Faten Abd Elzaher

Status epilepticus (SE), the most severe form of epilepsy, leads to brain damage. Uncertainty persists about the mechanisms that lead to the pathophysiology of epilepsy and the death of neurons. Overloading of intracellular iron ions has recently been identified as the cause of a newly recognized form of controlled cell death called ferroptosis. Inhibiting ferroptosis has shown promise as a treatment for epilepsy, according to recent studies. So, the current study aimed to assess the possible antiepileptic impact of CoQ10 either alone or with the standard antiepileptic drug sodium valproate (SVP) and to evaluate the targeted effect of COQ10 on hippocampal oxidative stress and ferroptosis in a SE rat model. Using a lithium-pilocarpine rat model of epilepsy, we evaluated the effect of SVP, CoQ10, or both on seizure severity, histological, and immunohistochemical of the hippocampus. Furthermore, due to the essential role of oxidative stress and lipid peroxidation in inducing ferroptosis, we evaluated malonaldehyde (MDA), reduced glutathione (GSH), glutathione peroxidase 4 (GPX4), and ferritin in tissue homogenate. Our work illustrated that ferroptosis occurs in murine models of lithium-pilocarpine-induced seizures (epileptic group). Nissl staining revealed significant neurodegeneration. A significant increase in the number of astrocytes stained with an astrocyte-specific marker was observed in the hippocampus. Effective seizure relief can be achieved in the seizure model by administering CoQ10 alone compared to SVP. This was accomplished by lowering ferritin levels and increasing GPX4, reducing MDA, and increasing GSH in the hippocampus tissue homogenate. In addition, the benefits of SVP therapy for regulating iron stores, GPX4, and oxidative stress markers were amplified by incorporating CoQ10 as compared to SVP alone. It was concluded that CoQ10 alone has a more beneficial effect than SVP alone in restoring histological structures and has a targeted effect on hippocampal oxidative stress and ferroptosis. In addition, COQ10 could be useful as an adjuvant to SVP in protecting against oxidative damage and ferroptosis-related damage that result from epileptic seizures.

Background: Liver cirrhosis is an important lethal health problem all over the world. Liver transplantation is the first efficient treatment. Unfortunately, it is limited due to many obstacles. Therefore, alternative treatments are required for cirrhosis. Platelet rich plasma (PRP) is a challenging measure for treatment of cirrhosis. Aim of the work: To assess the effect of PRP on experimentally induced liver fibrosis in albino rats.Material and Methods: Twenty-four adult female rats were included in this study. They were divided into three groups: Group I: a control group and included 6 adult rats that received 0.5 ml of olive oil. Group II: consisted of 12 rats. They were subdivided into subgroup IIA: it included 6 rats that received carbon tetrachloride (CCL4) for six weeks and were sacrificed after the last injection for induction of fibrosis, subgroup IIB: it included 6 rats that were left for spontaneous recovery for four weeks after the last CCL4 injection. Group III: it consisted of 6 rats that were subjected to fibrosis then they received PRP (1 ml/kg) twice weekly for four weeks and then were sacrificed. Liver specimens were prepared for histological and immune-histochemical techniques. Morphometrical and statistical studies were done. Results: CCL4 injection resulted in multiple injuries in hepatocytes including vacuolations in the cytoplasm and pyknotic nuclei. In addition, it resulted in hepatic fibrosis especially surrounding the central vein and portal areas. Treatment by PRP resulted in an obvious histological improvement in hepatic structure including apparently normal liver cells with acidophilic cytoplasm and vesicular nuclei and significant decrease (P