Prenatal Alcohol-Induced Neuroapoptosis In Rat Brain Cerebral Cortex: Protective Effect Of Folic Acid And Betaine
| Autor: | Ibrahim Sogut, Güngör Kanbak, Kazim Kartkaya, Aysegul Oglakci, Ferruh Yücel, Onur Uysal |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Cathepsin L Alcohol Apoptosis Cathepsin B Rats Sprague-Dawley chemistry.chemical_compound 0302 clinical medicine Betaine Pregnancy chemistry.chemical_classification Cerebral Cortex biology Calpain Caspase 3 Cytochromes c General Medicine Neuroprotective Agents Biochemistry Prenatal Exposure Delayed Effects Blood Alcohol Content Female medicine.medical_specialty Fetal alcohol syndrome 03 medical and health sciences Folic Acid Internal medicine medicine Animals Ethanol business.industry Central Nervous System Depressants medicine.disease Rats Disease Models Animal 030104 developmental biology Endocrinology Enzyme chemistry Animals Newborn Pediatrics Perinatology and Child Health biology.protein Neurology (clinical) business 030217 neurology & neurosurgery |
| Popis: | Alcohol consumption in pregnancy may cause fetal alcohol syndrome (FAS) in the infant. This study aims to investigate prenatal alcohol exposure related neuroapoptosis on the cerebral cortex tissues of newborn rats and possible neuroprotective effects of betaine, folic acid, and combined therapy. Pregnant rats were divided into five experimental groups: control, ethanol, ethanol + betaine, ethanol + folic acid, and ethanol + betaine + folic acid combined therapy groups. We measured cytochrome c release, caspase-3, calpain and cathepsin B and L. enzyme activities. In order to observe apoptotic cells in the early stages, TUNEL method was chosen together with histologic methods such as assessing the diameters of the apoptotic cells, their distribution in unit volume and volume proportion of cortical intact neuron nuclei. Calpain, caspase-3 activities, and cytochrome c levels were significantly increased in alcohol group while cathepsin B and L. activities were also found to be elevated albeit not statistically significant. These increases were significantly reversed by folic acid and betaine + folic acid treatments. While ethanol increased the number of apoptotic cells, this increase was prevented in ethanol + betaine and ethanol + betaine + folic acid groups. Morphometric examination showed that the mean diameter of apoptotic cells was increased with ethanol administration while this increase was reduced by betaine and betaine + folic acid treatments. We observed that ethanol is capable of triggering apoptotic cell death in the newborn rat brains. Furthermore, folic acid, betaine, and combined therapy of these supplements may reduce neuroapoptosis related to prenatal alcohol consumption, and might be effective on preventing fetal alcohol syndrome in infants. |
| Databáze: | OpenAIRE |
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