Association of folic acid, vitamin B12, and intelligence scores in epileptic children.

Epilepsy is a serious childhood disease associated with cognitive impairment. Our aim was to investigate the possible association of serum folic acid, vitamin B12, and intelligence scores in epileptic children. A group of 30 children with established diagnosis of idiopathic epilepsy for at least one year as well as another group of 30 nonepileptic healthy children as the control group were recruited for analysis. Cognitive performance was assessed by a battery of psychological tests that covers verbal and nonverbal intelligence. Serum B12 level was significantly lower in patients than the control group (264.17 ± 58.07, 450.55 ± 134.9, respectively). No significant difference was detected between patients and the control group regarding serum folic acid level. Verbal, performance, and total IQ were significantly lower in patients than the control group (83.2 ± 3.08 vs. 95.8 ± 6.22, 78.4 ± 10.68 vs. 91.3 ± 2.45, and 180.6 ± 6.58 vs. 93.5 ± 3.02, respectively). However, no significant correlation was detected in folic acid, vitamin B 12, and cognitive scores. Epileptic children were five times more at risk of having low IQ (verbal, performance, and total) < 85 than the control group (OR = 4.754, 95% CI 13.047-1031.316, p = .000). In conclusion, children with epilepsy might be at higher risk for cognitive dysfunction than normal children. No significant association was detected between cognitive performance and either folic acid or vitamin B12 in epileptic children receiving sodium valproate. Supplementation of those vitamins should be restricted to those with documented deficiency.

Modulatory effect of silymarin on nuclear factor-erythroid-2-related factor 2 regulated redox status, nuclear factor-κB mediated inflammation and apoptosis in experimental gastric ulcer.

Non-steroidal anti-inflammatory drugs (NSAIDs) consumption has been commonly associated with gastric mucosal lesions including gastric ulcer. Silymarin (SM) is a flavonoid mixture with anti-oxidant and anti-inflammatory activities which explain its protective role against hepatic and renal injuries. However, its impact on gastric ulcer has not yet been elucidated. Thus we went further to investigate the potential protective effects of SM against indomethacin-induced gastric injury in rats. Pretreatment with SM (50 mg/kg orally) attenuated the severity of gastric mucosal damage as evidenced by decreasing ulcer index (UI) and ulcer score, improvement of disturbed histopathologicl features to be insignificant with those induced by the reference anti-ulcer drug. Pretreatment with SM also suppressed gastric inflammation by decreasing myeloperoxidase activity, tumer necrosis factor-α (TNF- α) and interleukin 6 (IL6) levels along with nuclear factor kappa B p65 (NF-κB) expression. Meanwhile, SM prevent gastric oxidative stress via inhibition of lipid peroxides formation, enhancement of glutathione peroxidase, superoxide dismutase activities and up-regulation of nuclear factor-erythroid-2-related factor 2 (Nrf2), the redox-sensitive master regulator of oxidative stress signaling. In conclusion, the results herein revealed that SM has a gastro-protective effect which is mediated via suppression of gastric inflammation, oxidative stress, increased the anti-oxidant and the cyto-protective defense mechanisms.