ABSTRACT
PURPOSE: Perinatal hypoxic-ischemic (HI) brain injury remains a common cause of chronic handicapping conditions of cerebral palsy, mental retardation, learning disability, and epilepsy. HI brain injury induces cell death via either necrosis or apoptosis. Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family. It plays key roles in survival, differentiation, and maintenance of neurons. This study was to investigate the neuroprotective effects of BDNF via the mechanisms of anti-apoptosis in HI brain injury by using cortical astrocyte and neuronal cell culture. METHODS: Cortical astrocytes culture of 1-day-old Sprague-Dawley (SD) rat pups and embryonic cortical neuronal cell culture of SD rats at 14-day gestation were done. The Normoxia group was prepared in 5% CO2 incubators and the Hypoxia group and Hypoxia+BDNF group (after treatment with BDNF for 24 hours) were placed in 1% O2 incubators (94% N2, 5% CO2) for 6 or 18 hours. The expression of Bcl-2 and Bax were assessed by real-time PCR and western blot. The caspase-3 activation was evaluated by caspase activity assay kit. RESULTS: In astrocyte and neuronal cell, the expressions of Bcl-2 in the hypoxia groups were reduced compared to the normoxia groups, whereas, those in the Hypoxia+BDNF groups were increased compared to the hypoxia groups. However, the expressions of Bax and caspase-3 and the ratio of Bax/Bcl-2 were revealed reversely. In astrocyte, Hypoxia group for 6 hours was not significantly altered in Bcl-2, Bax expressions. CONCLUSION: BDNF neuroprotective effects on HI brain injury in neonatal rats may occur via anti-apoptotic mechanism.
Subject(s)
Animals , Humans , Pregnancy , Rats , Hypoxia , Apoptosis , Astrocytes , Blotting, Western , Brain Injuries , Brain , Brain-Derived Neurotrophic Factor , Caspase 3 , Cell Culture Techniques , Cell Death , Cerebral Palsy , Epilepsy , Incubators , Intellectual Disability , Learning Disabilities , Necrosis , Neurons , Neuroprotective Agents , Rats, Sprague-Dawley , Real-Time Polymerase Chain ReactionABSTRACT
PURPOSE: Retinopathy of prematurity (ROP) is one of the leading causes of blindness, with retinal detachment occurring due to oxygen toxicity in preterm infants. After premature delivery, oxygen levels are significantly increased compared to those in utero and oxygen therapy further increases oxygen levels in the developing retina. This hyperoxia results in reducing vascular endothelial growth factor (VEGF) level. After the cessation of oxygen therapy and the return to normal oxygen levels, the nonperfused portions of the retina become hypoxic. Retinal hypoxia stimulates VEGF which causes retinal neovascularization and retinal proliferation. Further inhibition of VEGF decreases retinal neovascularization. Recently, resveratrol was found to protect the spinal cord, kidney, and heart from ischemia-reperfusion injury through upregulation of nitric oxide (NO). Resveratrol has been reported to either suppress or enhance NO production. Resveratrol inhibits nitric oxide synthase (NOS) activity and modifies inducible nitric oxide synthase (iNOS) expression. In the present study, we aimed to determine whether or not resveratrol exhibits protective effects via mediation of NOS after a hypoxic retinal insult. METHODS: In the in vitro hypoxic retinal injury, primary retinal cell culture was performed using P0-2 Sprague-Dawley (SD) rats. Hypoxia insults were induced through 1% O2 exposure for sixteen hours. Western blotting and real-time PCR using iNOS, endothelia nitric oxide synthase (eNOS), neuronal nitric oxide synthase (nNOS) antibodies and mRNAs were performed. RESULTS: The expressions of iNOS antibody and mRNA were reduced after a hypoxic insult, whereas it was recovered after treatment with resveratrol. In contrast, those of eNOS and nNOS showed reversely. CONCLUSION: Resveratrol appeared to exert retinal protective effects via mediation of NOS on hypoxic retinal injury in neonatal rats.
Subject(s)
Animals , Humans , Infant, Newborn , Rats , Hypoxia , Antibodies , Blindness , Blotting, Western , Cell Culture Techniques , Heart , Hyperoxia , Infant, Premature , Kidney , Negotiating , Nitric Oxide , Nitric Oxide Synthase , Nitric Oxide Synthase Type I , Nitric Oxide Synthase Type II , Oxygen , Real-Time Polymerase Chain Reaction , Reperfusion Injury , Retina , Retinal Detachment , Retinal Neovascularization , Retinaldehyde , Retinopathy of Prematurity , RNA, Messenger , Spinal Cord , Stilbenes , Up-Regulation , Vascular Endothelial Growth Factor AABSTRACT
Non-typhoidal salmonella (NTS) is a common pathogen involved in food poisoning. It has various extraintestinal complications including encephalopathy. However, NTS associated encephalopathy is rarely reported. A previously healthy 14-year-old boy was admitted for altered level of consciousness. He had profuse watery diarrhea with fever on the day of admission. Physical examination was unremarkable except slightly increased bowel sounds and altered mental state. Cerebrospinal fluid analysis revealed mild pleocytosis. Meningoencephalitis was the presumptive diagnosis. His consciousness was recovered over 24 hours, bloody and mucoid diarrhea developed the next day after admission. NTS organism was isolated from his stool. After 1 week, he fully recovered neurologically but a mild watery diarrhea persisted at the time of discharge.