Aims: Parkinson's disease (PD) is the second most prevalent age‐related neurodegenerative disorder. The cerebellum plays a role in PD pathogenesis. Curcumin has numerous medicinal uses, mostly attributed to its potent antioxidant properties. This study investigated the potential protective influence of curcumin on the cerebellum of albino rats with rotenone‐induced PD.Methods: Forty adult male albino rats were randomized into four treatment groups: vehicle (group I); rotenone 3 mg/kg/day i.p. injection (group II); rotenone 3 mg/kg/day plus curcumin 30 mg/kg/day i.p. injection (group III); and curcumin 30 mg/kg/day i.p. injection (group IV).Results: Compared to group I, group II exhibited marked degenerative changes in hematoxylin & eosin‐stained sections and a reduction in Nissl granules in the Purkinje cells of the cerebellum. In group III, the neurotoxic effects in the cerebellum were reduced. Furthermore, the degenerated Purkinje and GFAP‐positive cells increased considerably in group II and were partially reduced in group III versus group II. Compared to group I, rats in group II showed reduced rotarod motor activity, partially restored in group III. Acetylcholine esterase, glutathione, and superoxide dismutase were significantly reduced, and malondialdehyde was significantly increased in group II compared to group I and was partially increased in group III.Conclusion: Curcumin attenuated neurotoxic effects and degenerative histological changes and alleviated induced oxidative stress in the cerebellar cortex of a PD rat model. Therefore, curcumin dietary supplementation may have neuroprotective effects against the development of cerebellum‐related PD symptoms.

Variety of pathological factors including viral hepatitis, alcohol and drug abuse, metabolic diseases, autoimmune diseases and congenital abnormalities can cause hepatic injury. Liver transplantation is the treatment of choice for end-stage liver diseases, however, it faces several difficulties. So the aim of the work is to evaluate the effect of bone marrow derived mesenchymal stem cells (BM-MSCs) on the liver structure in carbon tetra chloride CCL4 induced liver fibrosis in rats. BM-MSCs were isolated and characterized from long bones of twenty male albino rats. Sixty female rats were divided into the following two groups: Group I; thirty rats which were the control group. Group II; thirty rats were injected intra-peritoneal (IP) by CCL4 twice weekly for four weeks and was further subdivided into the following three subgroups: Subgroup IIA (CCL4 alone); included ten rats which were sacrificed after this four weeks. Subgroup IIB (CCL4/MSCs); included ten rats which were IP injected by a single dose of BM-MSCs and were sacrificed after four weeks. Subgroup IIC (CCL4/recovery); included ten rats which were left for another four weeks without any intervention. Histological examination of liver specimens showed that CCl4 caused variable pathological changes with elevated liver enzymes. Injection of BM-MSCs revealed an improvement in the histological picture of the liver and its enzymatic profile. On the other hand, most of the pathological lesion were still detected in rats of recovery group. BM-MSC could restore the liver structure and function in experimental model of liver fibrosis.

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.

Heba Fikry, Sara Abdel Gawad, Walaa Baher. International Journal of Stem Cells 2016;9:96-106. http://dx.doi.org/10.15283/ijsc.2016.9.1.96

Background: The most noticeable consequence of paraquat (PQ) toxicity is pulmonary fibrosis. Mesenchymal stem cells have the remarkable ability to self-renew and differentiate into many cell types. One such type is adipose tissue-derived Mesenchymal Stem Cells (AT-MSCs), which are derived from adipose tissue. Thus, the purpose of this study was to compare the effects of AT-MSCs and rapamycin on paraquat-induced acute lung injury and pulmonary fibrosis in a mouse model. Methods: Fifty female mice were randomly allocated to four groups. Group I (control group) received the drug solvent using the same route of administration for the same duration as the corresponding experimental groups. Group II (pulmonary fibrosis group) lung injury was induced by injection of PQ at a dosage of 40 mg/kg. Group III (AT-MSCs group) received 1.0 × 10⁵ cells/mouse of male AT-MSCs. Group IV (rapamycin group) received 2.5 mg/kg/day diluted in 1% Dimethyl sulfoxide orally for two weeks. Lung tissue was harvested at the end of the experiment and analyzed by light and electron microscopy in addition to immunohistochemistry evaluation of p53. Samples were also taken to -80 for identification of the Y chromosome (SRY gene) and biochemical testing in the lung tissue. The injured lung was improved with AT-MSCs. Just like the control group, they restored p53 levels. Results: Following injection with AT-MSCs, there was an increase in Y-chromosome expression levels. Treatment with AT-MSCs also reduced malondialdehyde levels in the lung tissues while increasing superoxide dismutase and reduced glutathione levels. The results showed that pulmonary fibrosis may be mitigated following AT-MSCs transplantation in PQ-poisoned mice by suppressing the synthesis of pro-inflammatory cytokines (interleukin-6 and tumor necrosis factor-alpha) in the lung tissues of the animals. The SRY gene’s expression was significantly upregulated in the AT-MSCs treatment group. Conclusion: This study provides more evidence that the immunomodulatory effects of AT-MSC transplantation can alleviate pulmonary inflammatory and fibrotic alterations more effectively than rapamycin. As a result, these cells are a very promising pharmacological therapy for acute lung injury and pulmonary fibrosis induced by PQ poisoning.