| Full text | |
| Author(s): |
Costa, Angelica Jardim
[1]
;
Erustes, Adolfo Garcia
[1]
;
Sinigaglia, Rita
[2]
;
Neves Girardi, Carlos Eduardo
[3]
;
da Silva Pereira, Gustavo Jose
[1]
;
Ureshino, Rodrigo Portes
[4, 5]
;
Smaili, Soraya Soubhi
[1]
Total Authors: 7
|
| Affiliation: | [1] Univ Fed Sao Paulo, Dept Pharmacol, BR-04044020 Sao Paulo, SP - Brazil
[2] Univ Fed Sao Paulo, Electron Microscopy Ctr, BR-04023060 Sao Paulo, SP - Brazil
[3] Univ Fed Sao Paulo, Dept Psychobiol, BR-04023062 Sao Paulo, SP - Brazil
[4] Univ Fed Sao Paulo, Dept Biol Sci, BR-09913030 Diadema, SP - Brazil
[5] Univ Fed Sao Paulo, Lab Mol & Translat Endocrinol, Escola Paulista Med, BR-04039032 Sao Paulo, SP - Brazil
Total Affiliations: 5
|
| Document type: | Journal article |
| Source: | PHARMACEUTICS; v. 13, n. 2 FEB 2021. |
| Web of Science Citations: | 0 |
| Abstract | |
The pharmacological modulation of autophagy is considered a promising neuroprotective strategy. While it has been postulated that lithium regulates this cellular process, the age-related effects have not been fully elucidated. Here, we evaluated lithium-mediated neuroprotective effects in young and aged striatum. After determining the optimal experimental conditions for inducing autophagy in loco with lithium carbonate (Li2CO3), we measured cell viability, reactive oxygen species (ROS) generation and oxygen consumption with rat brain striatal slices from young and aged animals. In the young striatum, Li2CO3 increased tissue viability and decreased ROS generation. These positive effects were accompanied by enhanced levels of LC3-II, LAMP 1, Ambra 1 and Beclin-1 expression. In the aged striatum, Li2CO3 reduced the autophagic flux and increased the basal oxygen consumption rate. Ultrastructural changes in the striatum of aged rats that consumed Li2CO3 for 30 days included electrondense mitochondria with disarranged cristae and reduced normal mitochondria and lysosomes area. Our data show that the striatum from younger animals benefits from lithium-mediated neuroprotection, while the striatum of older rats does not. These findings should be considered when developing neuroprotective strategies involving the induction of autophagy in aging. (AU) | |
| FAPESP's process: | 17/10863-7 - Study of lipophagy mediated by two-pore channels receptors |
| Grantee: | Gustavo José da Silva Pereira |
| Support Opportunities: | Regular Research Grants |
| FAPESP's process: | 12/08273-3 - Study of autophagy and neuroprotection in aging and in a Parkinson's Disease animal model |
| Grantee: | Rodrigo Portes Ureshino |
| Support Opportunities: | Scholarships in Brazil - Post-Doctoral |
| FAPESP's process: | 16/20796-2 - Study of estrogen receptors mediated autophagy against tau toxicity in cell and zebrafish models |
| Grantee: | Rodrigo Portes Ureshino |
| Support Opportunities: | Research Grants - Young Investigators Grants |
| FAPESP's process: | 13/20073-2 - Autophagy as a protective mechanism in senescent rats |
| Grantee: | Soraya Soubhi Smaili |
| Support Opportunities: | Regular Research Grants |
| FAPESP's process: | 13/20976-2 - Development, characterization and studies of autophagy and apoptosis in a Parkinson's Disease cell model |
| Grantee: | Adolfo Garcia Erustes |
| Support Opportunities: | Scholarships in Brazil - Doctorate |