Dosis: 75-175 mg – (30-70 g Sprossen)
Inhalt
1. Alzheimer
2. Alterung
3. Krebs
4. Schlaflosigkeit
5. Arthritis
6. Parkinson
7. MS
8. Überaktive Blase
9. Atopische Dermatitis
10. Haarausfall
11. Immunschwäche
12. Herzinsuffizienz
13. KHK
14. Hypertonie
15. Arteriosklerose
16. Adipositas
17. Thrombosen
18. Diabetes
19. Progerie
20. SARS-CoV-2
21. Gastritis
22. Sarkopenie
23. Bandscheibendegeneration
24. Hypercholesterinämire
25. Depressionen
26. Arthrose
27. Muskelkater
28. Osteoporose
29. Lungenfibrose
30. Autismus
- Alzheimer
Pre-Clinical Neuroprotective Evidences and Plausible Mechanisms of Sulforaphane in Alzheimer’s Disease
The increase in pre-clinical evidences consistently suggests that sulforaphane has a multi-faceted neuroprotective effect on AD pathophysiology. The anti-AD-like evidence of sulforaphane seen in cells and animals indicates the need to pursue sulforaphane research for relevant biomarkers in AD pre-symptomatic populations.
Sulforaphane – role in aging and neurodegeneration
In this review, we describe some of the molecular and physical characteristics of SFN, its mechanisms of action, and the effects that SFN treatment induces in order to discuss its relevance as a “miraculous” drug to prevent aging and neurodegeneration.
Efficacy of Sulforaphane in Neurodegenerative Diseases
The aim of this review is to summarize the experimental studies present on Pubmed that report the efficacy of SFN in the treatment of neurodegenerative disease, including Alzheimer’s disease (AD), Parkinson’s disease (PD), and multiple sclerosis (MS). Therefore, thanks to its beneficial effects, SFN could be useful as a supplement to counteracting neurodegenerative diseases.
2. Alterung
Sulforaphane promotes C. elegans longevity and healthspan via DAF-16/DAF-2 insulin/IGF-1 signaling
These results indicate that sulforaphane prolongs the lifespan and healthspan of C. elegans through insulin/IGF-1 signaling. Our results provide the basis for a nutritional sulforaphane-enriched strategy for the promotion of healthy aging and disease prevention.
Urolithin A induces mitophagy and prolongs lifespan in C. elegans and increases muscle function in rodents
In C. elegans, UA prevented the accumulation of dysfunctional mitochondria with age and extended lifespan. Likewise, UA prolonged normal activity during aging in C. elegans, including mobility and pharyngeal pumping, while maintaining mitochondrial respiratory capacity. These effects translated to rodents, where UA improved exercise capacity in two different mouse models of age-related decline of muscle function, as well as in young rats. Our findings highlight the health benefits of urolithin A and its potential application in strategies to improve mitochondrial and muscle function.
Sulforaphane – role in aging and neurodegeneration
In this review, we describe some of the molecular and physical characteristics of SFN, its mechanisms of action, and the effects that SFN treatment induces in order to discuss its relevance as a “miraculous” drug to prevent aging and neurodegeneration.
Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage
The results of this study suggest the following conclusions:
1. SFN delays the senescence of human MRC-5 and BJ fibroblasts in vitro
2. Cell senescence is associated with a progressive and marked increased rate of glucose metabolism through glycolysis, and this is countered by SFN treatment – glycolytic restriction previously found to delay senescence [7]
3. SFN decreased glucose metabolism on the approach to senescence by increasing the expression of TXNIP, curbing the entry of glucose into cells; decreasing HK2, curbing the entry of glucose into cellular metabolism; decreasing 6-phosphofructo-2-kinase, downregulating the formation of the allosteric enhancer of glycolysis F-2,6-P2; and increasing G6PD, downregulating the ChRE-mediated transcriptional enhancement of glycolysis by Mondo/Mlx/G6P
4. SFN also enhanced the clearance of proteins cross-linked by transglutaminase which otherwise increased in senescence
5. Screening of compounds to counter senescence-associated glycolytic overload may be an effective strategy to identify compounds with antisenescence activity
Sulforaphane prevents age-associated cardiac and muscular dysfunction through Nrf2 signaling
At the age of 21-22 months, male C57BL/6 mice were placed on SFN containing diet or control diet (n = 20 mice per group) for a total of 12 weeks. During the time period of SFN administration, 6 mice from the control group died. On the other hand, all mice in the SFN diet group survived until the end of the experiment at which time they were 24-25 months old (Figure 1a)
Nrf2 Signaling and the Slowed Aging Phenotype: Evidence from Long-Lived Models
Here, we review evidence for altered Nrf2 signaling in a variety of slowed aging models that accomplish lifespan extension via pharmacological, nutritional, evolutionary, genetic, and presumably epigenetic means.
3. Krebs
Frugal Chemoprevention: Targeting Nrf2 with Foods Rich in Sulforaphane
This review summarizes the current status of pre-clinical chemoprevention studies with sulforaphane and highlights the progress and challenges for the application of foods rich in sulforaphane and/or glucoraphanin in the arena of clinical chemoprevention.
3.1. Brustkrebs
Sulforaphane suppresses the growth of triple-negative breast cancer stem-like cells in vitro and in vivo
The effect of SFN on a stem-related embryonic oncogene CRIPTO-1/TDGF1 (CR1) was evaluated via enzyme-linked immunosorbent assay (ELISA). In vivo, BalbC/nude mice were supplemented with SFN before and after TNBC cell inoculation (daily i.p. injection of 50mg SFN/kg for 5 and 3 weeks respectively), and effects of SFN during mammary tumor initiation and growth were accessed with Nanostring gene analysis. We found that SFN can inhibit cell proliferation and mammosphere formation of CSCs in TNBC.
3.2. Prostatakrebs
Sulforaphane Reduces Prostate Cancer Cell Growth and Proliferation In Vitro by Modulating the Cdk-Cyclin Axis and Expression of the CD44 Variants 4, 5, and 7
SFN, therefore, does exert anti-tumor properties on these two prostate cancer cell lines by histone acetylation and altering the intracellular signaling cascade, but not through the same molecular mechanisms.
3.3. Hautkrebs
Dietary glucoraphanin-rich broccoli sprout extracts protect against UV radiation-induced skin carcinogenesis in SKH-1 hairless mice
Feeding broccoli sprout extracts providing daily doses of 10 μmol of glucoraphanin to SKH-1 hairless mice with prior chronic exposure to UV radiation (30 mJ cm-2 of UVB, twice a week, for 17 weeks) inhibited the development of skin tumors during the subsequent 13 weeks; compared to the controls, tumor incidence, multiplicity, and volume were reduced by 25, 47, and 70%, respectively, in the animals that received the protective agent. - Schlaflosigkeit
Effects of glucoraphanin-rich broccoli sprout extracts on sleep quality in healthy adults: An exploratory study
The visual analogue scale questionnaire on sleep quality (4.8 ± 1.6 vs. 6.4 ± 1.9) and area under the curve of melatonin concentration (109.7 ± 80.0 pg/mL・h vs. 143.5 ± 79.9 pg/mL・h) were significantly increased and prostaglandin D2 levels at 21:00 (44.2 ± 24.6 pg/mL vs. 20.2 ± 15.5 pg/mL) were significantly decreased in the sulforaphane group, although there were no significant differences between the groups. These suggest that sulforaphane may improve sleep quality by increasing melatonin and anti-inflammatory activity.
5. Arthritis
The anti-arthritis effect of sulforaphane, an activator of Nrf2, is associated with inhibition of both B cell differentiation and the production of inflammatory cytokines
In vitro, sulforaphane treatment significantly reduced the differentiation of lipopolysaccharide-stimulated murine splenocytes into plasma B cells and germinal-center B cells. Finally, sulforaphane significantly inhibited the production of IL-6, TNF-α, and IL-17 by human peripheral blood mononuclear cells stimulated with an anti-CD3 monoclonal antibody in a dose-dependent manner. Inhibition of differentiation into plasma B and Germinal Center B cells may be the mechanism underlying the anti-arthritic effect of sulforaphane.
6. Parkinson
Efficacy of Sulforaphane in Neurodegenerative Diseases
The aim of this review is to summarize the experimental studies present on Pubmed that report the efficacy of SFN in the treatment of neurodegenerative disease, including Alzheimer’s disease (AD), Parkinson’s disease (PD), and multiple sclerosis (MS). Therefore, thanks to its beneficial effects, SFN could be useful as a supplement to counteracting neurodegenerative diseases.
7. MS
Efficacy of Sulforaphane in Neurodegenerative Diseases
The aim of this review is to summarize the experimental studies present on Pubmed that report the efficacy of SFN in the treatment of neurodegenerative disease, including Alzheimer’s disease (AD), Parkinson’s disease (PD), and multiple sclerosis (MS). Therefore, thanks to its beneficial effects, SFN could be useful as a supplement to counteracting neurodegenerative diseases.
8. Überaktive Blase
Sulforaphane Ameliorates Bladder Dysfunction through Activation of the Nrf2-ARE Pathway in a Rat Model of Partial Bladder Outlet Obstruction
SFN treatment can ameliorate the increase of collagen fibers induced by obstruction. SFN treatment also increased the activity of SOD, GSH-Px, and CAT compared to the other groups. The level of bladder cell apoptosis was decreased in BOO rats with SFN treatment. Moreover, SFN could reduce the ratio of Bax/Bcl-2 expression. Furthermore, SFN could activate the Nrf2 expression with elevation of its target antioxidant proteins. Conclusions. The sulforaphane-mediated decrease of oxidative stress and activation of the Nrf2-ARE pathway may ameliorate bladder dysfunction caused by bladder outlet obstruction.
Bladder Hyperactivity Induced by Oxidative Stress and Bladder Ischemia: A Review of Treatment Strategies with Antioxidants
Sulforaphan, eine schwefelreiche Verbindung, die in Kreuzblütlern vorkommt, wirkt antioxidativ; Antiapoptose, Hemmung der mitochondrialen Dysfunktion; und Aktivitäten gegen Krebs. Die Behandlung mit Sulforaphan verlängerte das Miktionsintervall, unterdrückte die Kollagenablagerung und verbesserte die Blasencompliance in einem PBOO-Rattenmodell [ 55 , 142 ]. Liuet al. fanden heraus, dass Sulforaphan den Anstieg von MDA und die Reduktion von SOD, GSH und CAT bei PBOO-Ratten verbessert [ 55 ]. Darüber hinaus regulierte seine möglicherweise durch die Expression des Nrf2-Signalwegs vermittelte antioxidative Fähigkeit die zellulären antioxidativen Reaktionen in Übereinstimmung mit anderen Studien [ 143 , 144]. Daher hemmt die therapeutische Wirkung von Sulforaphan eine übermäßige ROS-Akkumulation, schützt die Zellorganelle vor oxidativer Schädigung und erhält in der Folge die Organfunktion [ 55 , 144 , 145 ].
9. Atopische Dermatitis
Sulforaphane has a therapeutic effect in an atopic dermatitis murine model and activates the Nrf2/HO-1 axis
The present study suggested that sulforaphane exerted a therapeutic effect in the AD mouse model through the activation of the Nrf2/HO-1 axis as well as the suppression of Janus kinase 1/STAT3 signaling pathway.
10. Haarausfall
Brassica oleracea extract, glucosinlates, and sulforaphane promote hair growth in vitro and ex vivo
We observed that BOE, glucosinlates, and sulforaphane can prevent the testosterone-induced inhibition of dermal papilla (DP) cells viability. BOE and sulforaphane can even hinder the testosterone-induced inhibition of HaCaT cells viability. Moreover, BOE, glucosinlates, and sulforaphane can up-regulate the cytokeratin gene expression in HaCaT cells, prevent the increase in Bax gene levels induced by testosterone in DP, and promote the growth of hair follicle of mice. These effects can be linked to the enhancement of DP and HaCaT cells activities and the prevention of the testosterone-induced cell apoptosis of DP cells.
11. Immunschwäche
Potential of Sulforaphane as a Natural Immune System Enhancer: A Review
SFN may prevent different types of cancer and has the ability to improve hypertensive states, to prevent type 2 diabetes–induced cardiomyopathy, and to protect against gastric ulcer. SFN may also help in schizophrenia treatment, and recently it was proposed that SFN has potential to help those who struggle with obesity. The mechanism underlying the health-promoting effect of SFN relates to its indirect action at cellular level by inducing antioxidant and Phase II detoxifying enzymes through the activation of transcription nuclear factor (erythroid-derived 2)-like (Nrf2). The effect of SFN on immune response is generating scientific interest, because of its bioavailability, which is much higher than other phytochemicals, and its capacity to induce Nrf2 target genes.
12. Herzinsuffizienz
Sulforaphane, a Natural Isothiocyanate Compound, Improves Cardiac Function and Remodeling by Inhibiting Oxidative Stress and Inflammation in a Rabbit Model of Chronic Heart Failure
In the CHF group, compared with the sham operation group, there was an increase in the heart weight to body weight ratio (HW/BW), the left ventricular weight to body weight ratio (LVW/BW), the left ventricular end diastolic diameter (LVEDD), the left ventricular end systolic diameter (LVESD), plasma brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) levels, the cardiac collagen volume fraction (CVF), apoptotic index, expression levels of collagen I, collagen III, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and malondialdehyde (MDA) in the myocardial tissue, and a decrease in the left ventricular shortening fraction (LVFS) and left ventricular ejection fraction (LVEF), and cardiac superoxide dismutase (SOD) activity. These changes were corrected in the SFN-treated group.
Sulforaphane prevents age-associated cardiac and muscular dysfunction through Nrf2 signaling
Our studies revealed a significant drop in Nrf2 activity and mitochondrial functions, together with a loss of skeletal muscle and cardiac function in the old control mice compared to the younger age group. In the old mice, SFN restored Nrf2 activity, mitochondrial function, cardiac function, exercise capacity, glucose tolerance, and activation/differentiation of skeletal muscle satellite cells. Our results suggest that the age-associated decline in Nrf2 signaling activity and the associated mitochondrial dysfunction might be implicated in the development of age-related disease processes. Therefore, the restoration of Nrf2 activity and endogenous cytoprotective mechanisms by SFN may be a safe and effective strategy to protect against muscle and heart dysfunction due to aging.
A decrease in cardiac/respiratory function is known to limit exercise capacity in the elderly (Farkhooy et al., 2018). Cardiac aging is an intrinsic process with profound cellular and molecular changes that results in impaired cardiac function (Vigorito & Giallauria, 2014). We examined whether SFN restored cardiac function in old mice. Old mice on control diet showed reduced ejection fraction (61.0 ± 1.0%), fractional shortening (32.1 ± 0.7%), and stroke volume (32.8 ± 9.2 µl) compared to young mice on control diet (Figure 3a-c). On the other hand, SFN supplementation improved the ejection fraction (76.0 ± 1.4), fractional shortening (44.2 ± 1.3%), and the stroke volume (51.6 ± 11.3 µl) in the old mice. While SFN also significantly increased these parameters in young mice, the effect on ejection fraction and fractional shortening was larger in the old mice. There was no significant effect of SFN supplementation on cardiac output in young mice, while cardiac output in old mice was significantly improved (Figure 3d). As a result, cardiac output in SFN-fed old mice was similar to that of young controls. We conclude that SFN-fed old mice developed resistance to age-associated loss of cardiac function.
13. KHK
Sulforaphane Protects against Cardiovascular Disease via Nrf2 Activation
Recent data have indicated that the beneficial effects of SFN in CVD are due to its antioxidant and anti-inflammatory properties. SFN activates NF-E2-related factor 2 (Nrf2), a basic leucine zipper transcription factor that serves as a defense mechanism against oxidative stress and electrophilic toxicants by inducing more than a hundred cytoprotective proteins, including antioxidants and phase II detoxifying enzymes. This review will summarize the evidence from clinical studies and animal experiments relating to the potential mechanisms by which SFN modulates Nrf2 activation and protects against CVD.
14. Hypertonie
The dietary phase 2 protein inducer sulforaphane can normalize the kidney epigenome and improve blood pressure in hypertensive rats
Mean arterial pressure was 20% higher in vehicle-treated SHRSP when compared to SD. Sulforaphane administration to SHRSP improved blood pressure and lowered this difference to 11%. Vehicle-treated SHRSP had significantly increased wall:lumen ratios in renal arteries, increased numbers of vascular smooth muscle cells (VSMCs), increased renal protein nitration, and decreased (11%) renal DNA methylation compared to SD. Sulforaphane administration to SHRSP significantly lowered arterial wall:lumen ratio by 35%, reduced the number of VSMCs, reduced the level of protein nitration, and increased methylated deoxycytosine levels by 14%.
15. Arteriosklerose
Activation of Nrf2 in endothelial cells protects arteries from exhibiting a proinflammatory state
Nrf2 prevents ECs at the atheroprotected site from exhibiting a proinflammatory state via the suppression of p38-VCAM-1 signaling. Pharmacological activation of Nrf2 reduces EC activation at atherosusceptible sites and may provide a novel therapeutic strategy to prevent or reduce atherosclerosis.
Sulforaphane attenuates the development of atherosclerosis and improves endothelial dysfunction in hypercholesterolemic rabbits
SFN administration significantly decreased HCD-induced elevations in serum TC, LDL-C, CRP, and LDH. while significantly increased HDL-C and GSH levels and normalized aortic SOD and NOx. Additionally, SFN significantly improved rabbit aortic endothelium-dependent relaxation to acetylcholine. Moreover, SFN significantly reduced the elevation in I/M ratio. This effect was confirmed by aortic histopathologic examination. The expression of NF-κB in aortic tissue showed a marked reduction upon treatment with SFN. In conclusion, this study reveals that SFN has the ability to ameliorate HCD-induced atherosclerotic lesions progression and vascular dysfunction, possibly via its lipid-lowering and antioxidant effects and suppression of NF-κB-mediated inflammation.
16. Adipositas
Sulforaphane attenuates obesity by inhibiting adipogenesis and activating the AMPK pathway in obese mice
SFN attenuated HFD-induced visceral adiposity, adipocyte hypertrophy and fat accumulation in the liver. Serum total cholesterol and leptin, and liver triglyceride levels were lower in HFD-SFN-fed mice than in HFD-fed mice. SFN decreased the expression of peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer-binding protein α (C/EBPα) and leptin in the adipose tissue of HFD-SFN mice and increased adiponectin expression. Phosphorylation of AMP-activated protein kinase α (AMPKα) and acetyl-CoA carboxylase in the adipose tissue of HFD-SFN-fed mice was elevated, and HMG-CoA reductase expression was decreased compared with HFD-fed mice. Thus, these results suggest that SFN may induce antiobesity activity by inhibiting adipogenesis through down-regulation of PPARγ and C/EBPα and by suppressing lipogenesis through activation of the AMPK pathway.
Sulforaphane induces adipocyte browning and promotes glucose and lipid utilization
SFN‐induced browning of white adipocytes enhanced the utilization of cellular fuel, and application of SFN is a promising strategy to combat obesity and obesity‐related metabolic disorder.
Sulforaphan reduziert Fettleibigkeit, indem es die Leptinresistenz umkehrt
Transcriptional profiling of six major metabolically relevant tissues highlights that sulforaphane suppresses fatty acid synthesis while promoting ribosome biogenesis, reducing ROS accumulation, and resolving inflammation, therefore representing a unique transcriptional program that leads to protection from obesity. Our findings argue for clinical evaluation of sulforaphane for weight loss and obesity-associated metabolic disorders.
Sulforaphane improves leptin responsiveness in high-fat high-sucrose diet-fed obese mice
The present findings suggest that intervention with SFN, a naturally occurring isothiocyanate, has the potential to improve leptin responsiveness in DIO.
Glucoraphanin: a broccoli sprout extract that ameliorates obesity-induced inflammation and insulin resistance
A recent study demonstrated that glucoraphanin, a precursor of the Nrf2 activator sulforaphane, ameliorates obesity by enhancing energy expenditure and browning of white adipose tissue, and attenuates obesity-related inflammation and insulin resistance by polarizing M2 macrophages and reducing metabolic endotoxemia.
17. Thrombosen
Sulforaphane prevents human platelet aggregation through inhibiting the phosphatidylinositol 3-kinase/Akt pathway
Therefore, sulforaphane is able to inhibit the PI3K/Akt pathway at two distinct sites. In conclusion, we have demonstrated that sulforaphane prevented platelet aggregation and reduced thrombus formation in flow conditions; our data also support that the inhibition of the PI3K/Akt pathway by sulforaphane contributes it antiplatelet effects.
18. Diabetes
Metabolic effects of sulforaphane oral treatment in streptozotocin-diabetic rats
Diabetic animals also presented elevated levels of serum triacylglycerols (TAG), urea, and creatinine, and all SFN doses were able to reverse these alterations. However, the same doses of SFN accentuated alterations in total cholesterol, alanine, and aspartate aminotransferase levels, and had no effect on hepatic TAG, HDL cholesterol, and uptake of 2-deoxy glucose in adipose tissue and soleum muscle. Based on the effects inferred by the present data, SFN presented some positive effects against diabetes induction, although the impairment of hepatic function and cholesterol levels were aggravated after treatment with the compound.
Sulforaphane reduces hepatic glucose production and improves glucose control in patients with type 2 diabetes
Sulforaphane suppressed glucose production from hepatic cells by nuclear translocation of nuclear factor erythroid 2-related factor 2 (NRF2) and decreased expression of key enzymes in gluconeogenesis. Moreover, sulforaphane reversed the disease signature in the livers from diabetic animals and attenuated exaggerated glucose production and glucose intolerance by a magnitude similar to that of metformin. Finally, sulforaphane, provided as concentrated broccoli sprout extract, reduced fasting blood glucose and glycated hemoglobin (HbA1c) in obese patients with dysregulated type 2 diabetes.
19. Progerie
Sulforaphane enhances progerin clearance in Hutchinson–Gilford progeria fibroblasts
To restore protein clearance in HGPS cells, we treated HGPS cultures with sulforaphane (SFN), an antioxidant derived from cruciferous vegetables. We determined that SFN stimulates proteasome activity and autophagy in normal and HGPS fibroblast cultures. Specifically, SFN enhances progerin clearance by autophagy and reverses the phenotypic changes that are the hallmarks of HGPS. Therefore, SFN is a promising therapeutic avenue for children with HGPS.
Progerin accumulation in nucleus pulposus cells impairs mitochondrial function and induces intervertebral disc degeneration and therapeutic effects of sulforaphane
SFN ameliorated the progerin-induced aging defects and mitochondrial dysfunction in NP cells and IDD in Lmna G609G/G609G mice.
20. SARS-CoV-2
Can Activation of NRF2 Be a Strategy against COVID-19?
We propose that a multifaceted anti-inflammatory strategy based on pharmacological activation of nuclear factor erythroid 2 p45-related factor 2 (NRF2) can be deployed against the virus. The strategy provides robust cytoprotection by restoring redox and protein homeostasis, promoting resolution of inflammation, and facilitating repair. NRF2 activators such as sulforaphane and bardoxolone methyl are already in clinical trials. The safety and efficacy information of these modulators in humans, together with their well-documented cytoprotective and anti-inflammatory effects in preclinical models, highlight the potential of this armamentarium for deployment to the battlefield against COVID-19.
Sulforaphane exhibits antiviral activity against pandemic SARS-CoV-2 and seasonal HCoV-OC43 coronaviruses in vitro and in mice
SFN inhibited in vitro replication of six strains of SARS-CoV-2, including Delta and Omicron, as well as that of the seasonal coronavirus HCoV-OC43. Further, SFN and remdesivir interacted synergistically to inhibit coronavirus infection in vitro. Prophylactic administration of SFN to K18-hACE2 mice prior to intranasal SARS-CoV-2 infection significantly decreased the viral load in the lungs and upper respiratory tract and reduced lung injury and pulmonary pathology compared to untreated infected mice. SFN treatment diminished immune cell activation in the lungs, including significantly lower recruitment of myeloid cells and a reduction in T cell activation and cytokine production. Our results suggest that SFN should be explored as a potential agent for the prevention or treatment of coronavirus infections.
21. Gastritis
Role of Sulforaphane in Protection of Gastrointestinal Tract Against H. pylori and NSAID-Induced Oxidative Stress
Our data from the H. pylori infection study clearly demonstrated that SFN inhibited H. pylori viability both in vitro and in vivo, and mitigated H. pylori-induced gastritis in mice and humans. Similar-ly, our study on NSAID-induced small intestinal injury showed that SFN not only mitigated aspirin-induced injury of small intestinal epithelial cells in vitro, but also ameliorated indomethacin-induced small intestinal injury in mice in vivo.
22. Sarkopenie
Sulforaphane prevents age-associated cardiac and muscular dysfunction through Nrf2 signaling
We tested whether SFN treatment would improve muscle strength and exercise capacity. For this purpose, we challenged young and old mice, fed with control or SFN diet, with involuntary physical exercise testing of muscle strength. First, we tested them for grip strength by making them hold on to a thick wire. Young and old mice fed with control diet were able to hold on for an average of 54 ± 5 and 39 ± 5 s, respectively. Young and old mice on SFN diet were able to hold on for longer periods of time, 64 ± 13 and 86 ± 12 s, respectively (Figure 2a). Surprisingly, the old mice fed SFN were able to hold on longer than the young mice fed SFN. In addition, we compared the exercise capacity of control and SFN-treated young and old mice by having them run on a motorized, speed-controlled, modular treadmill system (Handschin et al., 2007). Old mice on control diet had a lower exercise capacity compared to their young counterparts (Figure 2b). Feeding with an SFN-rich diet resulted in a significantly improved exercise capacity in the old mice. The SFN-fed old mice performed similarly to young animals on the treadmill.
Findings from the current study include that treadmill exercise capacity and responses to forelimb grip strength significantly improved in old mice fed the SFN diet. Treadmill exercise capacity was approximately 1.5 times higher in old mice fed SFN diet compared with mice fed control diet. When comparing forelimb grip strength, old SFN-fed mice remained hanging on a wire more than twice as long as old mice on control diet. Performance of old SFN-fed mice was even better than young mice. Increased Pax7- and MyoD-positive satellite cell progeny in EDL myofibers of SFN-fed mice suggests an improvement in muscle regeneration in aged mice. Overall, we have demonstrated that the SFN diet intervention improved exercise performance, grip strength, and increased muscle stem cell formation in old mice, suggesting that SFN may be a novel therapeutic approach to reduce sarcopenia in the aging population.
Sulforaphane causes a major epigenetic repression of myostatin in porcine satellite cells
These findings reveal a new mode of epigenetic repression of MSTN by the bioactive compound SFN. This novel pharmacological, biological activity of SFN in satellite cells may thus allow for the development of novel approaches to weaken the MSTN signaling pathway, both for therapies of human skeletal muscle disorders and for livestock production improvement.
23. Bandscheibendegeneration
Progerin accumulation in nucleus pulposus cells impairs mitochondrial function and induces intervertebral disc degeneration and therapeutic effects of sulforaphane
Progerin is involved in the pathogenesis of IDD. Also, SFN alleviates progerin‑induced IDD, which is associated with amelioration of aging defects and mitochondrial dysfunction. Thus, SFN shows promise for the treatment of IDD.
SFN protects against cellular senescence 13, 14 and represses matrix degradation in animal models of osteoarthritis 36, 37. Moreover, SFN prepared from a concentrated broccoli sprout extract reduced the fasting blood glucose level in obese patients with dysregulated type 2 diabetes, indicating that SFN is a both clinically potent and safe 21. We explored whether SFN could rescue progerin-induced aging defects in NP cells. Progerin-expressing cells were treated with vehicle or SFN at 5 μM for 72 h. SFN significantly decreased the proportion of SA-β-Gal‑positive NP cells (Figure S5A). Also, endogenous DNA damage was attenuated in the SFN-treated progerin group, as indicated by increased expression of LAP2, H3K27me3, and lamin B1; and decreased expression of γH2AX (Figure (Figure5A).5A). SFN also markedly reduced the proportions of TUNEL‑positive and apoptotic cells (Figures S5B, S5C).
24. Hypercholesterinämire
Diet rich in high glucoraphanin broccoli reduces plasma LDL cholesterol: Evidence from randomised controlled trials
Evidence from two independent human studies indicates that consumption of high glucoraphanin broccoli significantly reduces plasma LDL-C.
25. Depressionen
Sulforaphane produces antidepressant- and anxiolytic-like effects in adult mice
In summary, these findings demonstrated that SFN has antidepressant- and anxiolytic-like activities in stressed mice model of depression, which likely occurs by inhibiting the hypothalamic-pituitary-adrenal (HPA) axis and inflammatory response to stress. These data support further exploration for developing SFN as a novel agent to treat depression and anxiety disorders.
26. Arthrose
Sulforaphane Represses Matrix-Degrading Proteases and Protects Cartilage From Destruction In Vitro and In Vivo
An SFN-rich diet (3 μmoles/day SFN versus control chow) decreased the arthritis score in the DMM model of osteoarthritis in the mouse, with a concurrent block of early DMM-induced gene expression changes. SFN inhibits the expression of key metalloproteinases implicated in osteoarthritis, independently of Nrf2, and blocks inflammation at the level of NF-κB to protect against cartilage destruction in vitro and in vivo.
Sulforaphane protects against oxidative stress-induced apoptosis via activating SIRT1 in mouse osteoarthritis
The anti-apoptotic effect of SFN was reversed by SIRT1 small interfering RNA, implying that SIRT1 exerted a protective role against the effect of SFN on chondrocytes. The expression levels of C/EBP homologous protein, 78-kDa glucose regulated protein, Bax, Bcl-2 and cleaved caspase 3 were found to be downregulated in SFN-treated mice. Furthermore, SFN ameliorated cartilage degradation in the OA mouse model. These findings indicate that SFN exerted an anti-apoptotic effect on chondrocytes and ameliorated OA in vivo by activating the SIRT1 signaling pathway.
27. Muskelkater
Effect of a sulforaphane supplement on muscle soreness and damage induced by eccentric exercise in young adults: A pilot study
Sulforaphane supplement intake for 2 weeks increased NQO1 mRNA expression in peripheral blood mononuclear cells (PBMCs). Muscle soreness on palpation and ROM were significantly lower 2 days after exercise in the sulforaphane group compared with the control group. Serum MDA showed significantly lower levels 2 days after exercise in the sulforaphane group compared with the control group.
28. Osteoporose
Anabolic and Antiresorptive Modulation of Bone Homeostasis by the Epigenetic Modulator Sulforaphane, a Naturally Occurring Isothiocyanate
Our data indicate that the food-derived compound SFN epigenetically stimulates osteoblast activity and diminishes osteoclast bone resorption, shifting the balance of bone homeostasis and favoring bone acquisition and/or mitigation of bone resorption in vivo. Thus, SFN is a member of a new class of epigenetic compounds that could be considered for novel strategies to counteract osteoporosis.
29. Lungenfibrose
Sulforaphane attenuates pulmonary fibrosis by inhibiting the epithelial-mesenchymal transition
SFN showed a significant anti-fibrotic effect in TGF-β-treated cell lines and BLM-induced fibrosis in mice. These findings showed that SFN has anti-fibrotic activity that may be considered in the treatment of IPF.
30. Autismus
Sulforaphane treatment of autism spectrum disorder (ASD)
Our clinical impressions during the study, although blind to group assignment, were that 13 of the 40 participants improved noticeably with respect to sociability and behavior, usually observable by 4 wk; all were receiving sulforaphane.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4637098/
Sulforaphane prevents age-associated cardiac and muscular dysfunction through Nrf2 signaling
Sulforaphane and Other Nutrigenomic Nrf2 Activators: Can the Clinician’s Expectation Be Matched by the Reality?
Sulforaphane Glucosinolate Monograph
Chinesische Medizin 
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