Nahrungsergänzung » Pflanzen- und Tierhormone

Ecdysteron bei Osteoporose und degenerativen Knochen- und Knorpelsituationen? (Uni Göttingen)
Erhöht ausserdem Osteocalcin. Weit weniger "Nebenwirkungen" als das ach so gepriesene E2.

https://www.ncbi.nlm.nih.gov/pubmed/20171072
https://www.ncbi.nlm.nih.gov/pubmed/20554186
https://www.ncbi.nlm.nih.gov/pubmed/25822452

Ebenfalls Osteoporose. Schützt Mäuseknochen vor Glucocorticoid-verursachter Atrophie
https://www.ncbi.nlm.nih.gov/pubmed/28388784


ß-Ecdy zur Alzheimerprävention? Neue Publikation, auch hier als Alternative zu Östrogen-Substitution zu verstehen:
https://www.ncbi.nlm.nih.gov/pubmed/29330470

Parkinson:
https://www.ncbi.nlm.nih.gov/pubmed/27229883


Neuroprotektion durch neuronal mTor-signaling-Verstärkung und antiexzitatorisch
https://www.ncbi.nlm.nih.gov/pubmed/28373010
https://www.ncbi.nlm.nih.gov/pubmed/26048653

Anabol und Fettgewebe-modulierend:
https://www.ncbi.nlm.nih.gov/pubmed/24974955
https://www.ncbi.nlm.nih.gov/pubmed/22278942
http://www.ergo-log.com/ecdysteroids.html
http://www.ergo-log.com/anabolic-effect-...oping-list.html

Brassinoteroide:

https://www.sciencedaily.com/releases/20...&utm_source=TMD
We hope that one day brassinosteroids may provide an effective, natural, and safe alternative for age- and disease-associated muscle loss, or be used to improve endurance and physical performance," said Slavko Komarnytsky, Ph.D., a researcher involved in the work from the Plants for Human Health Institute, FBNS at North Carolina State University in Kannapolis, N.C. "Because some plants we eat contain these compounds, like mustards, in the future we may be able to breed or engineer these plants for higher brassinosteroid content, thus producing functional foods that can treat or prevent diseases and increase physical performance."

To make this discovery, Komarnytsky and colleagues exposed rat skeletal muscle cells to different amounts of homobrassinolide and measured protein synthesis in cell culture. The result was increased protein synthesis and decreased protein degradation in these cells. Healthy rats then received oral administration of homobrassinolide daily for 24 days. Changes in body weight, food consumption, and body composition were measured. Rats receiving homobrassinolide gained more weight and slightly increased their food intake. Body composition was measured using dual-emission X-ray absorptiometry analysis and showed increased lean body mass in treated animals over those who were not treated. This study was repeated in rats fed high protein diet and similar results were observed. Additionally, researchers used surgically castrated peri-pubertal rat models to examine the ability of homobrassinolide to restore androgen-dependent tissues after androgen deprivation following castration. Results showed increased grip strength and an increase in the number and size of muscle fibers crucial for increased physical performance.

"The temptation is to see this discovery as another quick fix to help you go from fat to fit," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal, "and to a very small degree, this may be true. In reality, however, this study identifies an important drug target for a wide range of conditions that cause muscle wasting


Und, weil Brassinosteroide in nur sehr geringen Mengen in entsprechenden Pflanzen vorhanden sind, wird an Alternativen geforscht. Im ersten Post genannte Ecdysteroide bilden dafür das Grundgerüst (Hier geht es aber in erster Linie um Pflanzenschutz/Ertragsteigerung)
https://www.ncbi.nlm.nih.gov/pubmed/28479230

Stress-protective properties of phytoecdysteroids].
[Article in Russian]
Syrov VN, Islamova ZhI, Égamova FR, Iuldasheva NKh, Khushbaktova ZA.
Abstract

Introduction of phytoecdysteroids (ecdysterone, turkesterone and ñyasterone) to rats subjected to prolonged immobilization stress significantly decreased involution of the thymus and spleen, contributed to normalization of increased mass of adrenal glands, and restored their content of ascorbic acid and cholesterol. In the liver of stressed animals, phytoecdysteroids prevented sharp decrease in the glycogen concentration, showed a clear trend toward normalization of the ratio of lactic and pyruvic acids, maintained homeostasis of macroergic phosphorus compounds, and increased the activity of antioxidant enzymes that inhibit lipid peroxidation. With respect to the stress-protective activity, the studied phytoecdysteroids are in some cases superior to eleutherococcus extract.


[The results of experimental study of phytoecdysteroids as erythropoiesis stimulators in laboratory animals].
[Article in Russian]
Syrov VN, Nasyrova SS, Khushbaktova ZA.
Abstract

Phytoecdysteroids alpha-ecdysone, 2-desoxyecdysterone, ecdysterone, sileneoside A, and turkesterone isolated from Rhaponticum carthamoides (Willd.) IIjin, Silene brahuica Boiss and Ajuga turkestanica (Rgl.) Repeated administration of brig increased the content of erythrocytes and hemoglobin in the blood of intact rats. The most active of them--ecdysterone, sileneoside A, and, particularly turkesterone, cause also a marked effect on red blood regeneration in hemotoxic phenylhydrazine anemia. In its capacity for simulating erythropoiesis turkesterone resembles the well-known steroidal anabolic drug nerobol.


Phytoecdysteroids-containing extract from Stachys hissarica plant and its wound-healing activity.
Ramazanov NS1, Bobayev ID1, Yusupova UY1, Aliyeva NK2, Egamova FR1, Yuldasheva NK1, Syrov VN1.
Author information
Abstract

A number of phytoecdysteroid compounds, such as ecdysterone, polipodin V, 2-deoxy-20-hydroxyecdysone, integristeron A and 2-deoxydizon were isolated from Stachys hissarica plant and their structures were confirmed by NMR, mass and IR spectroscopy. In addition, the biological activity of the S. hissarica plant's extract was tested on rats for wound healing activity. It was shown that the extract at repeated oral (per os) administration at a dose of 10 mg/kg speeds up the healing process of linear skin wounds in rats. The wound-healing activity of S. hissarica extract is confirmed to be effective and exceeds known drug methyluracil (2,4-dioxo-6-methyl-1,2,3,4-tetrahydropyrimidine), especially in case of alloxan induced diabetic animals.

Ursolsäure und insbesondere Tomatidine sind nach ersten Studien hochinteressante Substanzen für AA. Besunders beugen sie Muskelschwund und Kraftverlust sowie rheumatiden Erkrankungen vor.

Tomatidine enhances lifespan and healthspan in C. elegans through mitophagy induction via the SKN-1/Nrf2 pathway.
https://www.ncbi.nlm.nih.gov/pubmed/28397803

http://www.ergo-log.com/the-anabolic-eff...solic-acid.html
http://www.ergo-log.com/tomatidine-the-a...n-tomatoes.html
http://www.ergo-log.com/tomatidine-a-med...m-tomatoes.html

https://www.ncbi.nlm.nih.gov/pubmed/28397803

https://nutritionandhealinguk.co.uk/heal...muscles-strong/
https://www.gannikus.com/medizin/der-ana...kt-von-tomaten/

Wurde auch in Nature veröffentlicht:
Pblikation besagt, dass festgestellt wurde, dass Ecdysone als ein Aldosteron-Homolog betrachtet erden kann aufgrund seiner Struktur. Es ist auch wirksam an Mineralcorticoid-Rezeptoren und führt zu Nierenschäden. Allerdings wurden hier sehr hohe Dosen verabreicht wie ich finde, die durch normale Ecdysteroid-haltige Nahrungsmittel nie erreicht werden.

Oben habe ich einige Studien aufgeführt, die verschiedene vielversprechende Gesundheitseffekte nahelegen. Dabei ging es meist um beta-Ecdysteron. In der Nature-Studie wird immer von Ecdysone gesprochen, welches nicht das gleiche wäre.




https://www.ncbi.nlm.nih.gov/pubmed/30227391

Ecdysone Elicits Chronic Renal Impairment via Mineralocorticoid-Like Pathogenic Activities.

BACKGROUND/AIMS:
Ecdysteroids are steroidal insect molting hormones that also exist in herbs. Ecdysteroid-containing adaptogens have been popularly used to improve well-being and by bodybuilders for muscle growth. However, the use of ecdysone in mammals is also associated with kidney growth and enlargement, indications of disturbed kidney homeostasis. The underlying pathogenic mechanism remains to be clarified.

METHODS:
Virtual screening tools were employed to identify compounds that are homologous to ecdysone and to predict putative ecdysone-interacting proteins. The kidney effect of ecdysone was examined in vitro and in vivo and compared with that of aldosterone. Cellular apoptosis was estimated by terminal deoxynucleotidyl transferase dUTP nick end labeling. Cell motility was assessed by scratch-wound cell migration assay. Blood urea nitrogen was measured to evaluate renal function. Western immunblot analysis was employed to determine the expression profile of interested proteins.

RESULTS:
Computational molecular structure analysis revealed that ecdysone is highly homologous to aldosterone. Moreover, virtual screening based on compound-protein interaction profiles identified the Mineralocorticoid Receptor (MR) to potentially interact with ecdysone. Accordingly, to assess potential biological functions of ecdysone in mammals, ecdysone was applied to mineralocorticoid-sensitive inner medullar collecting duct cells. Ecdysone induced mesenchymal accumulation of extracellular matrix and epithelial dedifferentiation characterized by de novo expression of α-smooth muscle actin. In addition, ecdysone elicited cellular apoptosis and retarded cell motility, akin to the effect of aldosterone. In vivo, daily treatment of mice with ecdysone increased cell apoptosis in the kidney, impaired renal function and elicited early signs of renal fibrogenesis, marked by deposition of collagen and fibronectin in tubulointerstitium, reminiscent of the action of aldosterone. The MR signaling pathway is likely responsible for the cellular and pathobiological effects of ecdysone, as evidenced by strong ecdysone-induced MR nuclear translocation in renal tubular cells both in vitro and in vivo, while blockade of MR by concomitant spironolactone treatment largely abolished the detrimental effects of ecdysone.


Activation of mineralocorticoid receptor by ecdysone, an adaptogenic and anabolic ecdysteroid, promotes glomerular injury and proteinuria involving overactive GSK3β pathway signaling.

Abstract

Ecdysone is an arthropod molting hormone and has been marketed as a non-androgenic natural anabolic and adaptogen. However, the safety profile of ecdysone is largely undetermined. After ecdysone treatment for 2 weeks, mice developed albuminuria with histologic signs of glomerular injury, including hypertrophy, mesangial expansion, mild glomerulosclerosis and podocyte injury. A direct glomerulopathic activity of ecdysone seems to contribute, since addition of ecdysone to cultured glomerular cells induced cytopathic changes, including apoptosis, activation of mesangial cells, podocyte shape changes and a decreased expression of podocyte markers. To explore the molecular target responsible for the pathogenic actions, we employed an in silico modeling system of compound-protein interaction and identified mineralocorticoid receptor (MR) as one of the top-ranking proteins with putative interactions with ecdysone. The molecular structure of ecdysone was highly homologous to mineralocorticoids, like aldosterone. Moreover, ecdysone was capable of both inducing and activating MR, as evidenced by MR nuclear accumulation in glomerular cells both in vitro and in vivo following ecdysone treatment. Mechanistically, glycogen synthase kinase (GSK) 3β, which has been recently implicated in pathogenesis of glomerular injury and proteinuria, was hyperactivated in glomeruli in ecdysone-treated mice, concomitant with diverse glomerulopathic changes. In contrast, spironolactone, a selective blockade of MR, largely abolished the cytopathic effect of ecdysone in vitro and attenuated albuminuria and glomerular lesions in ecdysone treated mice, associated with a mitigated GSK3β overactivity in glomeruli. Altogether, ecdysone seems able to activate MR and thereby promote glomerular injury and proteinuria involving overactive GSK3β pathway signaling.

https://atlasofscience.org/are-ecdysteroids-insect-hormones/

Dieser offenbar renommierte Insektenforscher sagt, Ecdysterone seien gar keine Insekten-Hormone, also auch nicht für "molting" verantwortlich. In Wirklichkeit seien Ecdysterone eine pflanzliche Vitamin-D-Form:

In vertebrate animals, Ecd generally exhibit effects that are similar to the vitamin D3 (calciferol), eventually combined with anabolic growth effects similar to the androgenic steroid hormones. These conclusions can be documented by the pronounced anabolic effects of Ecd in domestic animals (rabbit, swine, cattle, sheep, Japanese quails). In addition, there exists a plethora of beneficial pharmacological effects in the human body (increased growth of bone and muscles, improved physical and mental state, improved muscle strength in athletes, metabolic stimulation, tonic effects, neurogenic, psychogenic, immunogenic, antiallergenic, anti- stressoric, anti-cancerogenic and many other more or less sufficiently supported data). A retrospective look at the history of vitamin D shows that the pioneers working on the elucidation of the rickets bone disease observed long ago (during 1930-ies) that the active compound was somehow related to 7-dehydrocholesterol, which could be converted from other sterols by UV-irradiation. They looked for the antirachitic vitamin D among the purely lipophilic fish oils and animal fat.

I am convinced that Ecd represent a previously overlooked, special group of the amphoteric, both partly lipid and partly water soluble class of the esential vitamin D. Ecd possess the 7-dehydrocholesterol unsaturation, which is stabilised by the conjugated 6-keto group. In contrast to the so far known precursors of calciferol (vitamin D3), which require activation by ultraviolet radiation and metabolic incorporation of 3 additional hydroxylic groups in the liver, the Ecd type of vitamin D6 (6 comes from the latin “Hexapoda” = insects) contains not only 3, but 6 or 7 prefabricated hydroxylic groups.

There are sufficient data which show that Ecd (Vitamin D6) can stimulate regeneration and tissue growth or enhance metabolic rates in insects, mammals and also in humans. Unfortunately, due to the limited supply of pure Ecd compounds, there are still limited pharmacological data on avitaminosis due to the lack of the vitamin D6. It is difficult to cure avitaminosis if you do not know or do not have the responsible vitamin. I have a feeling, however, that the defficiency of vitamin D6 (Ecd) could be behind the hitherto incurable diseases, especially those related to impaired regeneration, aberrant cell growth or disturbed neuromuscular functions. Investigations along these lines have been persistently hindered by an errant belief in the moulting hormones of insects.




https://www.researchgate.net/publication...Insect_Hormones

The theories of insect hormone action were created some 50-years ago by professional insect endocrinologists. Unfortunately, the scientists slowly passed out and their original results are almost inaccessible. I am one of a few old-fashioned endocrinologists who has survived. The modern topics and priorities are mostly concerned with the isolation of receptors, enzymes (e.g. esterase) and genes (e.g. Met) in the peripheral target tissues. By contrast, the most important hormones of the central neuroendocrine system (i.e. neuropeptides of the neurosecretory cells of the brain, corpora cardiaca, corpora allata) are usually neglected. I found, for example, that ecdysone and ecdysteroids, which were accidentally discovered in the search for an insect moulting hormone, are not true insect hormones. Moreover, the sesquiterpenoid JH-I, which is still believed to be the true juvenile hormone (JH), is also not an insect hormone. Indeed, JH-I turns out to be just one of 4000 juvenoid bioanalogues, mimicking the JH action. The JH-I is a trivial excretory product of exocrine, not endocrine, colleterial glands of the male Cecropia, Hyalophora cecropia (Linnaeus, 1758) silkworms. This paper describes briefly some neglected physiological problems of insect hormone action with the aim to encourage discussions about their interpretations.

Jetzt auch mal positives über Ecdysteroide bzgl. Lebensspanne:

https://www.sciencedirect.com/science/ar...4048?via%3Dihub

Phytoecdysteroid-enriched quinoa seed leachate enhances healthspan and mitochondrial metabolism in Caenorhabditis elegans


Highlights
•Quinoa enhanced C. elegans median lifespan, locomotory vigor, and mitochondrial respiration.
•Quinoa reduced AGE pigment, reactive oxygen species, and fat accumulation in C. elegans.
•20-hydroxyecdysone is a primary bioactive constituent of quinoa.

Abstract

Quinoa (Chenopodium quinoa Willd.) phytochemicals have exhibited metabolic benefit in mammals, though their effects on aging and mechanisms of action remain unknown. Caenorhabditis elegans offers a practical in vivo model to study bioactivity since major metabolic pathways are conserved across phyla. We explored the effects of phytoecdysteroid-enriched quinoa seed preparation, termed quinoa leachate (QL), on behavioral and biochemical endpoints of wild-type C. elegans health. QL treatment (1.0 mg/mL or less) increased median lifespan from 9 to 11 d, improved locomotory performance from 103.5 to 114.9 head thrashes/min, and enhanced basal respiration rate by 37%. QL also reduced advanced glycation end-product (AGE) pigments by 24%, reactive oxygen species (ROS) by 20%, and body fat by 14%. 20-Hydroxyecdysone (20HE), the primary phytoecdysteroid in QL, conferred statistically similar benefit compared to QL at equivalent doses. Data suggest that quinoa supplementation slows C. elegans aging and improves metabolic health, and 20HE is the primary bioactive constituent responsible for favorable effects.

Auch bereits vorhandene AGEs oder nur gewisser Schutz vor der Bildung neuer? Ist oft schwer zu interpretieren. Die meisten schützen ja nur davor, aber können bereits gebildete nicht auflösen.

Über Angiotensin 1-7 git es viele interessante Forschungen hinsichtlich Gesundheit und Anti-Age. Z.t wird das über Mas-Rezeptor vermittelt ... ß-Ecdy scheint das auch "zu können"




https://www.researchgate.net/publication...ia_Mas_receptor


20-Hydroxyecdysone activates the protective arm of the renin angiotensin system via Mas receptor

20-Hydroxyecdysone (20E) is a steroid hormone that plays a key role in insect development through nuclear ecdysone receptors (EcRs) and at least one membrane GPCR receptor (DopEcR) and displays numerous pharmacological effects in mammals. However, its mechanism of action is still debated, involving either an unidentified GPCR or the estrogen ER receptor. The goal of our study was to better understand 20E mechanism of action. A mouse myoblast cell line (C2C12) and the gene expression of myostatin (a negative regulator of muscle growth) was used as a reporter system of anabolic activity. Experiments using protein-bound 20E established the involvement of a membrane receptor. 20E-like effects were also observed with Angiotensin-(1-7), the endogenous ligand of Mas. Additionally, the effect on myostatin gene expression was abolished by Mas receptor knock-down using small interfering RNA (siRNA) or pharmacological inhibitors. 17-Estradiol (E2) also inhibited myostatin gene expression, but protein-bound E2 was inactive, and E2 activity was not abolished by angiotensin-(1-7) antagonists. A mechanism involving cooperation between Mas receptor and a membrane-bound palmitoylated estrogen receptor is proposed.The possibility to activate the Mas receptor with a safe steroid molecule is consistent with the pleiotropic pharmacological effects of ecdysteroids in mammals and indeed this mechanism may explain the close similarity between angiotensin-(1-7) and 20E effects. Our findings open a lot of possible therapeutic developments by stimulating the protective arm of the renin-angiotensin-aldosterone system (RAAS) with 20E.

20-Hydroxyecdysone inhibits inflammation via SIRT6-mediated NF-κB signaling in endothelial cells
Zhen Jin et al. Biochim Biophys Acta Mol Cell Res. 2023 Jun.


https://pubmed.ncbi.nlm.nih.gov/36958525/

r. In conclusion, the present study demonstrates that 20E exerts its effect through SIRT6-mediated deacetylation of NF-κB p65 (K310) to inhibit CD40 expression in ECs, and 20E may have therapeutic potential for the treatment of cardiovascular diseases.