Berberine supplementation may ameliorate the state of chronic inflammation.

PMID: 

Complement Ther Med. 2019 Oct ;46:81-86. Epub 2019 Aug 4. PMID: 31519292

Abstract Title: 

Effect of Berberine on C-reactive protein: A systematic review and meta-analysis of randomized controlled trials.

Abstract: 

OBJECTIVES: Clinical evidence suggests the beneficial effects of Berberine (BER) on inflammatory markers. However, these results are controversial. The aim of this systematic review was to assess the effects of BER on C-reactive protein (CRP) using clinical trials in adults.DESIGN: Systematic review and meta-analysis.MAIN OUTCOME MEASURES: We searched randomized controlled trials in PubMed and Scopus up to November 2018. The mean differences (MD) and confidence interval (CI) of CRP (mg/L) concentrations were pooled with a random- or a fixed-effects model depending on the results of heterogeneity tests.RESULTS: Of 1242 studies identified, 5 were included in the meta-analysis. Pooled analysis showed that serum levels of CRP were decreased after BER supplementation (MD:-0.64 mg/L, 95% CI(-0.67 to -0.61) P 

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Berberine ameliorates NSAIDs-induced intestinal injury by the repair of enteric nervous system.

PMID: 

Fundam Clin Pharmacol. 2019 Sep 13. Epub 2019 Sep 13. PMID: 31520444

Abstract Title: 

Berberine ameliorates NSAIDs-induced intestinal injury by the repair of enteric nervous system.

Abstract: 

The study was to detect the role of GDNF, PGP9.5 (a neuronal marker) and GFAP (EGCs' marker) in the mechanism of NSAIDs related to intestinal injury, and to clarify the protective effect of berberine in the treatment of NSAID-induced small intestinal disease. 40 males SD rats were divided randomly into five groups (A-E): Group A: control group; Group B: model group received diclofenac sodium 7.5mg/(kg*d) for five days; Group C,D,E: berberine low, medium and high dose groups were treated by 7.5mg/(kg*d) diclofenac sodium for five days then received berberine 25mg/(kg*d) ,50mg/(kg*d), 75mg/(kg*d) respectively, between the sixth and eighth day. Intestinal mucosa was taken on the ninth day to observe the general, histological injuries, and to measure the intestinal epithelial thickness. Then, immunohistochemistry was performed to detect the expression of PGP9.5 and GFAP, and Western blot was performed to detect GDNF expression. The histological score and the general score in the model group were respectively 5.75±1.04 and 4.83±0.92. Scores in berberine medium and high berberine group were lower compared with the model group (P

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Berberine inhibits adipocyte differentiation, proliferation and adiposity through down-regulating galectin-3.

PMID: 

Sci Rep. 2019 Sep 16 ;9(1):13415. Epub 2019 Sep 16. PMID: 31527742

Abstract Title: 

Berberine inhibits adipocyte differentiation, proliferation and adiposity through down-regulating galectin-3.

Abstract: 

This study is designed to investigate the effects of berberine (BBR) on galectin-3 (Gal-3) and the relationships to its suppressive activities on adipocyte differentiation, proliferation and adiposity. Our results showed that BBR greatly suppressed the differentiation and proliferation of mouse primary preadipocytes isolated from epididymal white adipose tissue (eWAT), during which the expression level of Gal-3 was down-regulated significantly. Overexpression of Gal-3 totally abolished the suppressive activities of BBR on Gal-3 expression, preadipocyte differentiation and proliferation. BBR reduced Gal-3 promoter activity, destabilized its mRNA and inhibited firefly luciferase activity of a recombinant plasmid containing the Gal-3 3' untranslated region (UTR). Furthermore, BBR up-regulated microRNA (miRNA) let-7d expression and the suppressive activity on Gal-3 3'UTR was abolished by point mutation on the let-7d binding site. In mice fed a high-fat diet (HFD), BBR up-regulated let-7d and down-regulated Gal-3 expression in eWAT; it also suppressed adipocyte differentiation and proliferation and reduced adiposity greatly. In summary, our study proves that BBR inhibits the differentiation and proliferation of adipocytes through down-regulating Gal-3, which is closely associated with its anti-obesity effect. Our results may support the future clinical application of BBR for the treatment of obesity or related diseases.

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Aronia berry extract inhibits TNF-α-induced vascular endothelial inflammation through the regulation of STAT3.

PMID: 

Food Nutr Res. 2019 ;63. Epub 2019 Aug 16. PMID: 31452653

Abstract Title: 

Aronia berry extract inhibits TNF-α-induced vascular endothelial inflammation through the regulation of STAT3.

Abstract: 

Background: Inflammation in endothelial cells induces production of inflammatory cytokines and monocytes adhesion, which are crucial events in the initiation of atherosclerosis. Aronia berry (), also called black chokeberry, contains abundant anthocyanins that have received considerable interest for their possible relations to vascular health.Objective: The aim of this study was to investigate whether an anthocyanin-rich extract obtained from aronia berry can attenuate inflammatory responses in vascular endothelial cells.Methods: As a model of vascular endothelial inflammation, human umbilical vein endothelial cells (HUVECs) pretreated with aronia berry extract were stimulated with tumor necrosis factor-alpha (TNF-α). The expression levels of cytokines and adhesion molecules were analyzed. To investigate the effects of aronia berry extract on the adhesion of THP-1 monocytic cell, the static adhesion assay was carried out. The possible molecular mechanisms by which aronia berry extract regulated vascular inflammatory responses were explored.Results: The mRNA expressions of interleukins (IL-1β, IL-6, and IL-8) and monocyte chemoattractant protein-1 (MCP-1) upregulated by TNF-α were significantly suppressed by pretreatment with aronia berry extract. Aronia berry extract decreased TNF-α-induced monocyte/endothelial adhesion and suppressed vascular cell adhesion molecule-1 (VCAM-1) expression, but did not affect intercellular adhesion molecule-1 (ICAM-1) expression. Moreover, aronia berry extract decreased the phosphorylation of signal transducer and activator of transcription 3 (STAT3) and the nuclear levels of STAT3 and interferon regulatory transcription factor-1 (IRF1). The nuclear translocation of nuclear factor-kappa B (NF-κB) was not inhibited by aronia berry extract.Conclusion: Aronia berry extract could exert anti-atherosclerotic effects on TNF-α-induced inflammation through inhibition of STAT3/IRF1 pathway in vascular endothelial cells.

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Consumption of noni and chokeberry juices lower blood pressure while energy drinks increase it.

PMID: 

Evid Based Complement Alternat Med. 2019 ;2019:6076751. Epub 2019 Aug 18. PMID: 31531115

Abstract Title: 

Effects of Acute Consumption of Noni and Chokeberry Juices vs. Energy Drinks on Blood Pressure, Heart Rate, and Blood Glucose in Young Adults.

Abstract: 

The purpose of this study has been to determine the effect of acute consumption of noni and chokeberry juices vs. energy drinks on blood pressure, heart rate, and blood glucose. The subjects divided into 4 groups, which consumed three portions of noni or chokeberry juices (30 mL or 200 mL, respectively) and energy drink (ED) or water (200 mL) at one-hour intervals. All participants had their blood pressure (BP), both systolic and diastolic BP (SBP and DBP), as well as heart rate (HR) and blood glucose (BG), measured. Consumption of noni juice caused a significantdecrease in SBP and DBP of 5.0% and 7.5%, respectively, while, the consumption of chokeberry juice slightly decreased only DBP by 3.6%. On the contrary, consumption of three portions of EDs caused a significant increase in DBP by 14.7%. The BG of participants consuming noni juice decreased by 7.3%,while the consumption of EDs increased BG by as much as 15.8%. Acute consumption of noni juice contributed to a significantly decreased SBP, DBP, and HR as well as a mild reduction of BG. Consumption of chokeberry juice caused only a slight reduction of DBP. Contrary to juices, EDs consumption resulted in an increase of blood pressure (especially DBP) and blood glucose. The results of the study showed that noni juice may be effective in lowering blood pressure and blood sugar levels, but there is a need to continue research on the long-term effect of this juice.

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Eugenol has a therapeutic effect on oxidative stress and apoptosis against cisplatin-induced testicular damage.

PMID: 

Andrologia. 2019 Oct ;51(9):e13353. Epub 2019 Jun 26. PMID: 31243800

Abstract Title: 

The antiapoptotic and antioxidant effects of eugenol against cisplatin-induced testicular damage in the experimental model.

Abstract: 

Testicular dysfunction or damage is among the critical side effects of chemotherapeutic drugs like cisplatin. This study was mapped out to assess the possible therapeutic effect of eugenol on cisplatin-induced testicular damage. In this experimental study, a single dose of cisplatin (15 mg/kg) was given intraperitoneally. After 72 hr of cisplatin injection, rats were sacrificed and testis tissues were removed. Tissues were examined by biochemical, histopathological and immunohistochemical methods. While tissue lipid peroxidation product and apoptotic marker levels increased, antioxidant enzyme activities of testis tissue were decreased in the cisplatin group. Additionally, histopathological damage was also determined in testis tissue. Contrary to all these results, the severity of damage in the tissue wasreduced histopathologically owing to eugenol treatment. The lipid peroxidation decreased and antioxidant enzyme activities increased in the eugenol treatment group. It has been determined that eugenol has a therapeutic effect on oxidative stress and apoptosis against cisplatin-induced testicular damage.

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Synergistic fungicidal activity with low doses of eugenol and amphotericin B against Candida albicans.

PMID: 

Biochem Biophys Res Commun. 2019 Oct 20 ;518(3):459-464. Epub 2019 Aug 20. PMID: 31443962

Abstract Title: 

Synergistic fungicidal activity with low doses of eugenol and amphotericin B against Candida albicans.

Abstract: 

Candida albicans frequently causes variety of superficial and invasive disseminated infections in HIV infected patients. Further, the emergence of non albicans species causing candidiasis predominantly in patients with advanced immune-suppression and drug resistance brings great apprehension. Hence, in this study we evaluate the capability of eugenol (EUG), a natural compound in combination with less toxic concentrations of amphotericin B (AmpB) for enhanced antifungal effects and reduced toxicity. Antifungal activity and time-kill assay were employed according to Clinical Laboratory Standard Institute (CLSI) guidelines with minor modifications on clinical isolates of Candida albicans. To confirm the synergistic interaction of EUG and AmpB, checkerboard experiments were employed. Interestingly, EUG-Amp B combination shows many fold higher anti-candida activity compared to single component treatment. Furthermore, our results depicts reactive oxygen species (ROS) driven killing and mitochondrial hyperpolarisation on treatment. Our data also suggests inhibition of calcium channel by EUG and predicts longer retainment of AmpB. Pronounced cellular damage was observed with combination treatment than to EUG and AmpB alone. Our finding is helpful for the removal of toxic concentrations of antifungal agents.

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Ferulic acid altered IL-17A/IL-17RA interaction and protected against imiquimod-induced psoriasis-like skin injury

PMID: 

Food Chem Toxicol. 2019 Jul ;129:365-375. Epub 2019 May 3. PMID: 31054998

Abstract Title: 

Ferulic acid altered IL-17A/IL-17RA interaction and protected against imiquimod-induced psoriasis-like skin injury in mice.

Abstract: 

Ferulic acid (FA), a phenolic phytochemical, is commonly found in grains, vegetables, and fruits. Interleukin-17A (IL-17A) and IL-17 receptor A (IL-17RA) interaction is one of important therapeutic targets for psoriasis. Here we analyzed the FA effects on IL-17A/IL-17RA interaction and psoriasis-like skin injury induced by imiquimod (IMQ). IL-17A-blocking assay and docking analysis showed that FA interacted with Trp-67, Gln-94, and Glu-95 residues of IL-17A via hydrogen bonds and consequently abolished the binding of IL-17RA to IL-17A. Mice were topically given with IMQ and orally given with various amounts of FA for 14 consecutive days. FA attenuated IMQ-induced psoriasis-like skin lesions in a dose-dependent manner, and the epidermal thickness of mice treated with 100 mg/kg FA was reduced by 53.48 ± 4.44% in comparison with sham. Global analysis of differentially expressed genes showed that IMQ and FA significantly affected immune response, metabolism, and mitogen-activated protein kinase signaling pathways. Immunohistochemical staining showed that FA inhibited the infiltration and the cytokine secretion of Th17 cell, dendritic cell, and granulocyte subsets in psoriatic skin tissues. In conclusion, we newly identified that oral administration of FA protected against IMQ-induced psoriatic skin injury in mice. Moreover, its protection was associatedwith the interference of IL-17A/IL-17RA interaction.

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The effect of ferulic acid on experimental traumatic brain damage in rats.

PMID: 

Bratisl Lek Listy. 2019 ;120(5):372-379. PMID: 31113201

Abstract Title: 

The effect of ferulic acid on experimental traumatic brain damage in rats.

Abstract: 

AIM: Traumatic brain injury is an important social health problem due to the fact that young adults are more likely to be affected, and advanced functional limitations are observed in survivors. In this study, we aimed to investigate the protective effect of ferulic acid in an experimental trauma model.MATERIAL AND METHODS: This study was performed in March 2016 at Dokuz Eylül University Experimental Animal Laboratory. Subjects were randomly divided into 4 groups Control, Ethyl Alcohol, Trauma, Trauma/Ferulic Acid groups. For histological findings, Cresyl violet; for immunohistochemical analysis, TUNEL and Active Caspase-3 staining were used. For biochemical analysis,Superoxide dismutase, Malondialdehyde, and Glutathione values ​​were examined.RESULTS: The application of ferulic acid has been shown to primarily reduce neuronal apoptosis, the levels of free radicals, and to effect oxidant/antioxidant balance positively by increasing the levels of antioxidants, such as Superoxide dismutase and Glutathione that are developed due to brain damage. Our study group has shown that ferulic acid decreased nerve tissue pathologies after generated brain trauma compared to injury groups.CONCLUSION: Addition of ferulic acid to the traditional head trauma treatment has the strength, and ability to increase the rate, and percentage of healing (Tab. 2, Fig. 4, Ref. 28).

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