Age-related change of neuropeptide Y-immunoreactive neurons in the cerebral cortex of aged rats

Senescence is the phenomenon by which physiological functions of organisms degenerate with time. Cellular senescence is marked by an inhibition of cell cycle progression. Beta-galactosidase accumulates in the lysosomes of aged cells. In this study, human dermal fibroblast cells (HDFs) were treated with 0.5 μM doxorubicin for 4 h to induce cellular senescence. Senescence-associated beta-galactosidase (SA-β-gal) activity was then measured 72 h after treatment with aerial parts of Dendranthema zawadskii var. lucidum (Nakai) J.H. Park (DZ) extract. Treatment with DZ extract significantly decreased SA-β-gal activity in a dose-dependent manner in HDFs. Additionally, DZ extract treatment reduced age-related oxidative stress and inflammation in the aortas of aged rats. The reactive oxygen species (ROS) levels in aortas of aged control rats were higher than those in young rats. However, DZ extract-fed aged rats showed significantly lower ROS levels than the aged control rats. When the aged rats were treated with DZ extract at either 0.2 or 1.0 mg∙kg−1∙day−1, NF-κB levels in aorta tissue decreased significantly compared to those in aorta tissue of the aged control rats without DZ treatment. In addition, DZ extract-fed aged rat aortas showed significant reductions in expression of iNOS and COX-2 induced by NF-κB translocation. Therefore, these results suggest that DZ effectively inhibited senescence-related NF-κB activation and inflammation. DZ extract may have a role in the prevention of the vascular inflammatory responses that occur during vascular aging.

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Muscarinic cholinergic receptor subtypes in cerebral cortex of Fisher 344 rats: A light microscope autoradiography study of age-related changes

Mechanisms of Ageing and Development ◽

10.1016/j.mad.2005.09.024 ◽

2006 ◽

Vol 127 (2) ◽

pp. 115-122 ◽

Cited By ~ 10

Author(s):

Seyed Khosrow Tayebati ◽

Maria Antonietta Di Tullio ◽

Francesco Amenta

Keyword(s):

Cerebral Cortex ◽

Light Microscope ◽

Cholinergic Receptor ◽

Receptor Subtypes ◽

Muscarinic Cholinergic Receptor ◽

Age Related ◽

Microscope Autoradiography ◽

Muscarinic Cholinergic ◽

Age Related Changes

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Lack of Autophagy Induction by Lithium Decreases Neuroprotective Effects in the Striatum of Aged Rats

Pharmaceutics ◽

10.3390/pharmaceutics13020135 ◽

2021 ◽

Vol 13 (2) ◽

pp. 135

Author(s):

Angelica Jardim Costa ◽

Adolfo Garcia Erustes ◽

Rita Sinigaglia ◽

Carlos Eduardo Neves Girardi ◽

Gustavo José da Silva Pereira ◽

...

Keyword(s):

Oxygen Consumption ◽

Ultrastructural Changes ◽

Ros Generation ◽

Autophagic Flux ◽

Aged Rats ◽

Neuroprotective Effects ◽

Striatal Slices ◽

Positive Effects ◽

Age Related ◽

Neuroprotective Strategy

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.

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