Protective effect of sterubin against neurochemical and behavioral impairments in rotenone-induced Parkinson's disease.

This study was conducted to evaluate how sterubin affects rotenone-induced Parkinson's disease (PD) in rats. A total of 24 rats were distributed into 4 equal groups: normal saline control and rotenone control were administered saline or rotenone (ROT), respectively, orally; sterubin 10 received ROT + sterubin 10 mg/kg po; and sterubin alone was administered to the test group (10 mg/kg). Rats of the normal saline and sterubin alone groups received sunflower oil injection (sc) daily, 1 h after receiving the treatments cited above, while rats of the other groups received rotenone injection (0.5 mg/kg, sc). The treatment was continued over the course of 28 days daily. On the 29th day, catalepsy and akinesia were assessed. The rats were then euthanized, and the brain was extracted for estimation of endogenous antioxidants (MDA: malondialdehyde, GSH: reduced glutathione, CAT: catalase, SOD: superoxide dismutase), nitrative (nitrite) stress markers, neuroinflammatory cytokines, and neurotransmitter levels and their metabolites (3,4-dihydroxyphenylacetic acid (DOPAC), dopamine (DA), norepinephrine (NE), serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), and homovanillic acid (HVA)). Akinesia and catatonia caused by ROT reduced the levels of endogenous antioxidants (GSH, CAT, and SOD), elevated the MDA level, and altered the levels of nitrites, neurotransmitters, and their metabolites. Sterubin restored the neurobehavioral deficits, oxidative stress, and metabolites of altered neurotransmitters caused by ROT. Results demonstrated the anti-Parkinson's activities of sterubin in ROT-treated rats.

Protective effect of sterubin against neurochemical and behavioral impairments in rotenone-induced Parkinson's disease

This study was conducted to evaluate how sterubin affects rotenone-induced Parkinson's disease (PD) in rats. A total of 24 rats were distributed into 4 equal groups: normal saline control and rotenone control were administered saline or rotenone (ROT), respectively, orally; sterubin 10 received ROT + sterubin 10 mg/kg po; and sterubin alone was administered to the test group (10 mg/kg). Rats of the normal saline and sterubin alone groups received sunflower oil injection (sc) daily, 1 h after receiving the treatments cited above, while rats of the other groups received rotenone injection (0.5 mg/kg, sc). The treatment was continued over the course of 28 days daily. On the 29th day, catalepsy and akinesia were assessed. The rats were then euthanized, and the brain was extracted for estimation of endogenous antioxidants (MDA: malondialdehyde, GSH: reduced glutathione, CAT: catalase, SOD: superoxide dismutase), nitrative (nitrite) stress markers, neuroinflammatory cytokines, and neurotransmitter levels and their metabolites (3,4-dihydroxyphenylacetic acid (DOPAC), dopamine (DA), norepinephrine (NE), serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), and homovanillic acid (HVA)). Akinesia and catatonia caused by ROT reduced the levels of endogenous antioxidants (GSH, CAT, and SOD), elevated the MDA level, and altered the levels of nitrites, neurotransmitters, and their metabolites. Sterubin restored the neurobehavioral deficits, oxidative stress, and metabolites of altered neurotransmitters caused by ROT. Results demonstrated the anti-Parkinson's activities of sterubin in ROT-treated rats.

Comparison between killed and living probiotic usage versus placebo for the prevention of necrotizing enterocolitis and sepsis in neonates.

UNLABELLED: The aim of the study is to compare the role of killed (KP) Lactobacillus acidophilus with living (LP) in reducing incidence of sepsis (NS) and necrotizing enterocolitis (NEC) in neonates. Randomized double blind placebo study, included 150 neonates admitted to NICU at day 1, sixty received oral (LP) and 60 received (KP) and 30 received placebo. One gram of stools was collected on admission, at day 7, at end of the study, as well as on suspected NEC or NS and was sent for culture. RESULTS: LP and KP were preventive factors for NEC with absolute risk reduction (AAR) 16, 15%, respectively and 18% for NS compared to placebo. Incidence of NEC and NS did not differ significantly between neonates supplemented with LP and those with KP. Preterm neonates supplemented with KP showed significantly lower incidence of NEC compared to placebo, while incidence of NS showed no significant difference between both groups. There is significant reduction in NS and NEC among neonates with positive Lactobacillus colonization of gut compared to those none colonized at day 7 (27.9 vs. 85.9%, 0 vs. 7.8%) and at day 14 (48.7 vs. 91.7% for NS and 0 vs. 20.8% for NEC). Overall comparison between the three groups showed statistical significant reduction in the incidence of NEC. Present conclusions are that early gut colonization with beneficial bacteria lowers the incidence of NEC and NS. KP retained similar benefits to live bacteria.

Cord blood brain derived neurotrophic factor: diagnostic and prognostic marker in fullterm newborns with perinatal asphyxia.

This prospective case control study was designed to evaluate cord blood brain derived neurotrophic factor level in full term newborns with perinatal asphyxia as a marker of central nervous system insult and predictor of severity of hypoxic ischemic encephalopathy, with follow up of its level during the reperfusion phase. The study included twenty fullterm neonates with perinatal asphyxia (cases) and twenty controls. Cord blood samples were obtained at birth and peripheral blood samples at 72 h postnatal from cases only. Plasma brain derived neurotrophic factor level was measured using enzyme linked immunosorbent assay. The clinical severity of encephalopathy was graded based on Sarnat and Sarnat staging. Cord Plasma brain derived neurotrophic factor level was significantly increased among cases compared to controls. Among cases, brain derived neurotrophic factor level at delivery and after 72 h significantly correlated with the severity of encephalopathy according to Sarnat staging being higher as severity increases. Brain derived neurotrophic factor level significantly increased after 72 h of life compared to its level at delivery among cases. Brain derived neurotrophic factor levels at delivery and at 72 h postnatal were predictors of severe Sarnat stage and poor outcome. We concluded that brain derived neurotrophic factor level as a marker of central nervous system insult is increased in full term newborns with perinatal asphyxia. It can serve as an indicator for the severity of encephalopathy and adverse outcomes.