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Posted: Wed Apr 17, 2019 9:57 am
Posted: Wed Apr 17, 2019 10:01 am
2019 Mar 8
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.
Posted: Wed Apr 17, 2019 10:45 am
Broccoli and broccoli sprouts, especially broccoli sprouts, are excellent sources of sulforaphane, more so than most other vegetables. Broccoli sprouts have up to 5 times as much sulforaphane than regular broccoli. Sulforaphane is readily available in supplement form and is very inexpensive (of course there are expensive options too) and is thought to have many health benefits.
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.
Posted: Sun Apr 21, 2019 1:46 am
2019 Mar 12
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.
Posted: Sat May 04, 2019 3:47 am
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.
Posted: Fri May 10, 2019 7:50 am
2019 Apr 4
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.
Posted: Sat Jun 08, 2019 2:04 am
2019 Mar 27
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.