Dementia is one of the most important problems nowadays. Aging is associated with learning and memory impairments. Diet rich in cholesterol has been shown to be detrimental to cognitive performance. This work was carried out to compare the effect of high cholesterol diet on the hippocampus of adult and aged male albino rats. Twenty adult and twenty aged male rats were used in this study. According to age, the rats were randomly subdivided into balanced and high cholesterol diet fed groups. The diet was 15 g/rat/day for adult rats and 20 g/rat/day for aged rats for eight weeks. Serial coronal sections of hippocampus and blood samples were taken from each rat. For diet effect evaluation, Clinical, biochemical, histological, immunohistochemical, and morphometric assessments were done. In compare to a balanced diet fed rat, examination of Cornu Ammonis 1 (CA 1) area in the hippocampus of the high cholesterol diet adult rats showed degeneration, a significant decrease of the pyramidal cells, attenuation and/or thickening of small blood vessels, apparent increase of astrocytes and apparent decrease of Nissl's granules content. Moreover, the high cholesterol diet aged rats showed aggravation of senility changes of the hippocampus together with Alzheimer like pathological changes. In conclusion, the high cholesterol diet has a significant detrimental effect on the hippocampus and aging might pronounce this effect. So, we should direct our attention to limit cholesterol intake in our food to maintain a healthy life style for a successful aging.
Background: This work was designed to clarify, for the first time up to our knowledge, the effects of high fructose diet (HFrD) induced metabolic syndrome (MetS) on the pituitarygonadal axis of adolescent male rats continuing through adulthood period and to evaluate the possible role of ginger extract in ameliorating these effects.
Materials and methods:Forty 4-week-old male albino rats, treated for 8 weeks, were randomly divided into 4 equal groups; control(fed standard diet), ginger extract treated (500 mg/kg once daily orally by gavage), HFrD induced MetS (fed a diet containing 60% fructose), HFrD and ginger groups. The assessment methods included biochemical, histological and immunohistochemical studies.Results: HFrD fed rats exhibited a picture similar to MetS in the form of increased body weight and serum levels of glucose and insulin with an elevated HOMA-IR reflecting insulin resistance as well as dyslipidemia. Lipid peroxidation (increased MDA) and oxidative stress (decreased SOD) were implicated in this syndrome. This group exhibited a significant decrease of testicular weight and the levels of reproductive hormones (LH, FSH & testosterone). The pituitary gonadotrophs showed electron dense nuclei, large cytoplasmic vacuoles, destructed organelles in addition to decreased number of secretory granules. Furthermore, testicular specimens presented marked alterations. There were disorganized shrunken tubules with irregular basement membranes, reduced germinal epithelial thickness, vacuolations and degenerated mitochondria in the spermatogenic cells.Beclin1 and PCNA immunoexpressions were significantly downregulated with HFrD induced MetS. Ginger extract supplementation proved to be a potent protective agent against these harmful effects through its antioxidant, hypoglycemic, insulinotropic, androgenic and hypolipidemic effects in addition to its ability to induce testicular autophagy.
Conclusions: Consumption of HFrD induced MetS and proved to have harmful effects on the pituitarytesticular axis. Moreover, this work provided a new insight into the possible use of ginger extract to alleviate the main features of MetS and protect the pituitarygonadal axis from the damaging effects of HFrD induced MetS.
The direct interactive effects of rosemary and acrylamide on the development of motor neurons in the spinal cord remains unknown. Our goal is to confirm the protective effects of rosemary against motor neuronal degeneration induced by acrylamide in the developing postnatal rat spinal cord using a postnatal rat model. We assigned the offspring of treated female rats into control, rosemary; acrylamide group; and recovery groups. This work depended on clinical, histopathological, morphometrically, immunohistochemical and genetic methods. In the acrylamide group, we observed oxidation, motor neuron degeneration, apoptosis, myelin degeneration, neurofilament reduction, reactive gliosis. Whoever, concomitant rosemary intake and withdrawal of acrylamide modulate these effects. These findings proof that dietary rosemary can directly protect motor neuron against acrylamide toxicity in the mammalian developing spinal cord.
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