PMID: 

Am J Cardiovasc Drugs. 2019 Nov 12. Epub 2019 Nov 12. PMID: 31713723

Abstract Title: 

Ubiquinol Improves Endothelial Function in Patients with Heart Failure with Reduced Ejection Fraction: A Single-Center, Randomized Double-Blind Placebo-Controlled Crossover Pilot Study.

Abstract: 

BACKGROUND: Endothelial dysfunction is reportedly associated with worse outcomes in patients with chronic heart failure. Ubiquinol is a reduced form of coenzyme Q10 (CoQ10) that may improve endothelial function.OBJECTIVE: We assessed the hypothesis that ubiquinol improves peripheral endothelial function in patients with heart failure with reduced ejection fraction (HFrEF).METHODS: In this randomized, double-blind, placebo-controlled, crossover pilot study, 14 patients with stable HFrEF were randomly and blindly allocated to ubiquinol 400 mg/day or placebo for 3 months. After a 1-month washout period, patients were crossed over to the alternative treatment. Before and after each treatment, we assessed peripheral endothelial function using the reactive hyperemia index (RHI) and analyzed it using the natural logarithm of RHI (LnRHI).RESULTS: Peripheral endothelial function as assessed by LnRHI tended to improve with ubiquinol 400 mg/day for 3 months (p = 0.076). Original RHI values were also compared, and RHI significantly improved with ubiquinol treatment (pre-RHI 1.57 [interquartile range (IQR) 1.39-1.80], post-RHI 1.74 [IQR 1.63-2.02], p = 0.026), but not with placebo (pre-RHI 1.67 [IQR 1.53-1.85], post-RHI 1.51 [IQR 1.39-2.11], p = 0.198).CONCLUSIONS: Ubiquinol 400 mg/day for 3 months led to significant improvement in peripheral endothelial function in patients with HFrEF. Ubiquinol may be a therapeutic option for individuals with HFrEF. Large-scale randomized controlled trials of CoQ10 supplementation in patients with HFrEF are needed.CLINICAL TRIAL REGISTRATION: Japanese University Hospital Medical Information Network (UMIN-ICDR). Clinical Trial identifier number UMIN000012604.

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PMID: 

Microorganisms. 2020 Jan 10 ;8(1). Epub 2020 Jan 10. PMID: 31936809

Abstract Title: 

Thymol Inhibits Biofilm Formation, Eliminates Pre-Existing Biofilms, and Enhances Clearance of Methicillin-Resistant(MRSA) in a Mouse Peritoneal Implant Infection Model.

Abstract: 

Methicillin-resistant(MRSA) is a common human pathogen that causes several difficult-to-treat infections, including biofilm-associated infections. The biofilm-forming ability ofplays a pivotal role in its resistance to most currently available antibiotics, including vancomycin, which is the first-choice drug for treating MRSA infections. In this study, the ability of thymol (a monoterpenoid phenol isolated from plants) to inhibit biofilm formation and to eliminate mature biofilms, was assessed. We found that thymol could inhibit biofilm formation and remove mature biofilms by inhibiting the production of polysaccharide intracellular adhesin (PIA) and the release of extracellular DNA (eDNA). However, cotreatment with thymol and vancomycin was more effective at eliminating MRSA biofilms, in a mouse infection model, than monotherapy with vancomycin. Comparative histopathological analyses revealed that thymol reduced the pathological changes and inflammatory responses in the wounds. Assessments of white blood cell counts and serum TNF-α and IL-6 levels showed reduced inflammation and an increased immune response following treatment with thymol and vancomycin. These results indicate that combinatorial treatment with thymol and vancomycin has the potential to serve as a more effective therapy for MRSA biofilm-associated infectionsthan vancomycin monotherapy.

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PMID: 

J Drug Target. 2020 Feb 5:1-10. Epub 2020 Feb 5. PMID: 31983246

Abstract Title: 

Thymoquinone and curcumin combination protects cisplatin-induced kidney injury, nephrotoxicity by attenuating NFκB, KIM-1 and ameliorating Nrf2/HO-1 signalling.

Abstract: 

This study evaluates the protective effects of Thymoquinone (Tq) and Curcumin (Cur) in models of cisplatin-induced renal toxicity. Proliferation studies were carried out in HEK-293 cells. Cisplatin(ip) 5 mg/kg BW was used to induce renal injury in Sprague-Dawley rats. 50 mg/kg BW Tq + 100 mg/kg BW Cur, with or without cisplatin-treatment were administered for 5 days. Tq + Cur combination synergistically reduced the proliferation inhibition of HEK-293 cells resulted from cisplatin treatment and brought down cisplatin-induced apoptosis in these cells.studies revealed serum levels of BUN, creatinine, CK and pro-inflammatory cytokines like TNF-α, IL-6 and MRP-1 to be elevated in the cisplatin-treated group while reducing glomerular filtration rate. Tq + Cur treatment significantly improved these conditions. The antioxidant enzyme levels and mitochondrial ATPases were restored upon treatment, which were lessened in the cisplatin-treated group. Cisplatin induced the expression of KIM-1, which was brought down by the combination treatment. Tq + Cur treatment increased the expressions of phosphorylated Akt, Nrf2 and HO-1 proteins while decreasing the levels of cleaved caspase 3 and NFκB in kidney homogenates. In summary, Tq + Cur had protective effects on cisplatin-induced nephrotoxicity and renal injury, which could be mediated by up-regulation of survival signals like Akt, Nrf2/HO-1 and attenuation of KIM-1, NFκB.

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PMID: 

Ital J Pediatr. 2019 Mar 12 ;45(1):36. Epub 2019 Mar 12. PMID: 30871574

Abstract Title: 

An observational study of fixed-dose Tanacetum parthenium nutraceutical preparation for prophylaxis of pediatric headache.

Abstract: 

BACKGROUND: Migraine is one of the most prevalent chronic pain manifestations of childhood. Despite the multitude of available treatments, parents are often concerned about chronic therapies and pediatricians have insufficient confidence in prescribing prophylactic drugs. Therefore, there is now growing interest for natural supplements used to control recurrent migraine headaches. Such approach may increase acceptance and adherence to long-term prophylaxis therapy in children.METHODS: This is an observational multicenter study performed in children (n = 91) with migraine, with (MO) or without aura (MA), or tension-type headache (TTH). A fixed-dose Andrographis paniculata, CoQ10, riboflavin, and magnesium, was administered for 16 weeks. Patients were evaluated at baseline (T0), at week 8 (T1) and at the end of treatment at week 16 (T2). A follow-up period occurred at week 20 (T3) and week 32 (T4).RESULTS: The herbal supplement significantly reduced the frequency of headaches in TTH patients during treatment period (T0: 11.97 + 1.92 vs T2: 5.13 + 1.93; p 

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PMID: 

Avicenna J Phytomed. 2020 Jan-Feb;10(1):70-77. PMID: 31921609

Abstract Title: 

enhances pentobarbital-induced sleeping behaviors.

Abstract: 

Objective: Sleep disorders are among the most common psychiatric and medical conditions. In the present study, the hypnotic effect ofwas studied in miceMaterials and Methods: The hydro-alcoholic extract (HAE) ofand three fractions of it, namely water fraction (WF), ethyl acetate fraction (EAF), and -hexane fraction (NHF), were intraperitoneally (ip) administrated to mice 30 min before injection of sodium pentobarbital (30 mg/kg, ip). Then, 30 min after administration of HAE, motor coordination (rota-rod test) was evaluated. Besides, LDof HAE was determined and the cytotoxicity of HAE was evaluated in PC12 cells using the MTT assay.Results: HAE 50-200 mg/kg increased the sleeping time. EAF was the only fraction which could prolong the sleep duration and decrease sleep latency. The LD50 value was 4.8 g/kg. The extract induced no cytotoxic effects in PC12 cell line.Conclusion: The results suggested thatpotentiates pentobarbital hypnosis without causing toxic effects. Probably, its effects are mediated by the components present in EAF of this plant.

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PMID: 

Med Sci Monit Basic Res. 2019 Aug 27 ;25:179-186. Epub 2019 Aug 27. PMID: 31451678

Abstract Title: 

Antifungal and Synergistic Effects of the Ethyl Acetate Extract of Tanacetum vulgare (L.) Against Candida albicans.

Abstract: 

BACKGROUND With the continued demand for new, effective, and safe endodontic therapies, the aim of this study was assessment of efficiency of the ethyl acetate (EthOAc) extract of Tanacetum vulgare (L.) against Candida albicans. MATERIAL AND METHODS The antifungal effectiveness of the EthOAc extract of T. vulgare was determined using the agar disk diffusion method. The inhibition zones induced by the EthOAc extract were compared after 5 minutes, 60 minutes, and 24 hours to those induced by standard solutions (2% chlorhexidine, saturated calcium hydroxide, and 2% sodium hypochlorite). Statistical analysis of the results was performed using the Kruskal-Wallis test and one-way ANOVA. RESULTS The inhibition zone of chlorhexidine against C. albicans was 30.3-19.3 mm, but in combination with EthOAc extract (100 mg/mL) of T. vulgare, this inhibition was from 32.7-30 mm, indicating that this combination exerted a marked synergistic effect against C. albicans. The inhibition zone of sodium hypochlorite (69.7-65 mm) was higher than the inhibition zone of EthOAc extract and chlorhexidine. The combination of EthOAc extract with sodium hypochlorite resulted in a loss of antifungal activity. Furthermore, the activity of the EthOAc extract against C. albicans was decreased after mixing the extract with dentine at a concentration of 25 mg/50µL (30.3-20.7 mm). The EthOAc extract did not show a genotoxic effect on lymphocyte cells. CONCLUSIONS The EthOAc extract of T. vulgare may be a useful tool to discover natural bioactive agents that have antifungal activity against C. albicans and could be used as endodontic therapies.

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PMID: 

Nutrients. 2019 Dec 18 ;12(1). Epub 2019 Dec 18. PMID: 31861497

Abstract Title: 

Protective Effect ofα-Linolenic Acid on Non-Alcoholic Hepatic Steatosis and Interleukin-6 and -10 in Wistar Rats.

Abstract: 

Consumption of omega-3 (n-3) polyunsaturated fatty acids (PUFA) is related to improvement in the inflammatory response associated with decreases in metabolic disorders of obesity, such as low-grade inflammation and hepatic steatosis. Linseed () oil is a primary source of n-3 fatty acids (FAs) of plant origin, particularlyα-linolenic acid, and provides an alternative for the ingestion of n-3 PUFA by persons allergic to, or wishing to avoid, animal sources. In our study, we evaluated the effect of the consumption of different lipidic sources on metabolic and inflammatory parameters in Wistar rats. We split 56 male rats into four groups that were fed for 60 days with the following diets: sesame oil, (SO,), linseed oil (LO), SO + LO (SLO), and a control group (CG) fed with animal fat. Our results reveal that the use of LO or SLO produced improvements in the hepatic tissue, such as lower values of aspartate aminotransferase, liver weight, and hepatic steatosis. LO and SLO reduced the weight of visceral fats, weight gain, and mediated the inflammation through a decrease in interleukin (IL)-6 and increase in IL-10. Though we did not detect any significant differences in the intestine histology and the purinergic system enzymes, the consumption ofα-linolenic acid appears to contribute to the inflammatory and hepatic modulation of animals compared with a diet rich in saturated FAs and or unbalanced in n-6/n-3 PUFAs, inferring possible use in treatment of metabolic disorders associated with obesity and cardiovascular diseases.

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PMID: 

Food Sci Nutr. 2019 Dec ;7(12):3873-3882. Epub 2019 Nov 19. PMID: 31890165

Abstract Title: 

Alpha-linolenic acid given as an anti-inflammatory agent in a mouse model of colonic inflammation.

Abstract: 

This study examined the relationship between the high-fat, high-sugar diet (HFHSD) and trinitrobenzene sulfonic acid (TNBS) induced mouse colitis, the therapeutic effect of alpha-linolenic acid (ALA) on mouse colitis, and the relationship between HFHSD and hyperlipidemia. We also examined the possible underlying mechanisms behind their interactions. Female BABL/c mice were fed with HFHSD for the 9 weeks. At the same time, ALA treatment (150 or 300 mg/kg) was administered on a daily basis. At the end of the 9 weeks, experimental colitis was induced by the intra-colonic administration of TNBS. Body weight, spleen weight, disease activity index (DAI), histological changes, T-cell-related cytokine level, and lipid profiles were measured after treatment. TNBS induced severe clinical manifestations of colitis and histological damage. Low-ALA (150 mg/kg) administration profoundly ameliorated TNBS-induced clinical manifestations, body weight loss, spleen weight loss, and histological damage. On the contrary, the high-ALA (300 mg/kg) administration did not ameliorate colitis and even exacerbated the symptoms. HFHSD consumption assisted TNBS in changing IL-12, IFN-γ, IL-2, and IL-17A in the liver. As expected, these changes were recovered through low-ALA. In addition, HFHSD had a significant impact on the total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and triglyceride (TG), which related to the increased risk of hyperlipidemia. In summation, HFHSD exacerbated the TNBS-induced colitis via the Th1/Th17 pathway. The Low-ALA (150 mg/kg) exhibited protectiveeffects against the TNBS-induced colitis via the Th1/Th2/Th17 pathway.

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PMID: 

Cell Death Dis. 2020 Feb 3 ;11(2):83. Epub 2020 Feb 3. PMID: 32015327

Abstract Title: 

α-Linolenic acid but not linolenic acid protects against hypertension: critical role of SIRT3 and autophagic flux.

Abstract: 

Although dietaryα-linolenic acid (ALA) or linolenic acid (LA) intake was reported to be epidemiologically associated with a lower prevalence of hypertension, recent clinical trials have yielded conflicting results. Comparable experimental evidence for the roles of these two different fatty acids is still lacking and the underlying mechanisms need to be further elucidated. Our data showed that ALA but not LA supplementation alleviated systolic blood pressure elevation and improved ACh-induced, endothelium-dependent vasodilation in both spontaneously hypertensive rats (SHRs) and AngII-induced hypertensive mice. In addition, SHRs displayed reduced vascular Sirtuin 3 (SIRT3) expression, subsequent superoxide dismutase 2 (SOD2) hyperacetylation and mitochondrial ROS overproduction, all of which were ameliorated by ALA but not LA supplementation. In primary cultured endothelial cells, ALA treatment directlyinhibited SIRT3 reduction, SOD2 hyperacetylation, mitochondrial ROS overproduction and alleviated autophagic flux impairment induced by AngII plus TNFα treatment. However, these beneficial effects of ALA were completely blocked by silencing SIRT3. Restoration of autophagic flux by rapamycin also inhibited mitochondrial ROS overproduction in endothelial cells exposed to AngII plus TNFα. More interestingly, SIRT3 KO mice developed severe hypertension in response to a low dose of AngII infusion, while ALA supplementation lost its anti-hypertensive and endothelium-protective effects on these mice. Our findings suggest that ALA but not LA supplementation improves endothelial dysfunction and diminishes experimental hypertension by rescuing SIRT3 impairment to restore autophagic flux and mitochondrial redox balance in endothelial cells.

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Unsurprisingly, research finds a strong correlation between Big Pharma physician compensation and increased rates of name-brand drug prescriptions