Neuroprotective agents: Is effective on toxicity in glial cells?

WOS: 000244480800002PubMed ID: 167583181. Glial cells are the most abundant cell population in the central nervous system. The aim of this study was to examine the effects of melatonin, 7-nitroindazole, and riluzole on glutamate toxicity in primary glial cell culture. 2. Glutamate toxicity was induced by addition of 100 mu M glutamate to the cultures, and then 100 mu M melatonin, 500 mu M 7-nitroindazole, and 10 (M riluzole were administered in different groups. Lactate Dehydrogenase activity and nitrite levels were determined at the 1st, 6th, and 24th h. 3. Melatonin, 7-nitroindazole, and riluzole decrease Lactate Dehydrogenase activity at the 1st, 6th, and 24th h (at all hours, p < 0.05). Nitrite levels were decreased by melatonin and riluzole at the 1st, 6th, and 24th h. 4. In this study, we observed that melatonin, 7-nitroindazole, and riluzole are effective as protective agents on glutamate toxicity in mixed glial cells

NADPH-d and Fos reactivity in the rat spinal cord following experimental spinal cord injury and embryonic neural stem cell transplantation

WOS: 000289922800002PubMed ID: 21376061Aims: The aim of this study is to determine the role of nitric oxide (NO) in neuropathic pain and the effect of embryonic neural stem cell (ENSC) transplantation on NO content in rat spinal cord neurons following spinal cord injury (SCI). Main methods: Ninety adult male Sprague-Dawley rats were divided into 3 groups (n =30, each): control (laminectomy), SCI (hemisection at T12-T13 segments) and SCI +ENSC. Each group was further divided into sub-groups (n = 5 each) based on the treatment substance (L-NAME, 75 mg/kg/i.p.; L-arginine, 225 mg/kg/i. p.; physiological saline, SF) and duration (2 h for acute and 28 days for chronic groups). Pain was assessed by tail flick and Randall-Selitto tests. Fos immunohistochemistry and NADPH-d histochemistry were performed in segments 2 cm rostral and caudal to SCI. Key findings: Tail-flick latency time increased in both acute and chronic L-NAME groups and increased in acute and decreased in chronic L-arginine groups. The number of Fos (+) neurons decreased in acute and chronic L-NAME and decreased in acute L-arginine groups. Following ENSC, Fos (+) neurons did not change in acute L-NAME but decreased in the chronic L-NAME groups, and decreased in both acute and chronic L-arginine groups. NADPH-d (+) neurons decreased in acute L-NAME and increased in L-arginine groups with and without ENSC transplantation. Significance: This study confirms the role of NO in neuropathic pain and shows an improvement following ENSC transplantation in the acute phase, observed as a decrease in Fos(+) and NADPH-d (+) neurons in spinal cord segments rostral and caudal to injury. (C) 2011 Elsevier Inc. All rights reserved.Scientific and Technological Research Council of Turkey (TUBITAK)Turkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK) [SBAG104S330]This study was supported by a grant from The Scientific and Technological Research Council of Turkey (TUBITAK-SBAG104S330)

Tidegluib provides neuroprotection in Parkinson's Disease model through Nrf2/are pathway

Conference of the Society-for-Free-Radical-Research-Europe (SFRR-E) -- JUN 08-11, 2016 -- Budapest, HUNGARYWOS: 000377617900060Soc Free Rad Res Europ