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1.
Int. j. morphol ; 38(3): 530-535, June 2020. graf
Artigo em Inglês | LILACS | ID: biblio-1098283

RESUMO

Dysregulated autophagy, whether excessive or downregulated, has been thought to be associated with neurodegenerative disorders including Parkinson's disease. Accordingly, the present study was carried out to investigate whether 3-methyladenine, an autophagy inhibitor, can modulate the effects of rotenone on dopaminergic neurons in primary mesencephalic cell culture. Cultures were prepared from embryonic mouse mesencephala at gestation day 14. Four groups of cultures were treated on the 10th DIV for 48 h as follows: the first was kept as an untreated control, the second was treated with 3-methyladenine alone (1, 10, 100, 200 mM), the third was treated with 20 nM rotenone and the fourth was co-treated with 20 nM rotenone and 3-methyladenine (1, 10, 100, 200 mM). On the 12th DIV, cultured cells were stained immunohistochemically against tyrosine hydroxylase and culture media were used to measure the levels of lactate dehydrogenase. 3methyladenine had no effects on both the survival of dopaminergic neurons and the release of lactate dehydrogenase. Rotenone significantly decreased the number of dopaminergic neurons and increased the levels of lactate dehydrogenase in the culture media. When cultures concomitantly treated with 3-methyladenine and rotenone, 3-methyladenine had no effect against rotenone-induced dopaminergic cell damage and lactate dehydrogenase release into the culture medium. In conclusion, the autophagy inhibitor 3-methyladenine could not modulate rotenone-induced dopaminergic cell damage in primary mesencephalic cell culture.


Se estima que la autofagia desregulada, ya sea excesiva o con baja regulación, está asociada con trastornos neurodegenerativos, incluyendo la enfermedad de Parkinson. En consecuencia, el se realizó este estudio para investigar si la 3metiladenina, un inhibidor de la autofagia,puede modular los efectos de la rotenona en las neuronas dopaminérgicas en el cultivo primario de células mesencefálicas. Los cultivos se prepararon a partir de mesencéfalo de ratón embrionario el día 14 de gestación. Cuatro grupos de cultivos se trataron en el 10º DIV durante 48 h de la siguiente manera: el primer grupo se mantuvo como un control no tratado, el segundo se trató con 3-metiladenina sola (1, 10, 100, 200 mM), el tercer grupo se trató con rotenona 20 nM y el cuarto se trató conjuntamente con rotenona 20 nM y 3-metiladenina (1, 10, 100, 200 mM). En el 12º DIV; las células cultivadas fueron tratadas mediante tinción inmunohistoquímica en tirosina hidroxilasa y se usaron medios de cultivo para medir los niveles de lactato deshidrogenasa. La 3-metiladenina no tuvo efectos tanto en la supervivencia de las neuronas dopaminérgicas como en la liberación de lactato deshidrogenasa. La rotenona disminuyó significativamente el número de neuronas dopaminérgicas y se observó un aumento de los niveles de lactato deshidrogenasa en los medios de cultivo. Cuando los cultivos tratados concomitantemente con 3-metiladenina y rotenona, la 3metiladenina no tuvo efecto contra el daño celular dopaminérgico inducido por la rotenona y la liberación de lactato deshidrogenasa en el medio de cultivo. En conclusión, el inhibidor de la autofagia 3-metiladenina no moduló el daño celular dopaminérgico inducido por la rotenona en el cultivo celular mesencefálico primario.


Assuntos
Animais , Camundongos , Doença de Parkinson , Rotenona/toxicidade , Adenina/análogos & derivados , Autofagia , Mesencéfalo , Adenina/farmacologia , Células Cultivadas , Morte Celular/efeitos dos fármacos , Neurônios Dopaminérgicos/efeitos dos fármacos , L-Lactato Desidrogenase/análise
2.
Artigo em Inglês | IMSEAR | ID: sea-176929

RESUMO

This study is conducted to investigate the prophylactic effect of thymoquinone (TQ), the major active ingredient of Nigella sativa seeds, against carbon tetrachloride (CCl4)-induced hepatic damage in Sprague-Dawley (SD) rats. Forty rats were divided into four even groups. The first group served as control. The second, third and fourth groups received CCl4, CCl4 and TQ, and TQ only, respectively for 5 weeks. CCl4 (2 ml/kg b.w.) was given orally by gastric tube twice a week on Sunday and Thursday. TQ (20 mg/kg b.w.) was given daily in corn oil by gastric tube. At the end of the experiment, rats were sacrificed, and blood samples and liver specimens were obtained for biochemical analysis and morphological examination, respectively. Control and TQ-treated rats showed normal serum activity for alanine (ALT) and aspartate (AST) aminotransferases, and normal liver histology. Treatment of rats with CCl4 significantly increased serum activity of ALT and AST aminotransferases compared to control rats. Histopathologically, livers from CCl4-treated rats showed dilatation of blood sinusoids and portal blood vessels, Kupffer cell activation, vacuolar degeneration of hepatocytes, focal areas of necrosis and mild hepatic fibrosis. Using transmission electron microscopy (TEM), CCl4 caused clear lesions in the liver including dilatation of endoplasmic reticula, increased extracellular matrix and formation of abundant fatty globules and numerous autophagosomes in hepatocytes. On the other hand, co-administration of TQ with CCl4 significantly decreased serum ALT and AST activities, and attenuated most of CCl4-induced hepatic pathological changes. The present study indicates that TQ has the potential to attenuate CCl4-induced hepatic damage in SD rats.

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