Znaleziono wyników: 3

Liczba wyników na stronie

Wyniki wyszukiwania

Wyszukiwano:
w słowach kluczowych: brain aging

Sortuj według:

Ogranicz wyniki do:

Molecular mechanism of PC12 cell death evoked by sodium nitroprusside, a nitric oxide donor

100%

Pytlowany M., Strosznajder J. B., Jesko H., Cakala M., Strosznajder R. P.

Acta Biochimica Polonica

2008

tom 55

nr 2

339-347

Nitric oxide (NO) is a potent extracellular and intracellular physiological messenger. However, NO liberated in excessive amounts can be involved in macromolecular and mitochondrial damage in brain aging and in neurodegenerative disorders. The molecular mechanism of its neurotoxic action is not fully understood. Our previous data indicated involvement of NO in the release of arachidonic acid (AA), a substrate for cyclo- and lipoxygenases (COX and LOX, respectively). In this study we investigated biochemical processes leading to cell death evoked by an NO donor, sodium nitroprusside (SNP). We found that SNP decreased viability of pheochromocytoma (PC12) cells in a concentration- and time-dependent manner. SNP at 0.1 mM caused a significant increase of apoptosis-inducing factor (AIF) protein level in mitochondria. Under these conditions 80% of PC12 cells survived. The enhancement of mitochondrial AIF level might protect most of PC12 cells against death. However, NO released from 0.5 mM SNP induced massive cell death but had no effect on protein level and localization of AIF and cytochrome c. Caspase-3 activity and poly(ADP-ribose) polymerase-1 (PARP-1) protein levels were not changed. However, PARP activity significantly decreased in a time-dependent manner. Inhibition of both COX isoforms and of 12/15-LOX significantly lowered the SNP-evoked cell death. We conclude that AIF, cytochrome cand caspase-3 are not responsible for the NO-mediated cell death evoked by SNP. The data demonstrate that NO liberated in excess decreases PARP-1 activity. Our results indicate that COX(s) and LOX(s) are involved in PC12 cell death evoked by NO released from its donor, SNP.

Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik

Flavonoids and the aging brain

80%

Schmitt-Schillig S., Schaffer S., Weber C. C., Eckert G. P., Muller W. E.

Journal of Physiology and Pharmacology. Supplement

2005

tom 56

nr 1

23-36

Like in all other organs, the functional capacity of the human brain deteriorates over time. Pathological events such as oxidative stress, due to the elevated release of free radicals and reactive oxygen or nitrogen species, the subsequently enhanced oxidative modification of lipids, protein, and nucleic acids, and the modulation of apoptotic signaling pathways contribute to loss of brain function. The identification of neuroprotective food components is one strategy to facilitate healthy brain aging. Flavonoids were shown to activate key enzymes in mitochondrial respiration and to protect neuronal cells by acting as antioxidants, thus breaking the vicious cycle of oxidative stress and tissue damage. Furthermore, recent data indicate a favorable effect of flavonoids on neuro-inflammatory events. Whereas most of these effects have been shown in vitro, limited data in vivo are available, suggesting a rather low penetration of flavonoids into the brain. Nevertheless, several reports support the concept that flavonoid intake inhibits certain biochemical processes of brain aging, and might thus prevent to some extent the decline of cognitive functions with aging as well as the development or the course of neurodegenerative diseases. However, more data are needed to assess the true impact of flavonoids on brain aging.

Mechanobiology of the brain in health and disease

80%

Sheridan G. K.

Acta Neurobiologiae Experimentalis

2019

tom 79

nr Suppl.1

Basic research into neurodegenerative disorders, like Alzheimer’s disease, is heavily focused on understanding genetic susceptibility and biochemical triggers of pathology, as well as disturbances to the intrinsic electrophysiological properties of affected neurons. Often overlooked is the role of mechanics, particularly mechanical properties and mechano‑sensitivity/‑responsiveness of neurons and glia. Recent evidence confirms that mechanical signals regulate CNS development and pathophysiology. In this talk, I will discuss the role of mechanics in both physiological and pathophysiological brain ageing. A defining pathophysiological hallmark of Alzheimer’s disease is the amyloid plaque; an extracellular deposit of aggregated fibrillar Aβ1‑42 peptides. Amyloid plaques are hard, brittle structures scattered throughout the hippocampus and cerebral cortex and are thought to cause hyperphosphorylation of tau, neurofibrillary tangles, and progressive neurodegeneration. Glia are highly mechanosensitive cells and can sense the mismatch between the normally soft mechanical environment of the brain and very stiff amyloid plaques via mechanosensing ion channels. Both ageing and peripheral infection augment amyloid plaque‑induced upregulation of mechanoresponsive ion channels in astrocytes. Further research is required to investigate whether modulating mechanically-gated channel opening will protect or exacerbate the disease state, and most importantly, if they are novel drug targets for age‑related dementia

Ograniczanie wyników

1 Acta Biochimica Polonica

1 Acta Neurobiologiae Experimentalis

1 Journal of Physiology and Pharmacology. Supplement

1 Cakala M.

1 Eckert G. P.

1 Jesko H.

1 Muller W. E.

1 Pytlowany M.

1 Schaffer S.

1 Schmitt-Schillig S.

1 Sheridan G. K.

1 Strosznajder J. B.

1 Strosznajder R. P.

1 Weber C. C.

1 2019

1 2008

1 2005

Wyniki wyszukiwania

Molecular mechanism of PC12 cell death evoked by sodium nitroprusside, a nitric oxide donor

Flavonoids and the aging brain

Mechanobiology of the brain in health and disease