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rehmannia/entzündungshemmung
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Seite 1 von 39 Ergebnisse
Bioassay-guided isolation of anti-inflammatory components from the root of Rehmannia glutinosa and its underlying mechanism via inhibition of iNOS pathway.
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BACKGROUND
The root of Rehmannia glutinosa (RR) is commonly used to reduce inflammation in various traditional Chinese herbal formulae; however, little is known regarding its active component(s).
OBJECTIVE
The objective of the present study was to examine the active component(s) responsible for the
Influence of traditional Chinese anti-inflammatory medicinal plants on leukocyte and platelet functions.
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The enzymes 5-lipoxygenase and elastase are therapeutic targets in dermatological disorders such as psoriasis. Fifteen extracts from traditional Chinese medicinal plants used to treat topical inflammations were screened for their inhibitory effect on lipoxygenase, cyclooxygenase and elastase
Hot water extracted Lycium barbarum and Rehmannia glutinosa inhibit liver inflammation and fibrosis in rats.
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Polysaccharide-rich Lycium barbarum and Rehmannia glutinosa have been considered to have immune-modulating activity. This study investigated the effects of water extracted Lycium barbarum and Rehmannia glutinosa (HE) on carbon tetrachloride (CCl(4))-induced liver injury in rats. Male Sprague-Dawley
Catalpol suppresses osteoclastogenesis and attenuates osteoclast-derived bone resorption by modulating PTEN activity.
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Excessive activation of osteoclast activity is responsible for many bone diseases, such as osteoporosis, rheumatoid arthritis, periprosthetic osteolysis, and periodontitis. Natural compounds that inhibit osteoclast formation and/or function have therapeutic potential for treating these diseases.
Characterization of the anti-diabetic and antioxidant effects of rehmannia glutinosa in streptozotocin-induced diabetic Wistar rats.
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This study investigated the effects of Rehmannia glutinosa individually as well as in combination with the oral hypoglycemic agent, metformin in streptozotocin (STZ)-induced diabetic Wistar rats. R. glutinosa ethanolic extract was prepared and the constituents were characterized using fractionation
Further Study of Influence of Panax notoginseng on Intestinal Absorption Characteristics of Triptolide and Tripterine in Rats with Tripterygium wilfordii.
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UNASSIGNED
Tripterygium wilfordii (TW) is widely employed to treat rheumatoid arthritis and autoimmune disorders clinically, which, however, accompany with disturbing hepatotoxicity and nephrotoxicity. The previous research showed that Panax notoginseng (PN) compatibly and significantly reduces the
Administration of Kyung-Ok-Ko reduces stress-induced depressive behaviors in mice through inhibition of inflammation pathway
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Ethnopharmacological relevance: Kyung-Ok-Ko (KOK), a traditional medicinal formula composed of Rehmannia glutinosa (Gaertn.) DC, Poria cocos (Schw.) Wolf, Korean Red Panax ginseng C.A.Mey, and honey, has been used to treat amnesia and
The effects of a novel botanical agent on lipopolysaccharide-induced alveolar bone loss in rats.
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BACKGROUND
The development of host-modulatory agents with low risk of adverse effects has been needed to treat periodontitis, a chronic inflammatory disease. A botanical mixture of extracts from two natural substances, Panax notoginseng and Rehmannia glutinosa Libosch, was developed as a novel
Topical application of Rehmannia glutinosa extract inhibits mite allergen-induced atopic dermatitis in NC/Nga mice.
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OBJECTIVE
Rehmannia glutinosa is known in Asia as a traditional herbal medicine with anti-inflammatory properties. Atopic dermatitis (AD) is an inflammatory skin disease associated with enhanced T-helper 2 (Th2) lymphocyte responses to allergens that results in elevated serum IgE levels and
Acteoside suppresses RANKL-mediated osteoclastogenesis by inhibiting c-Fos induction and NF-κB pathway and attenuating ROS production.
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Numerous studies have reported that inflammatory cytokines are important mediators for osteoclastogenesis, thereby causing excessive bone resorption and osteoporosis. Acteoside, the main active compound of Rehmannia glutinosa, which is used widely in traditional Oriental medicine, has
Rehmannia glutinosa inhibits tumour necrosis factor-alpha and interleukin-1 secretion from mouse astrocytes.
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We investigated whether an aqueous extract of Rehmannia glutinosa steamed root (RGAE) inhibits secretion of tumour necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) from primary cultures of mouse astrocytes. RGAE dose-dependently inhibited the TNF-alpha secretion by astrocytes stimulated
Catalpol reduces the production of inflammatory mediators via PPAR-γ activation in human intestinal Caco-2 cells.
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Catalpol, a major iridoid glycoside present in Rehmannia glutinosa, has been reported to show a variety of pharmacological properties. However, the molecular mechanism underlying the anti-inflammatory effect of catalpol in intestinal cells remains poorly understood. The present study was aimed at
Catalpol downregulates vascular endothelial‑cadherin expression and induces vascular hyperpermeability.
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Catalpol, an iridiod glucoside isolated from Rehmannia glutinosa, has been reported to possess anti‑inflammatory properties. However, the molecular mechanisms underlying this effect have not been fully elucidated. This study aimed to investigate the effects of catalpol on vascular permeability.
Role of catalpol in ameliorating the pathogenesis of experimental autoimmune encephalomyelitis by increasing the level of noradrenaline in the locus coeruleus.
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The endogenous neurotransmitter, noradrenaline, exerts anti-inflammatory and neuroprotective effects in vivo and in vitro. Reduced noradrenaline levels results in increased inflammation and neuronal damage. The primary source of noradrenaline in the central nervous system is tyrosine hydroxylase
Catalpol attenuates the neurotoxicity induced by beta-amyloid(1-42) in cortical neuron-glia cultures.
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A glia-mediated inflammation plays an important role in the pathogenesis of Alzheimer's disease (AD). In vitro, besides a direct neurotoxic effect on neurons, Abeta activates glia to produce an array of inflammatory factors including tumor necrosis factor-alpha (TNF-alpha), reactive oxygen species
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