Open AccessCyanidin prevents hippocampal cell death and promotes astrocytosis in kainic acid-induced neurodegeneration
Author(s) -
Sitthisak Thongrong,
Ratchaniporn Kongsui,
Napatr Sriraksa
Publication year - 2020
Publication title -
international journal of research in pharmaceutical sciences
Language(s) - English
Resource type - Journals
ISSN - 0975-7538
DOI - 10.26452/ijrps.v11i1.1918
Subject(s) - neurodegeneration , hippocampal formation , cyanidin , hippocampus , kainic acid , medicine , astrocyte , endocrinology , granule cell , chemistry , dentate gyrus , pathology , biochemistry , central nervous system , antioxidant , receptor , glutamate receptor , disease
Temporal lobe epilepsy (TLE) is one of the non-communicable diseases characterized by dentate granule cell dispersion (GCD) and the loss of the CA1 and CA3 neurons. This study investigated the effects of cyanidin on neurodegeneration after KA injection. Male Wistar rats were divided into a saline-injected group as a control, KA alone and cyanidin treated group at a dose of 10 mg/kg BW seven days before and after KA injection. The histomorphological analysis revealed that GCD was reduced in the ipsilateral hippocampus of cyanidin treated group when compared with KA alone (P<0.05). There was no neurodegeneration observed in the contralateral hippocampus. In contrast, neuronal degeneration was limited in the ipsilateral CA1 (P<0.01) and the hilar interneurons (P<0.001) of cyanidin treated group when compared with KA alone. However, there was no significant difference in the number of CA3 neurons of the ipsilateral between KA alone and cyanidin treated group. GFAP staining revealed a higher number of reactive astrocytes in the ipsilateral hilus (P<0.001) and molecular layer (P<0.05) of cyanidin treated group when compared with KA alone. Taken together, cyanidin could prevent neurodegeneration and promote astrocyte proliferation as well as mitigated GCD following KA-induced hippocampal injury.