Neuroprotective Effects of a Variety of Pomegranate Juice Extracts (PJE) Against the Excitotoxin Quinolinic Acid in Human Primary Neurons.

BACKGROUND: Quinolinic acid (QUIN) excitotoxicity is mediated by elevated intracellular Ca2+ levels, and nitric oxide (NO•) mediated oxidative stress leading to DNA damage, and cell death due to energy restriction. METHODS: We evaluated the effect of a series of pomegranate juice extracts (PJE), Helow, Malasi, Qusum, and Hamedh, with antioxidant properties on QUIN induced excitotoxicity on primary cultures of human neurons. RESULTS: We showed that Helow and Malasi can attenuate QUIN-induced excitotoxicity to a greater extent than Qusum and Hamedh from Oman. Similarly, both Helow and Malasi were able to attenuate QUIN-induced Ca2+ influx and nNOS activity to a greater extent compared to Qusum, and Hamedh. All extracts reduced the oxidative effects of increased NO• production, and hence preventing NAD+ depletion and cell death. CONCLUSION: In addition to the well-known antioxidant properties of these natural phytochemicals, the inhibitory effect of some of these compounds on specific excitotoxic processes such as calcium influx provides additional evidence for the beneficial health effects of PJE in excitable tissue, particularly within the CNS.

MRI features of epidural extramedullary hematopoiesis.

A case of beta-thalassemia intermedia with spinal cord compression due to extramedullary hematopoiesis, which was successfully treated by blood transfusion, is presented. Emphasis was made on the MRI appearance of extramedullary hematopoiesis on different pulse sequences. The theories that aimed to explain the involvement of the epidural space by extramedullary hematopoiesis are discussed.

Lymphocyte migration and multiple sclerosis: relation with disease course and therapy.

Lymphocyte migration into the central nervous system is a central event in lesion formation in multiple sclerosis. By using a fibronectin-coated membrane Boyden chamber assay, we observed that migration rates of immediately ex vivo lymphocytes from patients with relapsing-remitting, with or without concurrent clinical relapse, or with secondary progressive disease, were increased compared with healthy donors. Migration rates of lymphocytes from relapsing-remitting multiple sclerosis patients receiving either glatiramer acetate (Copaxone 20 mg daily) or interferon-beta1b (Betaseron 8 MIU, three times per week) were significantly reduced compared with untreated relapsing-remitting patients. In vitro treatment with interferon-beta1b (1,000 U/ml), but not glatiramer acetate (20 microg/ml), significantly reduced lymphocyte-migration rates, suggesting that the effects of these two therapeutic agents on migration result from different mechanisms of actions. Interferon-beta1b acts, at least in part, by a direct effect on this cell property, whereas glatiramer acetate effects are indirect.