Department of Pharmacology, School of Pharmacy, Nantong University, Jiangsu, China
Effects of sulforaphane in the central nervous system.
Sulforaphane (SFN) is an active component extracted from vegetables like cauliflower and broccoli. Activation of the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) signaling is a common mechanism for the anti-oxidative and anti-inflammatory activity of some herb-derived compounds, such as icariin and berberine. However, due to its peculiar ability in Nrf2 activation, SFN is recognized as an activator of Nrf2 and recommended as a supplementation for prevention and/or treatment of disorders like neoplasm and heart failure. In the central nervous system (CNS), the prophylactic and/or therapeutic effects of SFN have been revealed in recent years. For example, it has been reported to prevent the progression of Alzheimer's disease, Parkinson's disease, cerebral ischemia, Huntington's disease, multiple sclerosis, epilepsy, and psychiatric disorders via promotion of neurogenesis or inhibition of oxidative stress and neuroinflammation. SFN is also implicated in reversing cognition, learning, and memory impairment in rodents induced by scopolamine, lipopolysaccharide, okadaic acid, and diabetes. In models of neurotoxicity, SFN has been shown to suppress neurotoxicity induced by a wide range of toxic factors, such as hydrogen peroxide, prion protein, hyperammonemia, and methamphetamine. To date, no consolidated source of knowledge about the pharmacological effects of SFN in the CNS has been presented in the literature. In this review, we summarize and discuss the pharmacological effects of SFN as well as their possible mechanisms in prevention and/or therapy of disorders afflicting the CNS, aiming to get a further insight into how SFN affects the pathophysiological process of CNS disorders.
For those that don't know much about sulforaphane, sulforaphane is a naturally occurring compound in cruciferous vegetables like broccoli, cabbage, and kale. It’s activated only when vegetables are chopped or chewed. The highest levels of sulforaphane are found in raw vegetables. Considering how powerful this substance is (or at least claimed to be), you would think it would be studied intensely.
Raw vegetables have the highest levels of sulforaphane. Steaming vegetables for one to three minutes may be the best way to optimize sulforaphane levels when cooking.
Apparently It’s best to cook these type of vegetables below 284˚F (140˚C), as exceeding this temperature results in a loss of glucosinolates like glucoraphanin (don't know what those are). For this reason, it’s also best to avoid boiling or microwaving cruciferous vegetables. Instead it is suggested to eat them raw or lightly steamed to maximize their sulforaphane content.
Another very interesting attribute of sulforaphane is that is is supposed to help with pain.
Laboratory of Neurobiology, Tomsk State University, Tomsk, Russian Federation
Prenolica Limited (formerly Solagran Limited), Biotechnology Company, Melbourne, Victoria, Australia
Department of Radiology, University of Washington, Seattle, WA, USA
Plant polyprenols reduce demyelination and recover impaired oligodendrogenesis and neurogenesis in the cuprizone murine model of multiple sclerosis.
Recent studies showed hepatoprotective, neuroprotective, and immunomodulatory properties of polyprenols isolated from the green verdure of Picea abies (L.) Karst. This study aimed to investigate effects of polyprenols on oligodendrogenesis, neurogenesis, and myelin content in the cuprizone demyelination model. Demyelination was induced by 0.5% cuprizone in CD-1 mice during 10 weeks. Nine cuprizone-treated animals received daily injections of polyprenols intraperitoneally at a dose of 12-mg/kg body weight during Weeks 6-10. Nine control animals and other nine cuprizone-treated received sham oil injections. At Week 10, brain sections were stained for myelin basic protein, neuro-glial antigen-2, and doublecortin to evaluate demyelination, oligodendrogenesis, and neurogenesis. Cuprizone administration caused a decrease in myelin basic protein in the corpus callosum, cortex, hippocampus, and the caudate putamen compared with the controls. Oligodendrogenesis was increased, and neurogenesis in the subventricular zone and the dentate gyrus of the hippocampus was decreased in the cuprizone-treated group compared with the controls. Mice treated with cuprizone and polyprenols did not show significant demyelination and differences in oligodendrogenesis and neurogenesis as compared with the controls. Our results suggest that polyprenols can halt demyelination, restore impaired neurogenesis, and mitigate reactive overproduction of oligodendrocytes caused by cuprizone neurotoxicity.
Department of Anatomy, Faculty of Basic Medical Sciences, College of Health Sciences, University of Ilorin, Ilorin, Nigeria.
International Center for Genetic Engineering and Biotechnology, Italy
Kolaviron Protects the Prefrontal Cortex and Hippocampus against Histomorphological and Neurobehavioural Changes in Cuprizone Model of Multiple Sclerosis
This study explored the efficacy of kolaviron-a biflavonoid complex isolated from the seeds of Garcinia kola-in protecting against cuprizone (CPZ)-induced demyelination in both the prefrontal cortex and the hippocampus of Wistar rats.
Thirty rats were treated to receive 0.5 mL phosphate-buffered saline (group A, control), 0.5 mL corn oil (group B), 0.2% CPZ (group C), for 6 weeks, 0.2% CPZ for 3 weeks and then 200 mg/kg of Kv for 3 weeks (group D), or 200 mg/kg of Kv for 3 weeks followed by 0.2% CPZ for 3 weeks (group E). Rats were assessed for exploratory functions and anxiety-like behaviour before being euthanised and perfused transcardially with 4% paraformaldehyde. Prefrontal and hippocampal thin sections were stained in hematoxylin and eosin and cresyl fast violet stains.
CPZ-induced demyelination resulted in behavioural impairment as seen by reduced exploratory activities, rearing behaviour, stretch attend posture, center square entry, and anxiogenic characteristics. Degenerative changes including pyknosis, karyorrhexis, neuronal hypertrophy, and reduced Nissl integrity were also seen. Animals treated with Kv showed significant improvement in behavioural outcomes and a comparatively normal cytoarchitectural profile.
Blood Transfusion Research Center, High Institute for Research and Education in Transfusion Medicine, Tehran, Iran
Effects of Curcumin on Microglial Cells.
Microglia are innate immune system cells which reside in the central nervous system (CNS). Resting microglia regulate the homeostasis of the CNS via phagocytic activity to clear pathogens and cell debris. Sometimes, however, to protect neurons and fight invading pathogens, resting microglia transform to an activated-form, producing inflammatory mediators, such as cytokines, chemokines, iNOS/NO and cyclooxygenase-2 (COX-2). Excessive inflammation, however, leads to damaged neurons and neurodegenerative diseases (NDs), such as Parkinson's disease (PD), Alzheimer's disease (AD), Huntington's disease (HD), multiple sclerosis (MS) and amyotrophic lateral sclerosis (ALS). Curcumin is a phytochemical isolated from Curcuma longa. It is widely used in Asia and has many therapeutic properties, including antioxidant, anti-viral, anti-bacterial, anti-mutagenic, anti-amyloidogenic and anti-inflammatory, especially with respect to neuroinflammation and neurological disorders (NDs). Curcumin is a pleiotropic molecule that inhibits microglia transformation, inflammatory mediators and subsequent NDs. In this mini-review, we discuss the effects of curcumin on microglia and explore the underlying mechanisms.
Laboratory of Pharmacognosy, College of Pharmacy, Gachon University, Hambakmoero, Yeonsu-gu, Republic of Korea
Sulforaphane-Enriched Broccoli Sprouts Pretreated by Pulsed Electric Fields Reduces Neuroinflammation and Ameliorates Scopolamine-Induced Amnesia in Mouse Brain through Its Antioxidant Ability via Nrf2-HO-1 Activation.
Activated microglia-mediated neuroinflammation plays a key pathogenic role in neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, and ischemia. Sulforaphane is an active compound produced after conversion of glucoraphanin by the myrosinase enzyme in broccoli (Brassica oleracea var) sprouts. Dietary broccoli extract as well as sulforaphane has previously known to mitigate inflammatory conditions in aged models involving microglial activation. Here, we produced sulforaphane-enriched broccoli sprouts through the pretreatment of pulsed electric fields in order to trigger the biological role of normal broccoli against lipopolysaccharide-activated microglia. The sulforaphane-enriched broccoli sprouts showed excellent potency against neuroinflammation conditions, as evidenced by its protective effects in both 6 and 24 h of microglial activation in vitro. We further postulated the underlying mechanism of action of sulforaphane in broccoli sprouts, which was the inhibition of an inflammatory cascade via the downregulation of mitogen-activated protein kinase (MAPK) signaling. Simultaneously, sulforaphane-enriched broccoli sprouts inhibited the LPS-induced activation of the NF-κB signaling pathway and the secretions of inflammatory proteins (iNOS, COX-2, TNF-α, IL-6, IL-1β, PGE2, etc.), which are responsible for the inflammatory cascades in both acute and chronic inflammation. It also upregulated the expression of Nrf2 and HO-1 in normal and activated microglia followed by the lowered neuronal apoptosis induced by activated microglia. Based on these results, it may exhibit anti-inflammatory effects via the NF-κB and Nrf2 pathways. Interestingly, sulforaphane-enriched broccoli sprouts improved the scopolamine-induced memory impairment in mice through Nrf2 activation, inhibiting neuronal apoptosis particularly through inhibition of caspase-3 activation which could lead to the neuroprotection against neurodegenerative disorders. The present study suggests that sulforaphane-enriched broccoli sprouts might be a potential nutraceutical with antineuroinflammatory and neuroprotective activities.
Department of Neurology, Chung-Ang University Hospital, Chung-Ang University College of Medicine, Seoul, Korea
The Anti-Inflammatory Effect of Sulforaphane in Mice with Experimental Autoimmune Encephalomyelitis.
Multiple sclerosis (MS) is an immune-associated inflammatory disorder of the central nervous system and results in serious disability. Although many disease-modifying therapy drugs have been developed, these drugs have shown limited clinical efficacy and some adverse effects in previous studies, therefore, there has been reasonable need for less harmful and cost-effective therapeutics. Herein, we tested the anti-inflammatory effect of sulforaphane (SFN) in a mouse model of experimental autoimmune encephalomyelitis (EAE).
The EAE mice were randomly assigned into two experimental groups: the phosphate-buffered saline (PBS)-treated EAE group and SFN-treated EAE group. After EAE mice induction by auto-immunization against the myelin oligodendrocyte glycoprotein peptide, we evaluated EAE symptom scores and biochemical analyses such as infiltration of inflammatory cells and demyelination of the spinal cord. Furthermore, western blotting was performed using the spinal cords of EAE mice.
In the behavioral study, the SFN-treated EAE mice showed favorable clinical scores compared with PBS-treated EAE mice at the 13th day (1.30 ± 0.15 vs. 1.90 ± 0.18; P = 0.043) and 14th day (1.80 ± 0.13 vs. 2.75 ± 0.17; P = 0.003). Additionally, the biochemical studies revealed that SFN treatment inhibited the inflammatory infiltration, demyelinating injury of the spinal cords, and the up-regulation of inducible nitric oxide synthase in the EAE mice.
The SFN treatment showed anti-inflammatory and anti-oxidative effects in the EAE mice. Conclusively, this study suggests that SFN has neuroprotective effects via anti-inflammatory processing, so it could be a new therapeutic or nutritional supplement for MS.
Traditional Medicine and History of Medical Sciences Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran
Pistacia Genus as a Potential Source of Neuroprotective Natural Products.
Neuroprotective agents are able to defend the central nervous system against acute or chronic neuronal injuries. Even with the progress made over the last decades, most of the medications prescribed for the management of neurodegenerative diseases can only reduce their symptoms and slow down their progression. Based on natural product research, there are potential effective medicinal plants and phytochemicals for modulating neuronal functions and protecting against neurodegeneration. Plants in the genus Pistacia are also among valuable natural resources for neuroprotection research based on experiences in traditional medicine. Studies have supported the value of bioactive compounds of the genus Pistacia for central nervous system disorders such as Alzheimer's, Parkinson's, multiple sclerosis, cerebral ischemia, depression, and anxiety. Related literature has also revealed that most of the evidence on neuroprotection in the genus Pistacia is in the form of preliminary studies, mainly including models of behavior, motor function, and memory impairments in animals, neural toxicity, cerebral ischemia and seizure models, evaluation of their effects on antioxidant and inflammatory biomarkers, amyloid β aggregation, and acetylcholinesterase as well as investigations into some cellular pathways. Along with the phytonutrients in kernels such as pistachios, various phytochemicals, mostly terpenes, and phenolic compounds have also been identified in different plant parts, in particular their oleoresins, of species in the genus Pistacia. In this review, the pharmacology of neurological effects and related molecular mechanisms of the plants belonging to the genus Pistacia and its active constituents, as well as pharmacokinetics aspects, are discussed.
Instituto Maimonides de Investigación Biomédica de Córdoba (IMIBC), Av. Menendez Pidal, Cordoba, Spain
Extra-Virgin Olive Oil Modifies the Changes Induced in Non-Nervous Organs and Tissues by Experimental Autoimmune Encephalomyelitis Models
The School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China
Department of Immunology, Nanjing Medical University, Nanjing, China
Therapeutic Potential of ω-3 Polyunsaturated Fatty Acids in Human Autoimmune Diseases.
The recognition of ω-3 polyunsaturated acids (PUFAs) as essential fatty acids to normal growth and health was realized more than 80 years ago. However, the awareness of the long-term nutritional intake of ω-3 PUFAs in lowering the risk of a variety of chronic human diseases has grown exponentially only since the 1980s (1, 2). Despite the overwhelming epidemiological evidence, many attempts of using fish-oil supplementation to intervene human diseases have generated conflicting and often ambiguous outcomes; null or weak supporting conclusions were sometimes derived in the subsequent META analysis. Different dosages, as well as the sources of fish-oil, may have contributed to the conflicting outcomes of intervention carried out at different clinics. However, over the past decade, mounting evidence generated from genetic mouse models and clinical studies has shed new light on the functions and the underlying mechanisms of ω-3 PUFAs and their metabolites in the prevention and treatment of rheumatoid arthritis, systemic lupus erythematosus (SLE), multiple sclerosis, and type 1 diabetes. In this review, we have summarized the current understanding of the effects as well as the underlying mechanisms of ω-3 PUFAs on autoimmune diseases.
Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
Comparison of Food Intake in Multiple Sclerosis Patients and Healthy Individuals: A Hospital-Based Case-Controlled Study
Nutritional factors affect the incidence, severity of symptoms and progression of multiple sclerosis (MS). However, the role of specific nutritional factors remains largely unknown in MS. We conducted this hospital-based case-controlled study to investigate the association between dietary intake and risk of MS.
Materials & Methods:
This study was conducted on 93 MS patients and 94 age-matched controls from Oct 2015 to Sep 2016 in Tehran, Iran. MS was diagnosed based on 2010 McDonald criteria and Brain Magnetic Resonance Imaging. Dietary intake was assessed using a validated semi-quantitative food frequency questionnaire. Odds ratio and 95% confidence interval of MS was calculated in different food groups using multiple logistic regression models adjusted for potentially confounding variables and compared between the two groups.
There was no significant difference between the age (34.62 ±9.68 vs. 33.96±8.75) and BMI (23.96 ±4.07 vs. 24.47 ±4.07) of MS and control group, respectively. Higher intake of processed meat (OR (95% CI))=(2.07(1.18-3.63) and non-processed meat (1.38(1.13-1.68)) were found in the MS group compared with the control.
Higher intake of processed meat and non-processed meat was associated with increased risk of MS. Further studies on the probable role of these nutritional factors in the pathogenesis of MS are suggested.
Department of Physical Medicine & Rehabilitation, Rehabilitation Medicine Research Center, Mayo Clinic, Rochester
High fat diet consumption results in mitochondrial dysfunction, oxidative stress, and oligodendrocyte loss in the central nervous system.
Metabolic syndrome is a key risk factor and co-morbidity in multiple sclerosis (MS) and other neurological conditions, such that a better understanding of how a high fat diet contributes to oligodendrocyte loss and the capacity for myelin regeneration has the potential to highlight new treatment targets. Results demonstrate that modeling metabolic dysfunction in mice with chronic high fat diet (HFD) consumption promotes loss of oligodendrocyte progenitors across the brain and spinal cord. A number of transcriptomic and metabolomic changes in ER stress, mitochondrial dysfunction, and oxidative stress pathways in HFD-fed mouse spinal cords were also identified. Moreover, deficits in TCA cycle intermediates and mitochondrial respiration were observed in the chronic HFD spinal cord tissue. Oligodendrocytes are known to be particularly vulnerable to oxidative damage, and we observed increased markers of oxidative stress in both the brain and spinal cord of HFD-fed mice. We additionally identified that increased apoptotic cell death signaling is underway in oligodendrocytes from mice chronically fed a HFD. When cultured under high saturated fat conditions, oligodendrocytes decreased both mitochondrial function and differentiation. Overall, our findings show that HFD-related changes in metabolic regulators, decreased mitochondrial function, and oxidative stress contribute to a loss of myelinating cells. These studies identify HFD consumption as a key modifiable lifestyle factor for improved myelin integrity in the adult central nervous system and in addition new tractable metabolic targets for myelin protection and repair strategies.
Studies like this are not very useful because they do not specify the type of fats being consumed. There are good fats and bad fats. Diet high in good fats (omega 3s) have been shown to be very beneficial. And yes, studies high in bad fats may not be as healthy. There was a study released recently that indicated that many 'fat' studies done in the past have been flawed in how they were completed and basically invalidated many of the 'old school' conclusions made.
Few will disagree that foods high in omega 3 fats are beneficial and essential for good health.
Swiss Institute of Allergy and Asthma Research (SIAF), University of Zurich, Switzerland
The Influence of Dietary Fatty Acids on Immune Responses
Diet-derived fatty acids (FAs) are essential sources of energy and fundamental structural components of cells. They also play important roles in the modulation of immune responses in health and disease. Saturated and unsaturated FAs influence the effector and regulatory functions of innate and adaptive immune cells by changing membrane composition and fluidity and by acting through specific receptors. Impaired balance of saturated/unsaturated FAs, as well as n-6/n-3 polyunsaturated FAs has significant consequences on immune system homeostasis, contributing to the development of many allergic, autoimmune, and metabolic diseases. In this paper, we discuss up-to-date knowledge and the clinical relevance of the influence of dietary FAs on the biology, homeostasis, and functions of epithelial cells, macrophages, dendritic cells, neutrophils, innate lymphoid cells, T cells and B cells. Additionally, we review the effects of dietary FAs on the pathogenesis of many diseases, including asthma, allergic rhinitis, food allergy, atopic dermatitis, rheumatoid arthritis, multiple sclerosis as well as type 1 and 2 diabetes.
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