Hair loss in patients with inflammatory bowel disease.

PMID: 

Inflamm Bowel Dis. 2013 Jul ;19(8):1753-63. PMID: 23624889

Abstract Title: 

Hair loss in patients with inflammatory bowel disease.

Abstract: 

BACKGROUND: Little is known about the prevalence, causes, and management of hair loss in patients with inflammatory bowel disease (IBD). Despite the fact that there are relatively few case reports describing hair loss in IBD, anecdotally, it is a common clinical problem. Hair loss is associated with both acute and chronic illness, with nutritional deficiencies, and with adverse drug reactions, all of which are relevant to IBD.METHODS: A literature search was performed using PubMed from 1966 to July 2012 to identify all articles describing cases of and/or the cause of hair loss in patients with IBD.RESULTS: There is relatively little data describing the prevalence, cause, or course of hair loss in people with IBD. Because there are many potential reasons for hair loss in people with IBD, identifying the cause is not always possible. Telogen effluvium associated with acute or chronic flares of IBD is probably the commonest cause of disease-related hair loss, although the prevalence of this is unknown. Other causes include drug side effects and nutritional deficiencies. More recently shared genetic risk factors with alopecia areata and IBD have been identified.CONCLUSIONS: The potential causes of hair loss in IBD are protean, although its prevalence is unknown. A practical guide to assessing and managing patients with hair loss in IBD is presented.

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Rose crude polysaccharides are very promising and can potentially be used as natural chemopreventive agents.

PMID: 

Molecules. 2019 Apr 6 ;24(7). Epub 2019 Apr 6. PMID: 30959857

Abstract Title: 

Polysaccharide-Rich Fractions fromThunb.-Composition and Chemopreventive Potential.

Abstract: 

The huge health-beneficial potential of polysaccharides encourages the search for novel sources and applications of these compounds. One poorly explored source of polysaccharides is the rose. The content and biological activity of polysaccharides in rose organs is an almost completely unaddressed topic, therefore, polysaccharide-rich extracts (crude polysaccharides, CPLs) from petals, leaves, hips, and achenes ofThunb. were studied for their composition and the influence on various cellular processes involved in the development of cancer and other civilization diseases. The study revealed the presence of water-soluble and -insoluble polysaccharides (includingβ-glucans) and protein-polysaccharide conjugates in rose organs. Rose hips were found to be the most abundant source of polysaccharides. Different polysaccharide-rich extracts showed the ability to inhibit pro-inflammatory enzymes (COX-1, COX-2, hyaluronidase), a radical scavenging effect (againstDPPHand ABTS), and antiproliferative activity (in the A549 lung and SW480 colon cancer cell lines) in in vitro assays. Therefore, rose crude polysaccharides are very promising and can potentially be used as natural chemopreventive agents.

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Rosa rugosa flavonoids exhibited PPARα agonist-like effects on genetic severe hypertriglyceridemia of mice.

PMID: 

J Ethnopharmacol. 2019 Aug 10 ;240:111952. Epub 2019 May 15. PMID: 31100436

Abstract Title: 

Rosa rugosa flavonoids exhibited PPARα agonist-like effects on genetic severe hypertriglyceridemia of mice.

Abstract: 

ETHNOPHARMACOLOGICAL RELEVANCE: Rosa rugosa Thunb. is a traditional Chinese medicine that was used in the treatment of cardiovascular diseases and relative risk factors such as diabetes, hyperlipidemia, hypertension, and inflammation. Rosa rugosa flavonoids (RRFs) are the main components in Rosa rugosa Thunb. Several studies have demonstrated that RRFs can regulate plasma lipid contents, but the related mechanism of which has not yet been elucidated clearly.AIM OF THE STUDY: The goal of this study was to clarify the effects of RRFs on triglyceride metabolism and its related mechanisms.MATERIALS AND METHODS: RRFs were obtained by ethanol extraction from Rosa rugosa Thunb.. Transgenic mice expressing human Apolipoprotein C3 (ApoC3) were used as a mouse model of hypertriglyceridemia. Fenofibrate (FNB), a PPARα agonist, was used as a positive control drug of decreasing high triglyceride. FNB (100 mg/kg) or RRFs (300 mg/kg) were given to the mice by gavage daily. Two weeks later, the changes of plasma lipid levels in the mice were measured by commercial kits, the clearance of triglyceride was evaluated by oral fat load test, and expression of the genes related to lipid β-oxidation and synthesis was detected in the mice livers by real time PCR.RESULTS: RRFs, as well as FNB, were found to significantly reduce plasma triglyceride (TG) levels in ApoC3 transgenic mice after administration of the drug for two weeks. Plasma lipid clearance rate was increased and lipid content in the mice livers was reduced after administration of RRF. Treatment with RRFs up-regulated mRNA expression of PPARα and its downstream gene of ACOX, while down-regulated mRNA expression of the genes related to fatty acid synthesis (FASN, SREBP-1c, and ACC1). The expression of LPL was raised, while the expression of ApoC3 was decreased, and Foxo1 was inhibited by RRFs in the mice livers.CONCLUSION: RRFs can reduce plasma TG levels by repressing the expression of ApoC3 and inducing the expression of LPL in liver. RRFs could also reduce triglyceride in hepatocytes through increasingβ-oxidation and decreasing synthesis of the lipids. These findings show the potency of further clinical application of RRFs as a hypolipidemic drug for treatment of cardiovascular diseases.

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An aqueous polyphenol extract from Rosa rugosa tea has antiaging effects on Caenorhabditis elegans.

PMID: 

J Food Biochem. 2019 Apr ;43(4):e12796. Epub 2019 Feb 21. PMID: 31353595

Abstract Title: 

An aqueous polyphenol extract from Rosa rugosa tea has antiaging effects on Caenorhabditis elegans.

Abstract: 

Rosa rugosa aqueous polyphenol (RAP) is a kind of polyphenol from Rosa rugosa flower tea. In this study, the antiaging activities of RAP were studied in the model organism Caenorhabditis elegans. UHPLC-HESI-MS/MS was employed to identify the specific phenolic profile, revealing that there were 23 types of phenolic compounds in RAP and that quercetin glycoside was the principal component. RAP increased the mean lifespan of C. elegans and enhanced the thermotolerance and resistance to oxidative stress of C. elegans in a concentration-dependent manner. Furthermore, RAP showed powerful antioxidant effects in vitro and strong protection against oxidative DNA damage. RAP significantly improved the levels of total superoxide dismutase and total antioxidant capacity of C. elegans. In conclusion, RAP has antiaging effects on C. elegans, which might be related to its powerful antioxidant effects both in vitro and in vivo. PRACTICAL APPLICATIONS: In recent years, chronic diseases associated with aging have had a profound impact on quality of life. Many healthy foods have antiaging properties, especially flower teas, such as those made from Rosa rugosa. Our results indicated that Rosa rugosa tea is good for health and that RAP could potentially be developed as a bioactive product that could be used to combat aging.

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Sambucus nigra L. ameliorates UVB-induced photoaging and inflammatory response in human skin keratinocytes.

PMID: 

Cytotechnology. 2019 Sep 11. Epub 2019 Sep 11. PMID: 31512082

Abstract Title: 

Sambucus nigra L. ameliorates UVB-induced photoaging and inflammatory response in human skin keratinocytes.

Abstract: 

Sambucus nigra L. (Elderberry) is widely used as a dietary supplement in functional food and possesses many pharmacological activities to prevent ailments, such as the colds and fever, diabetes and cancer. However, research on its skin anti-aging effect is still limited. Here, we evaluated the recovery effects of elderberry extract (EB) in UVB-irradiated human skin keratinocytes (HaCaTs) and investigated whether EB represents a potential therapeutic agent against skin photoaging and inflammation. In this study, EB showed good efficiency on scavenging free radicals and dose-dependently reduced reactive oxygen species (ROS) generation. EB notably decreased UVB-induced matrix metalloproteinase-1 (MMP-1) expression and inflammatory cytokine secretion through the inhibition of mitogen-activated protein kinases/activator protein 1 (MAPK/AP-1) and nuclear factor-κB (NF-κB) signaling pathways, blocking extracellular matrix (ECM) degradation and inflammation in UVB-irradiated HaCaTs. In addition, EB improved nuclear factor E2-related factor 2/heme oxygenase-1 (Nrf2/HO-1) signaling to increase oxidative defense capacity, and enhanced transforming growth factor beta (TGF-β) signaling activation to promote procollagen type I synthesis, relieving UVB-induced skin cell damage. These results indicated that EB has the potential to ameliorate UVB-induced skin photoaging and inflammation.

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Anthocyanins could contribute to the management of chronic gut inflammatory diseases.

PMID: 

Mediators Inflamm. 2017 ;2017:3454023. Epub 2017 Mar 8. PMID: 28373746

Abstract Title: 

Cyanidin-3-O-Glucoside Modulates the In Vitro Inflammatory Crosstalk between Intestinal Epithelial and Endothelial Cells.

Abstract: 

Intestinal epithelium represents a protective physical barrier and actively contributes to the mucosal immune system. Polarized basolateral intestinal secretion of inflammatory mediators, followed by activation of NF-B signaling and inflammatory pathways in endothelial cells, efficiently triggers extravasation of neutrophils from the vasculature, therefore contributing to the development and maintenance of intestinal inflammation. Proper regulation of NF-B activation at the epithelial interface is crucial for the maintenance of physiological tissue homeostasis. Many papers reported that anthocyanins, a group of compounds belonging to flavonoids, possess anti-inflammatory effects and modulate NF-B activity. In this study, by using a coculture in vitro system, we aimed to evaluate the effects of TNF–stimulated intestinal cells on endothelial cells activation, as well as the protective effects of cyanidin-3-glucoside (C3G). In this model, TNF-induced nuclear translocation of NF-B and TNF-and IL-8 gene expression in Caco-2 cells, whereas C3G pretreatment dose-dependently reduced these effects. Furthermore, TNF–stimulated Caco-2 cells induced endothelial cells activation with increased E-selectin and VCAM-1 mRNA, leukocyte adhesion, and NF-B levels in HUVECs, which were inhibited by C3G. We demonstrated that selective inhibition of the NF-B pathway in epithelial cells represents the main mechanism by which C3G exerts these protective effects. Thus, anthocyanins could contribute to the management of chronic gut inflammatory diseases.

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Cyanidin-3-glucoside had an apoptogenic effect in the glioblastoma multiforme cell line.

PMID: 

World Neurosurg. 2017 Dec ;108:94-100. Epub 2017 Sep 1. PMID: 28867321

Abstract Title: 

Cytotoxic and Apoptogenic Effects of Cyanidin-3-Glucoside on the Glioblastoma Cell Line.

Abstract: 

OBJECTIVE: Glioblastoma multiforme (GBM) is the most prevalent and aggressive primary cerebral tumor. The median survival time is 15 months despite maximum treatment because the tumor is resistant to most therapeutic modalities. Several studies have indicated chemopreventive and chemotherapeutic activity of cyanidin-3-glucoside (C3G) as an anthocyanin component. We aimed to illustrate the cytotoxic and apoptogenic effects of C3G in the U87 cell line (human GBM cell line).METHODS: Cytotoxic activity was evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide tetrazolium assay after treatment with C3G at different concentrations in the U87 cell line. Cisplatin was used as a positive control for 24 and 48 hours. The percentage of apoptotic cells was determined using an Annexin V/propidium iodide assay, and the expression of bax, bcl2, and p53 genes was assessed using real-time polymerase chain reaction.RESULTS: Treatment of U87 cells with 40μg/mL of C3G resulted in 32% apoptotic cells after 24 hours. To further confirm that C3G treatment induced apoptosis in U87 cells, RNA expression of bax, bcl2, and p53 genes was investigated after treatment. Real-time polymerase chain reaction indicated that the expression of bax and p53 increased,whereas the expression of bcl2 decreased.CONCLUSIONS: C3G had an apoptogenic effect in the GBM cell line. New information regarding the therapeutic effects of C3G in GBM could ultimately lead to the production of new drugs.

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Effects of cyanidin 3-0-glucoside on cardiac structure and function in an animal model of myocardial infarction.

PMID: 

Food Funct. 2017 Nov 15 ;8(11):4089-4099. PMID: 28990610

Abstract Title: 

Effects of cyanidin 3-0-glucoside on cardiac structure and function in an animal model of myocardial infarction.

Abstract: 

Cyanidin 3-0-glucoside (CG) is a polyphenol with potential health benefits. In this study, we investigated, for the first time, the cardioprotective effects of CG in an animal model of myocardial infarction (MI), a major cause of death worldwide. Sham and MI rats were administered CG (10 mg kgday) daily for one week prior to surgery, and 8 weeks post-surgery. Echocardiography was performed to assess cardiac structure and function at 4 and 8 weeks. At 4 weeks, MI rats had significantly lower body mass when compared to control rats, and CG administration significantly prevented this decrease. Four-week MI rats also showed significantly increased left ventricle dilation, end systolic and end diastolic volumes in comparison to controls, and CG significantly prevented these adverse changes. Ejection fraction was significantly lower in 4-week MI rats in comparison to controls, and CG had no effect on this parameter. At 8 weeks, body mass was significantly lower in MI rats when compared to control rats, and CG significantly prevented this decrease. At 8 weeks, MI rats showed a significant increase in left ventricle dilation and isovolumic relaxation time, while ejection fraction was significantly lower when compared to controls; these parameters were not altered by CG treatment. Eight-week MI rats had significantly higher level of oxidative stress in heart tissue in comparison to controls, and CG administration did not prevent this increase. In conclusion, administration of CG was able to significantly preserve body mass in both 4 and 8 weeks MI rats, as well as significantly prevent cardiac dilation in 4 weeks MI rats. However, CG was unable to sustain this cardioprotection, as cardiac structure and function were not significantly improved in 8 weeks MI rats.

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Cyanidin-3-glucoside inhibits inflammatory activities in human fibroblast-like synoviocytes and in mice with collagen-induced arthritis.

PMID: 

Clin Exp Pharmacol Physiol. 2018 10 ;45(10):1038-1045. Epub 2018 Jun 21. PMID: 29779214

Abstract Title: 

Cyanidin-3-glucoside inhibits inflammatory activities in human fibroblast-like synoviocytes and in mice with collagen-induced arthritis.

Abstract: 

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by joint tissue inflammation. Cyanidin-3-glucoside (C3G) is a major component in the flavonoid family and has shown anti-inflammatory, anti-oxidant and anti-tumour activity. In this study, we investigated the effects of C3G on lipopolysaccharides (LPS)-induced inflammation on human rheumatoid fibroblast-like synoviocytes (FLS) and on collagen-induced arthritis (CIA) mice model. We treated FLS with C3G followed by LPS induction, the expressions of tumour necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β) and IL-6 and the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and mitogen-activated protein kinase (MAPK) signalling pathway were analyzed. CIA was induced in mice and the arthritic mice were treated with C3G for 3 weeks. Thedisease severity was compared between control and C3G treated mice. The serum levels of TNF-α, IL-1β and IL-6 were analyzed by ELISA. C3G inhibited LPS-induced TNF-α, IL-1β and IL-6 expression in FLS. Moreover, C3G inhibited LPS-induced p65 production and IκBa, p38, ERK and JNK phosphorylation. Administration of C3G significantly attenuated disease in mice with CIA and decreased the serum level of TNF-α, IL-1β and IL-6. C3G inhibited LPS-induced inflammation in human FLS by inhibiting activation of NF-κB and MAPK signalling pathway. C3G exhibited therapeutic effects in mice with CIA.

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