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Background:The contribution of high dietary cholesterol to encephalomyelitis and retinal diseases give more attention to overcome its neurotoxicity. These led physician and scientists of using anti-lepidemic statin drugs, however their long-term treatment may develop complication. Today many views recommended supplements of natural products especially fruit to get demand of needed antioxidant to scavenge bad free radicals liberated from inflammation. Pomegranate juice supplementation is used in the present study in combination with atorvastatin drug hoping to give synergistic effects and improve neurotoxicity.Material and methods: Eighty pregnant Wistar albino rats weighing 180 g to 200 g body weight were used. They were arranged into eight groups (n=8) such as control, atorvastatin (1 mg/kg), pomegranate (0.5 ml 50%/ rat), atorvastatin and pomegranate, hyper ccholesterolemic group (3% cholesterol diet for 6 weeks before onset of gestation), hypercholesterolemia and atorvastatin and/or pomegranate. All treatments were maintained throughout gestation and lactation period till 2 and 3 week-old. Offspring were sacrificed by diethyl ether and their cervical spinal cord were dissected and separated. The spinal cord was subjected for histological and transmission electron microscopical investigations, biochemical assays of neurotransmitters (dopamine, serotonin and γ-Aminobutyric acid), vascular endothelial growth factors, 8-hydroxydeoxyguanosine, caspase 3 and caspase 7 as well as comet assay). Results:The present findings revealed massive cell death and necrosis within ependymal canal as well as pyknosis and edematous lesions of neuronal cells in offspring of hypercholesterolemic mothers. At ultrastructural level, there is a detected demyelination and vacuolar degeneration of myelinated axons. Many of sensory and motor neuronal cells exhibited compacted chromatin materials of their nuclei. These were associated with depletion of assayed neurotransmitters (DA and 5-HT), overexpression of vascular endothelial growth factors, caspases 3 and 7 and 8-hydroxydeoxyguanosine. Stretched DNA damage (comet assay) with obvious head and tail region was detected in neuronal cells of offspring of hypercholesterolemic mothers and decreased post-pomegranatesupplementation. Atorvastatin and pomegranate supplementation exhibited apparent improvement comparing with single atorvastatin or pomegranate manifesting highly synergistic effects. Conclusion:Feeding pregnant on hypercholesterolemic diet induced spinal cord injury of their offspring and these can be improved by pomegranate juice supplementation in combination with atorvastatin-treatment.

Dietary consumption of processed high fat diet led to the development of metabolic diseases. This study aimed to demonstrate the retinopathy in a rat offspring maternally fed on high cholesterol and the improvement of pomegranate juice (PJ) administration and atorvastatin as potential treatment. Eighty pregnant Wistar albino rats were categorized into eight groups (n = 10); the control, PJ supplementation [0.4 m L (20%)]; atorvastatintreatment (10 mg/kg); and hypercholesterolemia (fed on 3% cholesterol for 6 weeks prior to conception, during pregnancy and lactation period. Retinas of 21-day-old rat offspring were investigated. Offspring maternally fed on a hypercholesterolemic diet exhibited internal retinal hemorrhage at the interphase between the pigment epithelium and photoreceptors leading to retinal detachment. In addition, widespread of degenerated stacked membrane of the photoreceptor outer segment and the neovascularization within the nuclear layers were observed. Offspring retina of a hypercholesterolemic mother exhibited a significant depletion of assayed neurotransmitters coinciding with a significant increase of the vacuolar endothelial growth factor apoptotic markers expressing pressing damaging of retinal cells. Co-administration of pomegranate juice to hypercholesterolemic mother rats treated with atorvastatin significantly improved the retinal structure and the assayed biochemical markers of offspring than that with atorvastatin-treatment. In conclusion, PJ showed a potent antiapoptotic and ant-angiogenesis activity and improved the histocytological pictures of rat offspring maternally subjected to hypercholesterolemia.

Aim: Recently, there is an increased average of developing cancers. Though, the chemotherapeutic-treatment is unfavorable during pregnancy due to its harmful effects on developing fetuses, physicians have two ways to minimize these effects either by termination of the pregnancy or minimizing its side effects. The present work aimed to illustrate the susceptibility of cardiac, lung and dorsal aorta function to the widely applicable drugs doxorubicin and cisplatin as well as 5-flurouracil. Materials and Methods: Mother albino rats were arranged into four-groups (control, doxorubicin, cisplatin and 5-flurouracil-treated groups). Each pregnant rat received intraperitoneal administration of 0.2 mg/kg body weight at 10 th and 14 th day of gestation and sacrificed at parturition (two doses). At parturition, serum of mother rats used to assess troponin I, heat shock protein 70, 8-hydroxydeoxyguanosine, vascular endothelial growth factor and adhesion molecules (ICAM-1 & VCAM-1). Isoenzyme electrophoresis of alkaline and acid phosphatases, glucose-6-phosphate dehydrogenase and lactic dehydrogenase were estimated in serum, myocardium and dorsal aorta of mother rats. The myocardium and lung were processed for histopathological investigations for both mothers and their offspring. Single strand (comet assay) and double strand DNA damage were carried out in heart and dorsal aorta of mother rats. Results: The present finding revealed that there are detected alterations of myocardial markers and lung amino acid metabolism as well as disruption of myocardial isoenzymes. 83Chinese Medicine DNA damage of myocardium and dorsal aorta were observed. Conclusions: The authors concluded that the metabolic activity of heart and lung is highly susceptible to doxorubicin and cisplatin treatment compared to 5-flurouracil and the therapeutic doses must be degraded.