Aloe vera and its components inhibit influenza a virus-induced autophagy and replication.

PMID: 

Am J Chin Med. 2019 ;47(6):1307-1324. Epub 2019 Sep 10. PMID: 31505936

Abstract Title: 

and its Components Inhibit Influenza A Virus-Induced Autophagy and Replication.

Abstract: 

ethanol extract (AVE) reportedly has significant anti-influenza virus activity, but its underlying mechanisms of action and constituents have not yet been completely elucidated. Previously, we have confirmed that AVE treatment significantly reduces the viral replication of green fluorescent protein-labeled influenza A virus in Madin-Darby canine kidney (MDCK) cells. In addition, post-treatment with AVE inhibited viral matrix protein 1 (M1), matrix protein 2 (M2), and hemagglutinin (HA) mRNA synthesis and viral protein (M1, M2, and HA) expressions. In this study, we demonstrated that AVE inhibited autophagy induced by influenza A virus in MDCK cells and also identified quercetin, catechin hydrate, and kaempferol as the active antiviral components of AVE. We also found that post-treatment with quercetin, catechin hydrate, and kaempferol markedly inhibited M2 viral mRNA synthesis and M2 protein expression. A docking simulation suggested that the binding affinity of quercetin, catechin hydrate, and kaempferol for the M2 protein may be higher than that of known M2 protein inhibitors. Thus, the inhibition of autophagy induced by influenza virus may explain the antiviral activity of AVE against H1N1 or H3N2.extract and its constituents may, therefore, be potentially useful for the development of anti-influenza agents.

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This meta-analysis suggests that pycnogenol may have a role in preventing cardiometabolic disease.

PMID: 

Pharmacol Res. 2019 Oct 1:104472. Epub 2019 Oct 1. PMID: 31585179

Abstract Title: 

Effects of Pycnogenol on Cardiometabolic Health: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.

Abstract: 

AIM: Clinical trials on the effect of pycnogenol supplementation on cardiometabolic health have been controversial. We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) to evaluate the potential effect of pycnogenol supplementation on cardiometabolic profile.METHODS: PubMed, Scopus, and ISI Web of Science databases were searched until October 2018. RCTs that evaluated the effects of pycnogenol on cardiometabolic parameters were included. DerSimonian and Laird random-effect models were used to compute the weighted mean differences (WMDs) and 95% confidence intervals (CIs).RESULTS: Twenty-four RCTs including 1594 participants were included in the meta-analysis. Pycnogenol significantly reduced fasting blood glucose (WMD: -5.86 mg/dl; 95% CI: -9.56, -2.15), glycated hemoglobin (WMD = -0.29%, 95%CI: -0.56, -0.01), systolic blood pressure (WMD: -2.54 mmhg; 95% CI: -4.08, -0.99), diastolic blood pressure (WMD: -1.76 mmhg; 95% CI: -3.12, -0.41), body mass index (WMD: -0.47 kg/m; 95% CI: -0.90, -0.03), LDL cholesterol (WMD: -7.12 mg/dl; 95% CI: -13.66, -0.58) and increased HDL cholesterol (WMD: 3.27 mg/dl; 95% CI: 0.87, 5.66).CONCLUSION: This meta-analysis suggests that pycnogenol may have a role in preventing cardiometabolic disease. However, further well-designed RCTs are recommended to evaluate its long-term effects and explore the optimal duration of use and dosage.

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Chronic venous insufficiency and venous microangiopathy: management with compression and pycnogenol.

PMID: 

Minerva Cardioangiol. 2019 Aug ;67(4):280-287. PMID: 31347820

Abstract Title: 

Chronic venous insufficiency and venous microangiopathy: management with compression and Pycnogenol®.

Abstract: 

BACKGROUND: The aim of this prospective supplement summer registry study was to evaluate the efficacy of Pycnogenol® in controlling symptoms of chronic venous insufficiency (CVI) and microcirculatory parameters: venous hypertension and microangiopathy. Pycnogenol® (Horphag Research) is the standardized extract of the bark of Pinus Pinaster.METHODS: During the summer period between June and August 142 patients were split into three groups: 1) Pycnogenol® 150 mg/day; 2) compression stockings; 3) and compression + Pycnogenol®.RESULTS: Venous pressure (ambulatory venous pressure, AVP) and refilling time (RT), microcirculatory and clinical measurements were comparable at inclusion. At 8 weeks variations in skin flux (RF), rate of ankle swelling (RAS), skin PO2-PCO2, Analogue Symptomatic Score (ASLS), Venous Disability and severity Scores and local oxidative stress (OS) indicated a statistically significant improvement by Pycnogenol® both as a single supplement and in association with compression in comparison with baseline. Pycnogenol® significantly improved the microcirculation in comparison with compression (P

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Protective effects of triple fermented barley extract on indomethacin-induced gastric mucosal damage in rats.

PMID: 

BMC Complement Altern Med. 2019 Feb 20 ;19(1):49. Epub 2019 Feb 20. PMID: 30786935

Abstract Title: 

Protective effects of triple fermented barley extract (FBe) on indomethacin-induced gastric mucosal damage in rats.

Abstract: 

BACKGROUND: Hordeum vulgare L (barley) contains numerous phenolic substances with proven anticancer, antioxidant and gastroprotective activities. Saccharification increases the functionality and bioavailability of these compounds thus can aid in the development of a natural product based medicine. This study aimed to investigate the possible gastroprotective effects of saccharification on the indomethacin (IND)-induced gastric ulcers in rats using Weissella cibaria- and Saccharomyces cerevisiae-triple fermented H. vulgare extract (FBe).METHODS: In total, 60 healthy male 6-week old Sprague-Dawley SD (SPF/VAF Outbred CrljOri:CD1) rats were commercially purchased. The FBe extract (100, 200, and 300 mg kg) was orally administered 30 min before an oral treatment of IND (25 mg kg). Six hours after IND treatment, variations in the histopathology, myeloperoxidase (MPO) activity, gross lesion scores, lipid peroxidation, and antioxidant defense system component (superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH)) levels were measured.RESULTS: FBe treatment showed significant (p 

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Injection of blood derived from rats chronically exposed to radiofrequency radiation at 500 microW/cm2 into healthy, unexposed pregnant rats resulted in pregnancy abnormalities.

PMID: 

Radiats Biol Radioecol. 2010 Jan-Feb;50(1):28-36. PMID: 20297678

Abstract Title: 

Impact of the blood serum from rats exposed to low-level electromagnetic fields on pregnancy, foetus and offspring development of intact female rats].

Abstract: 

This study evaluated possible adverse effects of injection of blood serum from rats exposed to microwaves at a power density of 500 microW/cm2 on pregnancy and foetal and offspring development in intact female rats. The study was performed with 59 pregnant Wistar rats. In utero mortality, embryo and foetal body weights and placenta weight were used for the evaluation of embryo and foetal development. Generally accepted integral and specific parameters were used for the evaluation of postnatal development of offspring during the first 30 days of life. It was shown that intra peritoneal injection of blood serum from IMF exposed rats (chronic 30-day RF exposure at 500 microW/cm2) to intact rats on the 10th day of pregnancy resulted in adverse effects on foetal and offspring development. Total mortality (in utero + postnatal) as well as delay in offspring development was higher in this group.

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Barley sprout extract protected the liver cells from oxidative stress by activating Nrf2 and increasing glutathione synthesis.

PMID: 

Nutrients. 2017 Nov 16 ;9(11). Epub 2017 Nov 16. PMID: 29144408

Abstract Title: 

Antioxidant Effect of Barley Sprout Extract via Enhancement of Nuclear Factor-Erythroid 2 Related Factor 2 Activity and Glutathione Synthesis.

Abstract: 

We previously showed that barley sprout extract (BSE) prevents chronic alcohol intake-induced liver injury in mice. BSE notably inhibited glutathione (GSH) depletion and increased inflammatory responses, revealing its mechanism of preventing alcohol-induced liver injury. In the present study we investigated whether the antioxidant effect of BSE involves enhancing nuclear factor-erythroid 2 related factor 2 (Nrf2) activity and GSH synthesis to inhibit alcohol-induced oxidative liver injury. Mice fed alcohol for four weeks exhibited significantly increased oxidative stress, evidenced by increased malondialdehyde (MDA) level and 4-hydroxynonenal (4-HNE) immunostaining in the liver, whereas treatment with BSE (100 mg/kg) prevented these effects. Similarly, exposure to BSE (0.1-1 mg/mL) significantly reduced oxidative cell death induced by-butyl hydroperoxide (-BHP, 300μM) and stabilized the mitochondrial membrane potential (∆ψ). BSE dose-dependently increased the activity of Nrf2, a potential transcriptional regulator of antioxidant genes, in HepG2 cells. Therefore, increased expression of its target genes, heme oxygenase-1 (HO-1), NADPH quinone oxidoreductase 1 (NQO1), and glutamate-cysteine ligase catalytic subunit (GCLC) was observed. Since GCLC is involved in the rate-limiting step of GSH synthesis, BSE increased the GSH level and decreased both cysteine dioxygenase (CDO) expression and taurine level. Because cysteine is a substrate for both taurineand GSH synthesis, a decrease in CDO expression would further contribute to increased cysteine availability for GSH synthesis. In conclusion, BSE protected the liver cells from oxidative stress by activating Nrf2 and increasing GSH synthesis.

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Microwave radiation can increase the expression of aquaporin 4 in the rat hippocampus.

PMID: 

Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2009 Sep ;27(9):534-8. PMID: 20137298

Abstract Title: 

[A aquaporin 4 expression and effects in rat hippocampus after microwave radiation].

Abstract: 

OBJECTIVE: To investigate the expression of aquaporin 4 (AQP4) after microwave exposure and the correlation with the brain injury by radiation.METHODS: 70 male rats were exposed to microwave whose average power density was 0, 10, 30 and 100 mW/cm(2) respectively. Rats were sacrificed at 6 h, 1 d, 3 d and 7 d after exposure. Immunohistochemistry and Western blot were used to detect the expression of AQP4 in protein level in rat hippocampus, and the expression of AQP4 in gene level was measured by in situ hybridization and RT-PCR.RESULTS: The expression of AQP4 in rat hippocampus was abnormal after 10, 30, 100 mW/cm(2) microwave exposure. The protein level showed increased at first and then recovered at 10 and 30 mW/cm(2) groups, while increased progressively in 100 mW/cm(2) group within 14 d (P

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Microwave exposure at a rate of 1mW/cm2 increased levels of plasma corticosterone, glucocorticoid receptor nuclear translocation, and apoptosis in the rat hippocampus.

PMID: 

J Radiat Res. 2008 Mar ;49(2):163-70. Epub 2008 Jan 16. PMID: 18198477

Abstract Title: 

Elevation of plasma corticosterone levels and hippocampal glucocorticoid receptor translocation in rats: a potential mechanism for cognition impairment following chronic low-power-density microwave exposure.

Abstract: 

The goal of this study was to investigate whether glucocorticoids (GCs) take part in cognition impairment after exposure to chronic low-power-density microwave (MW) fields. We exposed Wistar rats to a 2.45-GHz pulsed MW field at an average power density of 1 mW/cm(2) for 3 h daily, for up to 30 days. Our results show that MW-exposed rats had significant deficits in spatial learning and memory performance. MW exposure increased levels of plasma corticosterone, and consequently GC receptor (GR) nuclear translocation and apoptosis in the hippocampus. However, co-administration of the GR antagonist RU486 with MW exposure partially reversed the cognitive impairment and neuronal loss. These data indicate that GCs might contribute to the cognition deficit induced by chronic low-power-density MW exposure.

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Significant alterations in arterial blood pressure were observed in rats exposed to electromagnetic pulses while heart rate was not altered.

PMID: 

Int J Radiat Biol. 2007 Jun ;83(6):421-9. PMID: 17487681

Abstract Title: 

Electromagnetic pulses induce fluctuations in blood pressure in rats.

Abstract: 

PURPOSE: To investigate the effects of exposure to electromagnetic pulses (EMP) on functional indices of the cardiovascular system in male Sprague-Dawley rats.MATERIALS AND METHODS: A tapered parallel plate Gigahertz Transverse Electromagnetic cell (GTEM cell) with a flared rectangular coaxial transmission line was used to expose the rats to EMP (0.5 pps, total 200 pulses and whole-body averaged specific absorption rate 50 mW/kg at 200 kV/m or 75 mW/kg at 400 kV/m). Concurrent sham-exposed animals were used as controls. Cardiovascular functions, namely, heart rate, and systolic, mean and diastolic blood pressures were measured immediately and up to 4 weeks post-exposure using a non-invasive tail-cuff photoelectric sensor sphygmomanometer.RESULTS: The heart rates in sham- and EMP-exposed rats were not significantly changed. In the exposed rats, increased systolic blood pressure (SBP) occurred at 0 h and decreased SBP occurred at 1 day and 3 days after exposure. Significantly higher diastolic blood pressure (DBP) was found at 0 h and significantly lower DBP was found at 12 h, 1 day, and 1 month after exposure. Significantly higher mean arterial pressure (MAP) was noted at 0 h and significantly lower MAP was noted at 1 day.CONCLUSIONS: Significant alterations in arterial blood pressure were observed in rats exposed to EMP exposure while heart rate was not altered.

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Ultra high frequency electromagnetic field induce changes in rat neuronal cells.

PMID: 

Med Tr Prom Ekol. 2000(5):5-8. PMID: 10881537

Abstract Title: 

[Changes of neurocytes in CNS under general exposure to UHF field with local protection applied].

Abstract: 

Experiments on white rats were performed to study influence of UHF field on cortical sensomotor area under general exposure or with the head shielded. The changes in CNS caused by UHF field were not prevented completely by means of the shield. That is probably due to pathologic reflex impulses from the body receptors.

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