Verschiedenes » Autophagie

Autpophagie kommt zwar in vielen Beiträgen bereits vor. Aber es scheint mir ein ziemlich wichtige
eigenständige Anti-Aging-Komponente zu sein, die sich beeinflussen läßt. De Grey widmet sich in
einem Buch "Niemals alt" auch diesem Thema: "Die biologioschen Müllverbrennungsanlagen aufrüsten".
Es geht ihm um die Stoffe, die von den Lysosomen nicht recycled werden können und die
oft als "Lipofuszin" bezeichnet werden. Bekanntlich ist seine Lösung: ein Gen einschleusen, dass
ein Enzym generiert, das Lipofuscin klein kriegt. Er sucht es auf dem Friedhof.

Ich wollte allerdings auf diesen Artikel hinweisen:
https://www.fightaging.org/archives/2019...elated-disease/

Upregulation of Autophagy to Treat Age-Related Disease

Einige Möglichkeiten wurde hier ja schon diskutiert.

Etwas Off, dennoch mal diese Frage:

Ich lese wie hier in neueren Publikationen die mögliche neue pharmakologische Wirkstoffe-/Substanzen behandeln das Wort bzw. die Beschreibung: "small molecule".

Ist das eine Modeerscheinung oder ist das evtl. eije etablierte neuere Kategorie/Definition von Eigenschaften solcher Stoffe?

https://www.ncbi.nlm.nih.gov/pubmed/29115419

Effect of β‑ecdysterone on glucocorticoid‑induced apoptosis and autophagy in osteoblasts.

Abstract

The aim of the present study was to investigate the effect of glucocorticoids in osteoblasts and to examine the role of β‑ecdysterone in the pathogenesis of glucocorticoid‑induced osteoporosis. Osteoblasts were induced from bone marrow mesenchymal stem cells, which were isolated from C57BL/6 mice. Cell viability and apoptosis of osteoblasts were measured by Cell Counting Kit‑8 and flow cytometry analysis, respectively. The expression of related genes and proteins was measured by reverse transcription quantitative polymerase chain reaction and western blot analysis respectively. Dose‑dependent decreases in the cell proliferation and differentiation were observed in dexamethasone (Dex)‑treated osteoblasts, evidenced by downregulation in the activity of alkaline phosphatasedecreased expression levels of Runt‑related transcription factor 2 and osteocalcin, and upregulated expression of RANK ligand. Dex also induced apoptosis and inhibited autophagy of osteoblasts, evidenced by upregulated B‑cell lymphoma 2 (Bcl‑2)‑associated X protein/Bcl‑2 ratio and the activation of mammalian target of rapamycin (mTOR), and decreased expression levels of Beclin‑1, autophagy protein 5 and microtubule‑associated protein 1 light chain 3 II. The effects on cell proliferation, apoptosis and autophagy induced by Dex were reversed by β‑ecdysterone in a dose‑dependent manner. Therefore, β‑ecdysterone may be a promising candidate drug for the treatment of osteoporosis through inducing osteoblast autophagic activity by inactivating mTOR.



β‑Ecdysterone promotes autophagy and inhibits apoptosis in osteoporotic rats.
Tang YH1, Yue ZS1, Xin DW1, Zeng LR1, Xiong ZF1, Hu ZQ1, Xu CD1.
Author information



https://www.ncbi.nlm.nih.gov/pubmed/29138818

Osteoporosis is an aging process of skeletal tissues with characteristics of reductions in bone mass and microarchitectural deterioration of bone tissue. The present study aimed to investigate the effects of glucocorticoid‑induced osteoporosis on osteoblasts and to examine the roles of β‑ecdysterone (β‑Ecd) involved. In the present study, an in vivo model of osteoporosis was established through the subcutaneous implantation of prednisolone (PRED) into Sprague‑Dawley rats, with or without a subcutaneous injection of β‑Ecd (5 or 10 mg/kg body weight). Expression of Beclin‑1 and microtubule‑associated protein 1A/1B‑light chain 3I/II and apoptosis in lumbar vertebrae tissues was measured by immunofluorescence and TUNEL assays, respectively. Serum concentration of calcium and phosphorus, and the activity of tartrate‑resistant acid phosphatase (TRAP) and alkaline phosphatase (ALP) were measured by biochemical assay. Reverse transcription‑quantitative polymerase chain reaction and western blotting was used for detect the expression of related genes and proteins. PRED treatment inhibited bone formation by decreasing bone mineral density, and suppressing the expression of Runt‑related transcription factor 2 and bone morphogenetic protein 2, while enhancing the activity of alkaline phosphatase, upregulating the expression of receptor activator of nuclear factor-κB ligand, and increasing the serum content of calcium, phosphorus and tartrate‑resistant acid phosphatase in rats. Additionally, PRED was revealed to inhibit autophagy through the downregulation of Beclin‑1, autophagy protein 5 and microtubule‑associated protein 1A/1B‑light chain 3I/II expression, whereas it induced the apoptosis, through the activation of caspase‑3 and the suppression of apoptosis regulator BCL2 expression. Notably, the PRED‑induced alterations in bone formation, autophagy and apoptosis were revealed to be attenuated by β‑Ecd administration. In conclusion, the findings of the present study suggested that β‑Ecd may be a promising candidate for the development of therapeutic strategies for the treatment of osteoporosis, through the induction of autophagy and the inhibition of apoptosis in vivo.

Ein Trehalose oder Spermidin Nasenspray eventuell. Beides kann man sich gut selbst basteln.

Autophagy system as a potential therapeutic target for neurodegenerative diseases
https://pubmed.ncbi.nlm.nih.gov/35181396/

Zitat von Prometheus im Beitrag #6

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Nasenspray

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Zitat von Prometheus im Beitrag #6

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@Speedy

Denkst du, dass Trehalose oder Spermidin mit einem Nasenspray in effektiver Dosis bis ins ZNS gelangen? Da habe ich Zweifel...
Andererseits:

Zitat von Prometheus im Beitrag Die Hypothalamus-Lebensuhr

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Intranasal delivery of biologics to the central nervous system
https://www.sciencedirect.com/science/ar...169409X11002791

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Ich verfolge auch die Forschung zu fokussiertem Ultraschall:

Blood–brain barrier opening in Alzheimer's disease using MR-guided focused ultrasound
https://www.nature.com/articles/s41467-018-04529-6

Effektive Umgehung der BHS, aber immer noch zu invasiv:

Perispinal Delivery of CNS Drugs
https://link.springer.com/article/10.1007/s40263-016-0339-2

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Autophagy and pluripotency: self-eating your way to eternal youth
https://www.cell.com/trends/cell-biology...Fshowall%3Dtrue

Autophagy slows the aging of Germline stem cells in Drosophila through modulation of E-cadherin
https://www.biorxiv.org/content/10.1101/2022.03.31.486570v2

Zitat von Fichtennadel im Beitrag #4

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https://www.ncbi.nlm.nih.gov/pubmed/29115419

Effect of β‑ecdysterone on glucocorticoid‑induced apoptosis and autophagy in osteoblasts.

Abstract

The aim of the present study was to investigate the effect of glucocorticoids in osteoblasts and to examine the role of β‑ecdysterone in the pathogenesis of glucocorticoid‑induced osteoporosis. Osteoblasts were induced from bone marrow mesenchymal stem cells, which were isolated from C57BL/6 mice. Cell viability and apoptosis of osteoblasts were measured by Cell Counting Kit‑8 and flow cytometry analysis, respectively. The expression of related genes and proteins was measured by reverse transcription quantitative polymerase chain reaction and western blot analysis respectively. Dose‑dependent decreases in the cell proliferation and differentiation were observed in dexamethasone (Dex)‑treated osteoblasts, evidenced by downregulation in the activity of alkaline phosphatasedecreased expression levels of Runt‑related transcription factor 2 and osteocalcin, and upregulated expression of RANK ligand. Dex also induced apoptosis and inhibited autophagy of osteoblasts, evidenced by upregulated B‑cell lymphoma 2 (Bcl‑2)‑associated X protein/Bcl‑2 ratio and the activation of mammalian target of rapamycin (mTOR), and decreased expression levels of Beclin‑1, autophagy protein 5 and microtubule‑associated protein 1 light chain 3 II. The effects on cell proliferation, apoptosis and autophagy induced by Dex were reversed by β‑ecdysterone in a dose‑dependent manner. Therefore, β‑ecdysterone may be a promising candidate drug for the treatment of osteoporosis through inducing osteoblast autophagic activity by inactivating mTOR.

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Autophagy Balances Neuroinflammation in Alzheimer’s Disease
https://link.springer.com/article/10.1007/s10571-022-01269-6

Zitat von Speedy im Beitrag #8

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Zitat von Prometheus im Beitrag #6

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@Speedy

Denkst du, dass Trehalose oder Spermidin mit einem Nasenspray in effektiver Dosis bis ins ZNS gelangen? Da habe ich Zweifel...
Andererseits:

[quote="Prometheus"|p5550]Intranasal delivery of biologics to the central nervous system
https://www.sciencedirect.com/science/ar...169409X11002791

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Natural Activators of Autophagy Increase Maximal Walking Distance and Reduce Oxidative Stress in Patients with Peripheral Artery Disease: A Pilot Study
https://www.mdpi.com/2076-3921/11/9/1836/htm

Autophagy activation can partially rescue proteasome dysfunction-mediated cardiac toxicity
https://onlinelibrary.wiley.com/doi/10.1111/acel.13715

Autophagy promotes cell survival by maintaining NAD levels
https://www.cell.com/developmental-cell/...5807(22)00760-2

Role of autophagy in aging: The good, the bad, and the ugly
https://onlinelibrary.wiley.com/doi/full/10.1111/acel.13753

Nucleophagy delays aging and preserves germline immortality
https://www.nature.com/articles/s43587-022-00327-4

Enhancing autophagy by redox regulation extends lifespan in Drosophila
https://www.biorxiv.org/content/10.1101/790378v2

Hatten wir das schon?

Autophagie - Wann sie beginnt und ihre Auswirkungen

Der Begriff „Autophagie“ bezeichnet ein kleines Naturwunder: Die eigenständige Erneuerung unserer Zellen. Finde heraus, wie der sagenhafte Prozess funktioniert.

https://www.brain-effect.com/magazin/aut...re-auswirkungen

Targeting selective autophagy and beyond: From underlying mechanisms to potential therapies
https://www.sciencedirect.com/science/ar...090123224001991

Suppression of autophagy induces senescence in the heart
https://www.biorxiv.org/content/10.1101/2024.05.26.595978v1