under oxidative stress conditions.

Inhibition of protease-activated receptor 1 (PAR1) ameliorates cognitive performance and synaptic plasticity impairments in animal model of Alzheimer's diseases.

INTRODUCTION: Alzheimer's disease (AD) is a progressive brain disorder accompanied with synaptic failures and decline in cognitive and learning processes. Protease-activated receptor 1 (PAR1) is the major thrombin receptor in the brain that is implicated in synaptic plasticity and memory formation. In the current study, we hypothesized that inhibition of PAR1 would theoretically prevent amyloid beta (Aß) accumulation in the brain and then contribute to reduce risk of AD. The aim of the present study was to evaluate the effect of PAR1 inhibition by using SCH (as an inhibitor of PAR1) on spatial learning, memory, and synaptic plasticity in the CA1 region of the hippocampus in rat model of Alzheimer's disease. METHODS: For the induction of Alzheimer's disease, amyloid beta (Aß) 1-42 was injected in the CA1 region of the hippocampus. The rats were divided into four groups: group I (surgical sham); group II rat mode of Alzheimer's disease (AD); group III (SCH) (25 µg/kg) intraperitoneally (i.p.), and group IV (AD + SCH). After 14 days of protocol, the rats in group III received SCH and 30 min after injection behavioral and electrophysiological tests were performed. Learning and memory ability was assessed by Morris water maze and novel object recognition tests. Extracellular evoked field excitatory postsynaptic potentials (fEPSP) were recorded in the stratum radiatum of the CA1 area. RESULTS: Our results showed that AD rats showed impairments in learning and memory, and long-term potentiation (LTP) was not induced in these rats. However, injection of SCH overcame the AD-induced impairment in LTP generation in the CA1 area of the hippocampus and improved learning and memory impairment.