ninfo.se   
medforsk laboratories


ninfo.se    Research and development      guarantees/certificates  

Public studies on ingredients:
Animal Study, Bacterial, Human In Vitro, Human Study, In Vitro Study.

Research & Studies:

"Do not tell everything. You can be stopped. Truth is not in everyone's interest."

Sulforaphane

There are 324 good studies at Sulforaphane. Here's a selection:
Abstracts with Sulforaphane Research

2007
Sulforaphane has a novel chemopreventive mechanism in human colon cancer cells and prostate epithelial cells, namely the inhibition of histone deacetylase (HDAC). 

Abstract Title:
Sulforaphane retards the growth of human PC-3 xenografts and inhibits HDAC activity in human subjects.
Abstract Source:
Exp Biol Med (Maywood). 2007 Feb;232(2):227-34. PMID: 17259330
Abstract Author(s):
Melinda C Myzak, Philip Tong, Wan-Mohaiza Dashwood, Roderick H Dashwood, Emily Ho
Article Affiliation:
Linus Pauling Institute, Molecular and Cellular Biology Program, Oregon State University, Corvallis, Oregon 97331, USA.
Abstract:
Sulforaphane (SFN) is an isothiocyanate found in cruciferous vegetables such as broccoli. This anticarcinogen was first identified as a potent inducer of Phase 2 enzymes, but evidence is mounting that SFN acts through other cancer chemopreventive mechanisms. We recently reported on a novel mechanism of chemoprotection by SFN in human colon cancer cells and prostate epithelial cells, namely the inhibition of histone deacetylase (HDAC). In the present investigation, we sought to test whether SFN also might inhibit HDAC activity in vivo. When consumed in the diet at an average daily dose of 7.5 mumol per animal for 21 days, SFN suppressed the growth of human PC-3 prostate cancer cells by 40% in male nude mice. There was a significant decrease in HDAC activity in the xenografts, as well as in the prostates and mononuclear blood cells (MBC), of mice treated with SFN, compared to controls. There also was a trend towards increased global histone acetylation in the xenografts, prostates, and MBC. In human subjects, a single dose of 68 g BroccoSprouts inhibited HDAC activity significantly in peripheral blood mononuclear cells (PBMC) 3 and 6 hrs following consumption. These findings provide evidence that one mechanism through which SFN acts as a cancer chemopreventive agent in vivo is through the inhibition of HDAC activity. Moreover, the data suggest that HDAC activity in PBMC may be used as a biomarker for assessing exposure to novel dietary HDAC inhibitors in human subjects.
Article Published Date : Feb 01, 2007
Study Type : Human Study
Additional Links
Substances : Sulforaphane : CK(624) : AC(303)
Diseases : Colon Cancer : CK(749) : AC(430), Prostate Cancer : CK(1586) : AC(463), Prostate Cancer: Prevention : CK(243) : AC(33)
Pharmacological Actions : Chemopreventive : CK(2835) : AC(787), Enzyme Inhibitors : CK(473) : AC(251), Histone deacetylase inhibitor : CK(48) : AC(37)


______________________________________________________________________
2018
Protective effects of sulforaphane in experimental vascular cognitive impairment.
Abstract Title:

Protective effects of sulforaphane in experimental vascular cognitive impairment: Contribution of the Nrf2 pathway.
Abstract Source:
J Cereb Blood Flow Metab. 2018 Jan 1:271678X18764083. Epub 2018 Jan 1. PMID: 29533123
Abstract Author(s):
Leilei Mao, Tuo Yang, Xin Li, Xia Lei, Yang Sun, Yongfang Zhao, Wenting Zhang, Yanqin Gao, Baoliang Sun, Feng Zhang
Article Affiliation:
Leilei Mao
Abstract:
The major pathophysiological process of vascular cognitive impairment (VCI) is chronic cerebral ischemia, which causes disintegration of the blood-brain barrier (BBB), neuronal death, and white matter injury. This study aims to test whether sulforaphane (Sfn), a natural activator of nuclear factor erythroid 2-related factor 2 (Nrf2), reduces the chronic ischemic injury and cognitive dysfunction after VCI. Experimental VCI was induced in rats by permanent occlusion of both common carotid arteries for six weeks. This procedure caused notable neuronal death in the cortex and hippocampal CA1, myelin loss in the corpus callosum and hippocampal fimbria, accumulation of myelin debris in the corpus callosum, and remarkable cognitive impairment. Sfn treatment alleviated these ischemic injuries and the cognitive dysfunction. Sfn-mediated neuroprotection was associated with enhanced activation of Nrf2 and upregulation of heme oxygenase 1. Sfn also reduced neuronal and endothelial death and maintained the integrity of BBB after oxygen-glucose deprivation in vitro in an Nrf2 dependent manner. Furthermore, Nrf2 knockdown in endothelial cells decreased claudin-5 protein expression with downregulated claudin-5 promoter activity, suggesting that claudin-5 might be a target gene of Nrf2. Our results demonstrate that Sfn provides robust neuroprotection against chronic brain ischemic injury and may be a promising agent for VCI treatment.
Article Published Date : Dec 31, 2017
Study Type : Animal Study
Additional Links
Substances : Sulforaphane : CK(624) : AC(303)
Diseases : Cognitive Decline/Dysfunction : CK(1163) : AC(215)
Pharmacological Actions : Neuroprotective Agents : CK(2360) : AC(1099), Nrf2 activation : CK(177) : AC(86)
______________________________________________________________________

2007

Sulforaphane has immunomodulatory properties.

Abstract Title:
Immunomodulatory activity of Sulforaphane, a naturally occurring isothiocyanate from broccoli (Brassica oleracea).
Abstract Source:
Phytomedicine. 2007 Aug;14(7-8):538-45. Epub 2006 Nov 3. PMID: 17084602
Abstract Author(s):
P Thejass, G Kuttan
Article Affiliation:
Department of Immunology, Amala Cancer Research Centre, Amala Nagar, Thrissur, Kerala State 680555, India.
Abstract:
The effect of Sulforaphane on the immune system was studied using BALB/c mice. Intraperitoneal administration of five doses of Sulforaphane (500 microg/dose/animal/day) was found to enhance the total WBC count (12,950 cells/mm3) on 9th day. Bone marrow cellularity (23 x 10(6) cells/femur) and number of alpha-esterase positive cells (1346.66/4000 cells) were also increased by the administration of Sulforaphane. Treatment with Sulforaphane along with the antigen, sheep red blood cells (SRBC), produced an enhancement in the circulating antibody titre and the number of plaque forming cells (PFC) in the spleen. Maximum number of PFC (315.83 PFC/10(6) spleen cells) was obtained on the 6th day. Administration of Sulforaphane also showed an enhancement in the phagocytic activity of peritoneal macrophages. Moreover administration of Sulforaphane significantly reduced the elevated level of TNF-alpha production by LPS stimulated macrophages. These results indicate the immunomodulatory activity of Sulforaphane.
Article Published Date : Aug 01, 2007
Study Type : Animal Study
Additional Links
Substances : Sulforaphane : CK(624) : AC(303)
Diseases : Immune Disorders: Low Immune Function : CK(489) : AC(118)
Pharmacological Actions : Immunomodulatory : CK(1287) : AC(358)
______________________________________________________________________


2016
Sulforaphane improves neuronal mitochondrial function in brain tissue in acute carbon monoxide poisoning.

Abstract Title:
Sulforaphane Improves Neuronal Mitochondrial Function in Brain Tissue in Acute Carbon Monoxide Poisoning Rats.
Abstract Source:
Basic Clin Pharmacol Toxicol. 2016 Dec 16. Epub 2016 Dec 16. PMID: 27983767
Abstract Author(s):
Mingjun Bi, Qin Li, Dadong Guo, Xiaoyu Ding, Weikang Bi, Yueheng Zhang, Yong Zou
Article Affiliation:
Mingjun Bi
Abstract:
Carbonmonoxide (CO) poisoning is one of the leading causes of toxicity-related mortality and morbidity worldwide, primarily manifested by acute and delayed central nervous system (CNS) injuries and other organ damages. However, its definite pathogenesis is poorly understood. The aim of the present study was to explore the pathogenesis of the ultrastructural and functional impairment of mitochondria and the protection of sulforaphane (SFP) at different dosages on hippocampus neurons in rats after exposure to CO. We found that CO poisoning could induce advanced cognitive dysfunction, while the mitochondrial ultrastructure of neurons in rats of the CO poisoning group was seriously damaged and mitochondrial membrane potential (ΔΨm) was accordingly reduced by transmission electron microscopy (TEM) and JC-1 fluorescent probe assay. CO poisoning could also increase the expressions of both nuclear factor erythroid 2-related factor 2 (Nrf-2) and Thioredoxin-1 (Trx-1) proteins and their mRNA in brain tissue with immunohistochemistry and quantitative PCR (qPCR) techniques. Early administration of either middle-dose or high-dose SFP could efficiently improve mitochondrial structure and function, enhance the anti-oxidative stress ability, and thus exerting a positive effect against brain damage induced by acute CO poisoning. This article is protected by copyright. All rights reserved.
Article Published Date : Dec 15, 2016
Study Type : Animal Study
Additional Links
Substances : Sulforaphane : CK(624) : AC(303)
Diseases : Carbon Monoxide Poisoning : CK(2) : AC(1)
Pharmacological Actions : Antioxidants : CK(8430) : AC(3132), Neuroprotective Agents : CK(2360) : AC(1099), Nrf2 activation 
______________________________________________________________________

2002

Sulforaphane inhibits extracellular, intracellular, and antibiotic-resistant strains of Helicobacter pylori and prevents benzo[a]pyrene-induced stomach tumors.

Abstract Title:
Sulforaphane inhibits extracellular, intracellular, and antibiotic-resistant strains of Helicobacter pylori and prevents benzo[a]pyrene-induced stomach tumors.
Abstract Source:
Proc Natl Acad Sci U S A. 2002 May 28;99(11):7610-5. PMID: 12032331
Abstract Author(s):
Jed W Fahey, Xavier Haristoy, Patrick M Dolan, Thomas W Kensler, Isabelle Scholtus, Katherine K Stephenson, Paul Talalay, Alain Lozniewski
Abstract:
Gastric infection with Helicobacter pylori is a cosmopolitan problem, and is especially common in developing regions where there is also a high prevalence of gastric cancer. These infections are known to cause gastritis and peptic ulcers, and dramatically enhance the risk of gastric cancer. Eradication of this organism is an important medical goal that is complicated by the development of resistance to conventional antimicrobial agents and by the persistence of a low level reservoir of H. pylori within gastric epithelial cells. Moreover, economic and practical problems preclude widespread and intensive use of antibiotics in most developing regions. We have found that sulforaphane [(-)-1-isothiocyanato-(4R)-(methylsulfinyl)butane], an isothiocyanate abundant as its glucosinolate precursor in certain varieties of broccoli and broccoli sprouts, is a potent bacteriostatic agent against 3 reference strains and 45 clinical isolates of H. pylori [minimal inhibitory concentration (MIC) for 90% of the strains is <or=4 microg/ml], irrespective of their resistance to conventional antibiotics. Further, brief exposure to sulforaphane was bactericidal, and eliminated intracellular H. pylori from a human epithelial cell line (HEp-2). In complementary experiments, sulforaphane blocked benzo[a]pyrene-evoked forestomach tumors in ICR mice. This protection resulted from induction of phase 2 detoxication and antioxidant enzymes, and was abrogated in mice lacking the nrf2 gene, which regulates phase 2 enzymes. Thus, the dual actions of sulforaphane in inhibiting Helicobacter infections and blocking gastric tumor formation offer hope that these mechanisms might function synergistically to provide diet-based protection against gastric cancer in humans.
Article Published Date : May 28, 2002
Study Type : Animal Study
Additional Links
Substances : Broccoli : CK(1031) : AC(334), Sulforaphane : CK(624) : AC(303)
Diseases : Gastric Cancer : CK(622) : AC(198), Helicobacter Pylori Infection : CK(506) : AC(104)
Additional Keywords : Multi-Drug Resistant Pathogens : CK(16) : AC(15)
______________________________________________________________________


2017
Sulforaphane is a protective agent against acetaminophen-induced liver damage.

Abstract Title:
The effect of sulforaphane on oxidative stress and inflammation in rats with toxic hepatitis induced by acetaminophene.
Abstract Source:
Bratisl Lek Listy. 2017 ;118(8):453-459. PMID: 29050482
Abstract Author(s):
E Dokumacioglu, H Iskender, M S Aktas, B Hanedan, A Dokumacioglu, T M Sen, A Musmul
Article Affiliation:
E Dokumacioglu
Abstract:
OBJECTIVE: The aim of the present study was to reveal the possible effect of sulforaphane on oxidative stress and inflammation in rats liver with toxic hepatitis induced by acetaminophene.
BACKGROUND: Sulforaphane is a compound with high antioxidant properties. Acetaminophen, which is a para-aminophenol derivative, can lead to fatal hepatic necrosis with direct hepatotoxic effects at high doses.
METHODS: Thirty six male Sprague-Dawley rats were randomly divided into four groups. Control group (n = 9) was fed with standard rat chow and water for 3 days. Group APAP (n = 9) received a single dose acetaminophen 1 g/kg by oral gavage in addition to standard chow and water. Group SFN (n = 9) received sulforaphane 500μg/kg by oral gavage in addition to standard chow and water for 3 days. Group APAP+SFN (n = 9) received sulforaphane 500 μg/kg and a single dose acetaminophen 1 g/kg by oral gavage in addition to standard chow and water. Acetaminophen was administered three hours after SFN administration.
RESULTS: Neopterin, MDA, AST, ALT and CRP levels of group APAP were significantly increased compared to control group. GSH level of group APAP was significantly lower than in the control group.
CONCLUSION: Sulforaphane is a protective agent against acetaminophen-induced liver damage and it can be added in the treatment protocol (Tab. 1, Fig. 5, Ref. 51).
Article Published Date : Dec 31, 2016
Study Type : Animal Study
Additional Links
Substances : Sulforaphane : CK(624) : AC(303)
Diseases : Acetaminophen (Tylenol) Toxicity : CK(166) : AC(61)
Pharmacological Actions : Anti-Inflammatory Agents : CK(4861) : AC(1630), Antioxidants : CK(8430) : AC(3132), Hepatoprotective
Problem Substances : Acetaminophen : CK(204) : AC(68), Paracetamol : CK(121) : AC(36)
______________________________________________________________________

2017

Sulforaphane may be a potential compound that can inhibit Aβ oligomer production in Alzheimer's disease.

Abstract Title:
Sulforaphane Inhibits the Generation of Amyloid-β Oligomer and Promotes Spatial Learning and Memory in Alzheimer's Disease (PS1V97L) Transgenic Mice.
Abstract Source:
J Alzheimers Dis. 2018 ;62(4):1803-1813. PMID: 29614663
Abstract Author(s):
Ting-Ting Hou, He-Yun Yang, Wei Wang, Qiao-Qi Wu, Yuan-Ruhua Tian, Jian-Ping Jia
Article Affiliation:
Ting-Ting Hou
Abstract:
Abnormal amyloid-β (Aβ) aggregates are a striking feature of Alzheimer's disease (AD), and Aβ oligomers have been proven to be crucial in the pathology of AD. Any intervention targeting the generation or aggregation of Aβ can be expected to be useful in AD treatment. Oxidative stress and inflammation are commonpathological changes in AD that are involved in the generation and aggregation of Aβ. In the present study, 6-month-old PS1V97L transgenic (Tg) mice were treated with sulforaphane, an antioxidant, for 4 months, and this treatment significantly inhibited the generation and aggregation of Aβ. Sulforaphane also alleviated several downstream pathological changes that including tau hyperphosphorylation, oxidative stress, and neuroinflammation. Most importantly, the cognition of the sulforaphane-treated PS1V97L Tg mice remained normal compared to that of wild-type mice at 10 months of age, when dementia typically emerges in PS1V97L Tg mice. Pretreating cultured cortical neurons with sulforaphane also protected against neuronal injury caused by Aβ oligomers in vitro. These findings suggest that sulforaphane may be a potential compound that can inhibit Aβ oligomer production in AD.
Article Published Date : Dec 31, 2017
Study Type : Transgenic Animal Study
Additional Links
Substances : Sulforaphane : CK(624) : AC(303)
Diseases : Alzheimer's Disease : CK(1292) : AC(382)
Pharmacological Actions : Neuroprotective Agents : CK(2360) : AC(1099)
______________________________________________________________________
2011

Sulforaphane protects against cisplatin-induced liver and mitochondrial damage.​​​​​​​

Abstract Title:
Protective effect of sulforaphane pretreatment against cisplatin-induced liver and mitochondrial oxidant damage in rats.
Abstract Source:
Toxicology. 2011 Aug 15 ;286(1-3):20-7. Epub 2011 May 6. PMID: 21575670
Abstract Author(s):
Leobardo Gaona-Gaona, Eduardo Molina-Jijón, Edilia Tapia, Cecilia Zazueta, Rogelio Hernández-Pando, Mariel Calderón-Oliver, Guillermo Zarco-Márquez, Enrique Pinzón, José Pedraza-Chaverri
Article Affiliation:
Departamento de Biología, Facultad de Química UNAM, UNAM, México, D.F., Mexico.
Abstract:
In the present work was analyzed whether sulforaphane (SFN) may protect against cisplatin (CIS)-induced hepatic damage, oxidant stress and mitochondrial dysfunction. Four groups of male Wistar rats were studied: control, CIS, CIS+SFN and SFN. SFN was given i.p. (500μg/kg/d × 3 days) before CIS administration (single i.p. injection, 10mg/kg). Rats were sacrificed 3 days after CIS injection to evaluate hepatic damage (histological analysis, liver/body weight ratio and serum activity of aspartate aminotransferase and alanine aminotransferase), oxidant stress (lipid peroxidation and protein carbonyl and glutathione content), antioxidant enzymes (catalase, glutathione reductase, glutathione peroxidase, glutathione-S-transferase and superoxide dismutase) in liver homogenates and isolated mitochondria and mitochondrial function (oxygen consumption using either malate/glutamate or succinate as substrates and the activity of mitochondrial complex I, II, II-III, IV and V). Furthermore it was evaluated if SFN is able to scavenge some reactive oxygen species in vitro. It was found that SFN prevents CIS-induced (a) hepatic damage, (b) oxidant stress and decreased activity of antioxidant enzymes in liver and mitochondria and (c) mitochondrial alterations in oxygen consumption and decreased activity of mitochondrial complex I. It was also found that the scavenging ability of SFN for peroxynitrite anion, superoxide anion, singlet oxygen, peroxyl radicals,hydrogen peroxide and hydroxyl radicals was very low or negligible. The hepatoprotective effect of SFN was associated to the preservation of mitochondrial function, antioxidant enzymes and prevention of liver and mitochondrial oxidant stress.
Article Published Date : Aug 15, 2011
Study Type : Animal Study
Additional Links
Substances : Sulforaphane : CK(624) : AC(303)
Diseases : Chemically-Induced Liver Damage : CK(634) : AC(255), Chemotherapy-Induced Toxicity: Cisplatin : CK(319) : AC(133), Oxidative Stress : CK(3871) : AC(1382)
Pharmacological Actions : Anticarcinogenic Agents : CK(1099) : AC(519), Antineoplastic Agents : CK(1158) : AC(639), Antioxidants : CK(8430) : AC(3132)
Problem Substances : Cisplatin : CK(30) : AC(7)
Adverse Pharmacological Actions : Hepatotoxic : CK(335) : AC(96)
______________________________________________________________________
2017

Sulforaphane supplementation normalize endothelial dysfunction associated with type 2 diabetes.

Abstract Title:
The Sulforaphane and pyridoxamine supplementation normalize endothelial dysfunction associated with type 2 diabetes.
Abstract Source:
Sci Rep. 2017 Oct 30 ;7(1):14357. Epub 2017 Oct 30. PMID: 29085055
Abstract Author(s):
Ana Pereira, Rosa Fernandes, Joana Crisóstomo, Raquel M Seiça, Cristina M Sena
Article Affiliation:
Ana Pereira
Abstract:
In this study we investigate pyridoxamine (PM) and/or sulforaphane (SFN) as therapeutic interventions to determine whether activators of NFE2-related factor 2 (Nrf2) can be used in addition with inhibitors of advanced glycation end products (AGE) formation to attenuate oxidative stress and improve endothelial dysfunction in type 2 diabetes. Goto-kakizaki (GK) rats, an animal model of non-obese type 2 diabetes, were treated with or without PM and/or SFN during 8 weeks and compared with age-matched Wistar rats. At the end of the treatment, nitric oxide (NO)-dependent and independent vasorelaxation in isolated aorta and mesenteric arteries were evaluated. Metabolic profile, NO bioavailability and vascular oxidative stress, AGE and Nrf2 levels were also assessed.Diabetic GK rats presented significantly lower levels of Nrf2 and concomitantly exhibited higher levels of oxidative stress and endothelial dysfunction. PM and SFN as monotherapy were capable of significantly improving endothelial dysfunction in aorta and mesenteric arteries decreasing vascular oxidative damage, AGE and HbA1c levels. Furthermore, SFN + PM proved more effective reducing systemic free fatty acids levels, normalizing endothelial function, NO bioavailability and glycation in GK rats. Activators of Nrf2 can be used therapeutically in association with inhibitors of AGE and cross-linking formation to normalize endothelial dysfunction in type 2 diabetes.
Article Published Date : Oct 29, 2017
Study Type : Animal Study
Additional Links
Substances : Sulforaphane : CK(624) : AC(303)
Diseases : Diabetes Mellitus: Type 2 : CK(3572) : AC(624), Endothelial Dysfunction : CK(1210) : AC(237)
Pharmacological Actions : Antioxidants : CK(8430) : AC(3132), Nrf2 activation : CK(177) : AC(86)
______________________________________________________________________
2018

Sulforaphane exerted a concentration-dependent inhibitory effect on the inflammatory cytokine production by the immune cells.

Abstract Title:
Broccoli and human health: immunomodulatory effect of sulforaphane in a model of colon cancer.
Abstract Source:
Int J Food Sci Nutr. 2018 Mar 7:1-8. Epub 2018 Mar 7. PMID: 29513123
Abstract Author(s):
Hanna Bessler, Meir Djaldetti
Article Affiliation:
Hanna Bessler
Abstract:
The favourable properties of broccoli on human health are due to their abundant content of vitamins, minerals and isothiocyanates, the sulforaphane (SFN) being the most important. SFN is created from its precursor glucoraphanin and it is released by myrosinase enzymes produced during crushing of the plant. SFN has been shown to possess anti-inflammatory and anticancer properties. The aim of the study was to determine if SFN may affect the immune dialogue between human peripheral blood mononuclear cells (PBMCs) and HT-29 and RKO human colon cancer cells lines. Non- or mitogen-stimulated PBMCs were incubated with various concentrations of SFN, and the secretion of TNFα, IL-1β, IL-6, IFNγ, IL-2, IL-10 and IL-1ra was determined. In addition, the effect of SFN on the production of these cytokines by PBMCs co-cultured with colon carcinoma cells was examined. SFN exerted a concentration-dependent inhibitory effect on the inflammatory cytokine production by the immune cells. The impact of SFN on the interaction between immune and colon cancer cells underscores its capacity for cancer prevention and development.
Article Published Date : Mar 06, 2018
Study Type : In Vitro Study
Additional Links
Substances : Broccoli Sprouts : CK(199) : AC(29), Sulforaphane : CK(624) : AC(303)
Diseases : Colon Cancer : CK(749) : AC(430)
Pharmacological Actions : Anti-Inflammatory Agents : CK(4861) : AC(1630), Chemotherapeutic : CK(397) : AC(152), Immunomodulatory : CK(1287) : AC(358)
______________________________________________________________________

You will find much more in the following links on the Sulforaphane:

______________________________________________________________________ 
http://www.greenmedinfo.com/substance/sulforaphane
https://www.ncbi.nlm.nih.gov/pubmed/?term=broccoli
https://www.ncbi.nlm.nih.gov/pubmed/?term=sulforaphane
https://www.ncbi.nlm.nih.gov/pubmed/?term=sulforaphane+cancer
https://www.ncbi.nlm.nih.gov/pubmed/?term=sulforaphane+breast
https://www.ncbi.nlm.nih.gov/pubmed/?term=sulforaphane+autism
https://www.ncbi.nlm.nih.gov/pubmed/?term=sulforaphane+nrf2


Sulforaphane ameliorated rotenone-induced motor function deficits in mice.
(a) Chemical structure of sulforaphane. Animals were submitted to the combined protocol of sulforaphane and rotenone (b). Body weights were measured every five days for the full 60 days (c). Animals underwent behavioural tests on day 60. Spontaneous activity in the cylinder (d), adhesive removal test (e) and challenging beam (f) were measured. Each value is presented as mean ± SEM, n = 3. *P < 0.05, **P < 0.01 vs. control group; #P < 0.05, ##P < 0.01 rotenone group vs. rotenone + sulforaphane treatment group.

Effects of sulforaphane on the cell viability and clonogenic ability of NSCLC cells. (a) Time- and concentration-dependent inhibition of NSCLC cell viability by sulforaphane (SFN). Cells were treated with various concentrations of sulforaphane for 24 h (upper panel), 48 h (middle panel) and 72 h (lower panel), and cell viability was evaluated by MTT assay. (b) Inhibition of the clonogenic ability of NSCLC cells by sulforaphane. H1975 (upper panel), PC9/gef (middle panel) and A549 (lower panel) cells were treated with various concentrations of sulforaphane for 6 days and cultured for an additional 8 days in the absence of sulforaphane. The numbers of foci were scored, and the data are presented as relative foci-forming ability (FFA). Data are expressed as mean ± SD of three independent experiments. *p < 0.05; **p < 0.01; and ***p < 0.001, as analyzed with the unpaired t-test
Effects of sulforaphane on the cell viability and clonogenic ability of NSCLC cells. (a) Time- and concentration-dependent inhibition of NSCLC cell viability by sulforaphane (SFN). Cells were treated with various concentrations of sulforaphane for 24 h (upper panel), 48 h (middle panel) and 72 h (lower panel), and cell viability was evaluated by MTT assay. (b) Inhibition of the clonogenic ability of NSCLC cells by sulforaphane. H1975 (upper panel), PC9/gef (middle panel) and A549 (lower panel) cells were treated with various concentrations of sulforaphane for 6 days and cultured for an additional 8 days in the absence of sulforaphane. The numbers of foci were scored, and the data are presented as relative foci-forming ability (FFA). Data are expressed as mean ± SD of three independent experiments. *p < 0.05; **p < 0.01; and ***p < 0.001, as analyzed with the unpaired t-test






Sulforaphane in Broccoli
_______________________
PubMed
PubMed comprises more than 28 million citations for biomedical literature from MEDLINE, life science journals, and online books. 
In PubMed
There are  16619 on Broccoli.
There are 1796 on Sulforaphane.
_______________________

212 Diseases Researched for Sulforaphane

Oxidative Stress3172
Inflammation1335
Prostate Cancer2135
DNA damage726
Breast Cancer1925
Colon Cancer1125
Breast Cancer: Triple Negative524
Pancreatic Cancer1524
Cancers: All1221
Bladder Cancer617
Helicobacter Pylori Infection517
Diabetes Mellitus: Type 2515
Insulin Resistance314
Prostate Cancer: Prevention414
Diesel Exhaust Particle Toxicity312
Glutathione Deficiency312
Air Pollution Linked Toxicity211
Cancer Metastasis911
Liver Cancer911
Lung Cancer711
Skin Diseases211
Anemia: Sickle Cell110
Asthma110
Autism110
Autism Spectrum Disorders110
Bladder Degeneration110
COPD110
Cancers: Drug Resistant510
Cystic Fibrosis110
Fatty Liver110
Gastritis110
Hyperinsulinism110
Lung Diseases110
Prostate: PSA Doubling110
Pulmonary Fibrosis110
Radical Prostatectomy110
Respiratory Diseases110
Schizophrenia110
Cognitive Decline/Dysfunction48
Endothelial Dysfunction38
Lipopolysaccharide-Induced Toxicity68
Cerebral Ischemia47
Chemotherapy-Induced Toxicity: Cisplatin47
Adenomatous Polyposis Coli36
Chemically-Induced Liver Damage46
Colorectal Cancer46
Melanoma46
Cancer Stem Cells55
Endothelial Damage15
Glioblastoma45
Hypoxia45
Immune Disorders: Low Immune Function35
Neurodegenerative Diseases45
Ovarian Cancer55
Acetaminophen (Tylenol) Toxicity24
Aflatoxicosis34
Alzheimer's Disease34
Aspirin-Induced Toxicity24
Brain Injury: Traumatic24
Brain: Microglial Activation24
Chemotherapy-Induced Toxicity: Doxorubicin34
Depression24
Diabetic Complications24
Gastric Cancer34
Intestinal Polyps24
Leukemia44
NSAID-induced toxicity24
Obesity24
Organ Transplantation: Pancreatic Islet Cells24
Skin Cancer34
Skin Cancer: Prevention24
Spinal Cord Injuries24
Traumatic Brain Injury24
Aging Skin23
Benzo[a]pyrene-induced Toxicity23
Blood-Brain-Barrier Disorders23
Brain Cancer33
Brain Damage23
Cadmium Poisoning23
Carcinoma: Non-Small-Cell Lung23
Cervical Cancer33
Chemotherapy-Induced Toxicity23
Diabetes Mellitus: Type 1: Prevention23
Diabetic Nephropathy23
Drug-Induced Toxicity: Indomethacin23
Gastric Ulcer23
Intestinal Diseases23
Liver Damage: Aflatoxin-Induced23
Low Disorders: Low TH123
Melanoma: Metastatic23
Multiple Myeloma23
Myocardial Ischemia23
Oral Cancer23
Osteosarcoma23
Parkinson's Disease33
Petroleum Exposure And Toxicity23
Polycyclic aromatic hydrocarbon (PAH) toxicity23
Rheumatoid Arthritis23
Skin Diseases: Photo-Aging23
Advanced Glycation End products (AGE)12
Aging12
Amphetamine Addiction/Withdrawal12
Anxiety Disorders12
Atherosclerosis12
Bacterial Infections and Mycoses22
Bladder Dysfunction12
Bladder Outlet Obstruction12
Brain Edema12
Brain Hypoxia22
Brain Inflammation12
Breast Cancer: Metastatic22
Cancers: Multi-Drug Resistant12
Carbon Monoxide Poisoning12
Cardiovascular Diseases22
Chemical Exposure12
Chemical Weapon Agent Injury12
Depressive Disorder12
Diabetes Mellitus: Type 112
Diabetes: Memory Problems12
Duchenne's Muscular Dystrophy12
Epstein-Barr Virus Infections12
Gastrointestinal Cancer12
Glioma22
Gout12
Head and Neck Cancer22
Hypertension12
Hypoglycemia22
Immune Dysregulation: TH1/TH2 imbalance12
Intoxication12
Ischemia12
Kidney Diseases12
Lead Poisoning12
Light Sensitivity12
Liver Disease12
Low Immune Function: Natural Killer Cells12
Malathion Toxicity12
Mercury Poisoning12
Muscle Damage: Exercise-Induced12
Muscle Fatigue12
Muscle Soreness12
Myocardial Infarction12
Nasopharyngeal Cancer12
Nephropathy12
Neurologic Disorders12
Neuropathic Pain12
Nicotine/Tobacco Toxicity12
Nonalcoholic fatty liver disease (NAFLD)12
Organ Transplantation12
Promyelocytic leukemia22
Respiratory Syncytial Virus Infections12
Respiratory Tract Infections12
Salivary Gland Adenoid Cystic Carcinoma.22
Salivary Gland Diseases22
Schwannoma: Vestibular12
Seizures12
Serotonin Disorders12
Smoking12
Stroke12
Stroke: Recovery12
Testicular Injury: Chemical/Metal Induced12
Tumors22
Allergies11
Androgen-Induced Diseases11
Aortic Plaques11
Arsenic Poisoning11
Bone Destructive Diseases: Over-Active Osteoclasts11
Brain Injury: Hippocampal Damage11
Breast Cancer: HER-2 Overexpressed11
Breast Cancer: Prevention11
Cardiac Hypertrophy11
Cardiovascular Disease: Prevention11
Cholesterol: LDL/HDL ratio11
Colon Cancer: Prevention11
Colorectal Tumors11
Dopamine Deficiency11
Drug-Induced Toxicity11
Dystrophic retinal detachment (DRD)11
Encephalomyelitis11
Excitotoxicity11
Fungal Infection11
Gastrointestinal Diseases11
Gram-Negative Bacterial Infections11
Gram-Positive Bacterial Infections11
HDL: Low11
HIV Infections11
Hepatitis C11
Heterocyclic Aromatic Amine Induced Toxicity11
Hydrogen Peroxide Induced Toxicity11
Hyperglycemia11
IgE-Mediated Hypersensitivity11
Keloid11
Kidney Damage11
Leukemia: Acute promyelocytic leukemia11
Liver Cancer: Prevention11
Lung Cancer: Prevention11
Macular Degeneration11
Medulloblastoma11
Melanism11
Microcystis aeruginosa11
Mitochondrial Diseases11
Multiple Sclerosis11
Oral Cancer: Prevention11
Osteoporosis: Over-active Osteoclasts11
Pancreatic Cancer Stem Cell11
Pesticide Toxicity11
Prediabetes11
Restenosis11
Retinal Diseases11
Stomach Cancer11
Striatonigral Degeneration: Autosomal Dominant11
Sunburn11
Ultraviolet Radiation Induced Damage11


89 Pharmacological Actions Researched for Sulforaphane.

Antioxidants59144
Anticarcinogenic Agents72124
Apoptotic79118
Anti-Inflammatory Agents3383
Chemopreventive4380
Antiproliferative4174
Nrf2 activation2760
Neuroprotective Agents2649
Phase II Detoxification Enzyme Inducer1440
Cell cycle arrest2529
NF-kappaB Inhibitor1922
Cytoprotective521
Hepatoprotective821
Histone deacetylase inhibitor918
Anti-metastatic1417
Tumor Necrosis Factor (TNF) Alpha Inhibitor1217
Enzyme Inhibitors716
Chemosensitizer1215
Chemotherapeutic915
Cyclooxygenase 2 Inhibitors1215
Interleukin-6 Downregulation1015
Interleukin-1 beta downregulation1014
Antineoplastic Agents1013
Glutathione Upregulation312
Genoprotective211
Anti-Allergic Agents110
Insulin Down-Regulation110
MicroRNA modulator1010
Matrix metalloproteinase-2 (MMP-2) inhibitor59
Matrix metalloproteinase-9 (MMP-9) inhibitor68
NF-E2-Related Factor-2 (Nrf2) Modulator78
Anti-Apoptotic47
Cardioprotective56
Renoprotective46
Anti-Angiogenic45
Immunomodulatory35
Superoxide Dismutase Up-regulation15
Antidepressive Agents24
Antiviral Agents34
Bcl-2 protein down-regulation44
Anti-Bacterial Agents33
Anti-Ulcer Agents23
Hypoxia inducible factor-1 alpha (HIF-1α) inhibitor23
Radioprotective23
Telomerase Inhibitor33
Tumor Suppressor Protein p53 Upregulation33
Angiogenesis Inhibitors12
Anti-Anxiety Agents12
Anticonvulsants12
Antinoceceptive12
Autophagy Inhibitors12
Chemoprotective Agents12
Detoxifier22
Epidermal growth factor receptor (EGFR) inhibitor12
Gastroprotective12
Heme oxygenase-1 up-regulation22
Hypolipidemic12
Hypotensive12
Interleukin-17 downregulation12
Interleukin-18 down-regulation12
Interleukin-2 upregulation12
Leptin Down-Regulation12
Phase I Detoxification Enzyme Inducer12
Prostaglandin PGE2 downregulation12
Proteasome Inhibitors22
Serotonergic12
Vascular Endothelial Growth Factor Inhibitors12
Wnt/β-catenin signaling pathway modulation22
Anti-Fibrotic11
Anti-Proliferative11
Antifungal Agents11
Antimitotic Agents11
Autophagy Up-regulation11
Beta-Defensin-2 Up-Regulation11
Caspase-3 Activation11
Cell Differentiation Inducer11
Cytotoxic11
Estrogen Receptor Modulators11
Interferon Gamma Reducer11
Interleukin-8 downregulation11
P21 Activation11
Postaglandin PGE2 downregulation11
Quinone Reductase-Inducer11
Radiopharmaceuticals11
Radiosensitizer11
Survivin Down-Regulation11
Vascular Cell Adhesion Molecule-1 Inhibitor11
Vascular Endothelial Growth Factor Regulator11
Wnt/β-catenin pathway down-regulation11

Stockholm - Charlottenberg - Hamburg - Copenhagen - Oslo - London