Mohammed Farahna

Anti-plasmodial effects of Azadirachta indica in experimental cerebral malaria: Apoptosis of cerebellar Purkinje cells of mice as a marker

Background: Malaria is a major public health problem in the world, but treatment of malaria is becoming more difficult due to increasing drug resistance. Therefore, the need for alternative drugs is acute. Aims: This study investigated the antiplasmodial and protective effect of an ethanolic extract of the leaves from a traditionally used medicinal plant, Azadirachta indica (Neem) in a mouse model of malaria. Materials and Methods: Swiss albino mice were intraperitoneally infected with 10×106 Plasmodium berghei ANKA, a rodent malaria parasite. The presence of parasites was checked by microscopic examination of blood samples daily. Ethanolic extracts of Neem at 300, 500 and 1000 mg/kg were administered intraperitoneally daily for five days from the day parasitaemia reach 5% of parasite inoculation. Intraperitoneal chloroquine and artemether were used as standard drug treatment controls. Symptoms of neurological or respiratory disorder, mortality, weight and temperature were recorded. Histological sections of brain were prepared and examined after staining with hematoxylin-eosin and immunohistochemistry for apoptotic cells. Results: All Neem treatment groups displayed parasitaemia that gradually increased during treatment, and showed signs of terminal illness (i.e. hypothermia, ptosis and convulsions) within 2–4 days post-treatment. In contrast, the chloroquine and artemether groups showed no cerebral malaria symptoms and no deaths. Apoptosis in Purkinje cells, cerebral haemorrhage and oedema were found in some of the mice treated with Neem and chloroquine. Conclusions: Azadirachta indica (Neem) extract was not protective against malaria symptoms and signs in this mouse model. However, a difference in the number of apoptotic Purkinje cells between the untreated control group and Neem treatment at 500 mg/kg suggests that Neem may have some neuronal protective effect.

High fiber probiotic fermented mare's milk reduces the toxic effects of mercury in rats.

Background: Since the advent of the Industrial Revolution in the late 19th century, we have all been unfortunately exposed to an increasingly toxic and polluted world. Among the most dangerous of these pollutants is mercury, which is considered to be the most toxic non-radioactive heavy metal. Fermented foods may help cleanse the body of heavy metals. Fermentation breaks down the nutrients in foods by the action of beneficial microorganisms and creates natural chelators that are available to bind toxins and remove them from the body. Aims: The current study was designed to determine the impact of feeding a high fiber probiotic fermented mares milk on the biological effects of mercury toxicity in rat model. Methods and Materials: The high fiber fermented mares milk containing probiotics was prepared and its sensory properties, chemical composition, and antioxidant activity were determined. A rat model of mercury toxicity was used. The effect of feeding the high fiber probiotic fermented mares milk to rats, along with mercury ingestion, was determined by the analysis of several biochemical markers in serum and histopathological examinations of brain and kidney. Results: The high fiber fermented mares milk containing probiotics was found to be acceptable by all test panels and volunteers. Mercury ingestion was found to cause biochemical and histopathological alterations in rat serum and tissues. The mercury-treated rats showed a decrease in body weight and an increase in kidney weight. Sera of the mercury treated rats showed alterations in biochemical parameters, and histopathological changes in brain and kidney. However, the rats fed high fiber fermented mare`s milk along with mercury ingestion showed improved histopathology of kidney and brain, and there was restoration of the biochemical parameters in serum to almost normal values. Conclusions: Feeding high fiber fermented mare`s milk may reduce the toxic effects of mercury.

Signaling pathways bridging fate determination of neural crest cells to glial lineages in the developing peripheral nervous system

Fate determination of neural crest cells is an essential step for the development of different crest cell derivatives. Peripheral glia development is marked by the choice of the neural crest cells to differentiate along glial lineages. The molecular mechanism underlying fate acquisition is poorly understood. However, recent advances have identified different transcription factors and genes required for the complex instructive signaling process that comprise both local environmental and cell intrinsic cues. Among others, at least the roles of Sox10, Notch, and neuregulin 1 have been documented in both in vivo and in vitro models. Cooperative interactions of such factors appear to be necessary for the switch from multipotent neural crest cells to glial lineage precursors in the peripheral nervous system. This review summarizes recent advances in the understanding of fate determination of neural crest cells into different glia subtypes, together with the potential implications in regenerative medicine.

Garcinia kola aqueous suspension prevents cerebellar neurodegeneration in long-term diabetic rat – a type 1 diabetes mellitus model

ETHNOPHARMACOLOGICAL RELEVANCE The development of compounds able to improve metabolic syndrome and mitigate complications caused by inappropriate glycemic control in type 1 diabetes mellitus is challenging. The medicinal plant with established hypoglycemic properties Garcinia kola Heckel might have the potential to mitigate diabetes mellitus metabolic syndrome and complications. AIM OF THE STUDY We have investigated the neuroprotective properties of a suspension of G. kola seeds in long-term type 1 diabetes mellitus rat model. MATERIALS AND METHODS Wistar rats, made diabetic by single injection of streptozotocin were monitored for 8 months. Then, they were administered with distilled water or G. kola oral aqueous suspension daily for 30 days. Body weight and glycemia were determined before and after treatment. After sacrifice, cerebella were dissected out and processed for stereological quantification of Purkinje cells. Histopathological and immunohistochemical analyses of markers of neuroinflammation and neurodegeneration were performed. RESULTS Purkinje cell counts were significantly increased, and histopathological signs of apoptosis and neuroinflammation decreased, in diabetic animals treated with G. kola compared to diabetic rats given distilled water. Glycemia was also markedly improved and body weight restored to non-diabetic control values, following G. kola treatment. CONCLUSIONS These results suggest that G. kola treatment improved the general condition of long-term diabetic rats and protected Purkinje cells partly by improving the systemic glycemia and mitigating neuroinflammation.

Stromal control of chronic lymphocytic leukemia cells

License. The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. Permissions beyond the scope of the License are administered by Dove Medical Press Limited. Information on how to request permission may be found at: http://www.dovepress.com/permissions.php Research and Reports in Biology 2013:4 23–32 Research and Reports in Biology Dovepress

Garcinia kola seeds may prevent cognitive and motor dysfunctions in a type 1 diabetes mellitus rat model partly by mitigating neuroinflammation

Abstract Background We reported recently that extracts of seeds of Garcinia kola, a plant with established hypoglycemic properties, prevented the loss of inflammation-sensible neuronal populations like Purkinje cells in a rat model of type 1 diabetes mellitus (T1DM). Here, we assessed G. kola extract ability to prevent the early cognitive and motor dysfunctions observed in this model. Methods Rats made diabetic by single injection of streptozotocin were treated daily with either vehicle solution (diabetic control group), insulin, or G. kola extract from the first to the 6th week post-injection. Then, cognitive and motor functions were assessed using holeboard and vertical pole behavioral tests, and animals were sacrificed. Brains were dissected out, cut, and processed for Nissl staining and immunohistochemistry. Results Hyperglycemia (209.26 %), body weight loss (–12.37 %), and T1DM-like cognitive and motor dysfunctions revealed behavioral tests in diabetic control animals were not observed in insulin and extract-treated animals. Similar, expressions of inflammation markers tumor necrosis factor (TNF), iba1 (CD68), and Glial fibrillary acidic protein (GFAP), as well as decreases of neuronal density in regions involved in cognitive and motor functions (–49.56 % motor cortex, –33.24 % medial septal nucleus, –41.8 % /–37.34 % cerebellar Purkinje /granular cell layers) were observed in diabetic controls but not in animals treated with insulin or G. kola. Conclusions Our results indicate that T1DM-like functional alterations are mediated, at least partly, by neuroinflammation and neuronal loss in this model. The prevention of the development of such alterations by early treatment with G. kola confirms the neuroprotective properties of the plant and warrant further mechanistic studies, considering the potential for human disease.

Signaling Pathways Sustaining Antibiotic Resistance: Lessons From Methicillin-Resistant Staphylococcus aureus

Multidrug-resistant bacteria constitute a major public health burden, as these lethal pathogens of fish, birds, and mammals cause difficult-to-treat health care–associated or community-acquired infections in humans. Indeed, recent information from the World Health Organization highlighted that drug-resistant infections already kill hundreds of thousands a year globally, and by 2050, that figure could be more than 10 million, with an associated economic burden of up to

Signaling pathways bridging microbial-triggered inflammation and cancer

100 trillion, if prompt actions are not taken. Staphylococcus aureus is a leading cause of fatal bacterial infections worldwide, with a death rate of about 20% of cases in industrialized countries (and even more in developing countries). Moreover, the economic implications of growing methicillin-resistant S. aureus (MRSA) incidence in community patients and farm animal lineages suggest that the burden of MRSA infections could even be more considerable than reported. This chapter endeavors to review the state of the knowledge of biological processes and signaling molecules accounting for the development of resistance in bacteria, with a particular emphasis on evidence from resistant and persistent variants of S. aureus .