These results suggest that vascular aging can be suppressed by hydrogen-rich water.

PMID: 

Sci Rep. 2018 11 14 ;8(1):16822. Epub 2018 Nov 14. PMID: 30429524

Abstract Title: 

Administration of hydrogen-rich water prevents vascular aging of the aorta in LDL receptor-deficient mice.

Abstract: 

The main cause of arteriosclerosis is atherosclerosis in the aorta. Atherosclerosis is recognized as a chronic inflammatory condition that begins with the dysfunction or activation of arterial endothelium. Low-density lipoprotein (LDL) and especially its oxidized form play a key role in endothelial dysfunction and atherogenesis. Recent studies showed that senescent cells are involved in the development and progression of atherosclerosis, and eliminating senescent cells suppresses the senescence-associated secretory phenotype. We previously reported that molecular hydrogen-rich water (HW) has antioxidant and anti-inflammatory effects in numerous diseases. Here, we used LDL receptor-deficient mice fed a high-fat diet (HFD) for 13 weeks as a model for atherosclerosis and evaluated the effects of continuous administration of HW. The numbers of endothelial cells in the atheroma expressing the senescence factors p16and p21 decreased in HFD-fed mice given HW compared with HFD-fed mice given control water. Furthermore, macrophage infiltration and Tnfα expression in the atheroma were also suppressed. These results suggest that vascular aging can be suppressed by HW.

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Hydrogen water is the therapeutic agent in electrolyzed-alkaline water and attenuates high fat diet-induced nonalcoholic fatty liver disease.

PMID: 

World J Gastroenterol. 2018 Dec 7 ;24(45):5095-5108. PMID: 30568387

Abstract Title: 

Effects of alkaline-electrolyzed and hydrogen-rich water, in a high-fat-diet nonalcoholic fatty liver disease mouse model.

Abstract: 

AIM: To identify the effect of hydrogen-rich water (HRW) and electrolyzed-alkaline water (EAW) on high-fat-induced non-alcoholic fatty acid disease in mice.METHODS: Mice were divided into four groups: (1) Regular diet (RD)/regular water (RW); (2) high-fat diet (HFD)/RW; (3) RD/EAW; and (4) HFD/EAW. Weight and body composition were measured. After twelve weeks, animals were sacrificed, and livers were processed for histology and reverse-transcriptase polymerase chain reaction. A similar experiment was performed using HRW to determine the influence and importance of molecular hydrogen (H) in EAW. Finally, we compared the response of hepatocytes isolated from mice drinking HRW or RW to palmitate overload.RESULTS: EAW had several properties important to the study: (1) pH = 11; (2) oxidation-reduction potential of -495 mV; and (3) H= 0.2 mg/L. However, in contrast to other studies, there were no differences between the groups drinking EAW or RW in either the RD or HFD groups. We hypothesized that the null result was due to low Hconcentrations. Therefore, we evaluated the effects of RW and low and high HRW concentrations (L-HRW = 0.3 mg H/L and H-HRW = 0.8 mg H/L, respectively) in mice fed an HFD. Compared to RW and L-HRW, H-HRW resulted in a lower increase in fat mass (46%61%), an increase in lean body mass (42%28%), and a decrease in hepatic lipid accumulation (

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Effects of the long-term consumption of hydrogen-rich water on the antioxidant activity and the gut flora in female juvenile soccer players.

PMID: 

Med Gas Res. 2018 Oct-Dec;8(4):135-143. Epub 2019 Jan 9. PMID: 30713665

Abstract Title: 

Effects of the long-term consumption of hydrogen-rich water on the antioxidant activity and the gut flora in female juvenile soccer players from Suzhou, China.

Abstract: 

Expending a considerable amount of physical energy inevitably leads to fatigue during both training and competition in football. An increasing number of experimental findings have confirmed the relationship between the generation and clearance of free radicals, fatigue, and exercise injury. Recently, hydrogen was identified as a new selective antioxidant with potential beneficial applications in sports. The present study evaluated the effect of 2-month consumption of hydrogen-rich water on the gut flora in juvenile female soccer players from Suzhou. As demonstrated by enzyme linked immunosorbent assay and 16S rDNA sequence analysis of stool samples, the consumption of hydrogen-rich water for two months significantly reduced serum malondialdehyde, interleukin-1, interleukin-6, tumour necrosis factor-α levels; then significantly increased serum superoxide dismutase, total antioxidant capacity levels and haemoglobin levels of whole blood. Furthermore, the consumption of hydrogen-rich water improved the diversity and abundance of the gut flora in athletes. All examined indices, including the shannon, sobs, ace, and chao indices, were higher in the control group than those proposed to result from hydrogen-rich water consumption prior to the trial, but these indices were all reversed and were higher than those in the controls after the 2-month intervention. Nevertheless, there were some differences in the gut flora components of these two groups before the trial, whereas there were no significant changes in the gut flora composition during the trial period. Thus, the consumption of hydrogen-rich water for two months might play a role modulating in the gut flora of athletes based on itsselective antioxidant and anti-inflammatory activities. The study protocol was approved by the ethics committee of the Suzhou Sports School (approved number: SSS-EC150903).

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Hydrogen-rich water activates the PI3K/Akt pathway, thereby mediates mice astrocytes to exert the biological function of antioxidant.

PMID: 

Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2019 Jun ;31(6):762-767. PMID: 31315738

Abstract Title: 

[Protective effect of hydrogen-rich water on oxidative stress cell model and the impact of the phosphatidylinositol 3 kinase/protein kinase B pathway].

Abstract: 

OBJECTIVE: To explore the protective effect of hydrogen-rich water on the oxidative stress injury of astrocytes in mice and its effect on phosphatidylinositol 3 kinase/protein kinase B (PI3K/Akt) signal pathway.METHODS: In vitro, mice astrocytes were cultured and the logarithmic growth period cells were taken for experiment. (1) Experiment one: some cells were acted by 1.25, 2.50, 5.00, 10.00μmol/L hydrogen peroxide (HO) for 20 minutes to determine the appropriate concentration required for astrocyte damage induced by HO; cultivating 3, 6, 9, and 12 hours with hydrogen-rich water of 25, 50, 100, and 200μmol/L, respectively, to determine the concentration and time of hydrogen-rich water pretreatment; the 50 μmol/L hydrogen-rich water was cultured together with PI3K/Akt signal pathway inhibitors wortmannin (WM) 200 nmol/L or 400 nmol/L to determine the best inhibition concentration of wortmannin.Astrocyte activity was detected by methyl thiazolyl tetrazolium (MTT) colorimetry. (2) Experiment two: some cells were divided into blank control group, HOinjury group, hydrogen-rich water pretreatment group (HW+HOgroup), and co-culture of hydrogen-rich water and wortmannin pretreatment group (HW+WM+HOgroup). The mRNA expressions of PI3K and Akt were detected by reverse transcription-polymerase chain reaction (RT-PCR); the protein expressions of PI3K, Akt and phosphorylated Akt (p-Akt) were detected by Western Blot.RESULTS: (1) Experiment one: the survival rate of the blank control group was 100%. Cell activity gradually decreased with the increase of HOconcentration, and the survival rate of the HOaction 20 minutes cells of 2.50μmol/L was reduced to about 50%, so a cell injury model was established at this concentration. With the increase of hydrogen-rich water pretreatment concentration, and the duration of action, the cell survival rate increased first and then decreased. The cell survival rate was highest when 50 μmol/L hydrogen-rich water was pretreated with 9 hours, so a hydrogen-rich water pre-protection model was established. After 200 nmol/L or 400 nmol/L wortmannin was cultured together with hydrogen-rich water, cell activity was inhibited, and the cell survival rate of 200 nmol/L wortmannin group was no significantly different compared with that of HOinjury group, so the astrocyte suppression model was established. (2) Experiment two: compared with the blank control group, the mRNA expressions of PI3K and Akt and the protein expressions of PI3K, Akt and p-Akt were significantly decreased in the HOinjury group. Compared with the HOinjury group, the PI3K, Akt mRNA expressions and PI3K, Akt, p-Akt protein expressions were significantly increased in the HW+HOgroup [PI3K mRNA (2): 0.843±0.019 vs. 0.631±0.038, Akt mRNA (2): 0.591±0.025 vs. 0.558±0.037, PI3K/β-actin: 1.277±0.008 vs. 0.757±0.004, Akt/β-actin: 1.308±0.015 vs. 0.682±0.006, p-Akt/β-actin: 1.210±0.005 vs. 0.614±0.005, all P

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Hydrogen rich water improved ventilatory, perceptual and lactate responses to exercise.

PMID: 

Int J Sports Med. 2019 Oct 1. Epub 2019 Oct 1. PMID: 31574544

Abstract Title: 

Hydrogen Rich Water Improved Ventilatory, Perceptual and Lactate Responses to Exercise.

Abstract: 

The potential anti-fatigue and performance benefits of hydrogen rich water (HRW) have resulted in increased research interest over the past 5 years. The aim of this study was to assess physiological and perceptual responses to an incremental exercise protocol after administration of 600 ml HRW within 30 min before exercise. This randomized, double blinded placebo-controlled cross over study included twelve healthy males aged 27.1±4.9 years. The exercise protocol consisted of a 10 min warm-up at 1.0 W.kg, followed by 8 min at 2.0, 3.0, and 4.0 W.kg, respectively. Cardio-respiratory variables, lactate and ratings of perceived exertion (RPE) were assessed in the last minute of each step. A significantly lower blood lactate was found with HRW (4.0±1.6 and 8.9±2.2 mmol.l) compared to Placebo (5.1±1.9 and 10.6±3.0 mmol.l) at 3.0, and 4.0 W.kg, respectively. Ventilatory equivalent for oxygen and RPE exhibited significantly lower values with HRW (32.3±7.2, and 17.8±1.2 points, respectively) compared to Placebo (35.0±8.4, and 18.5±0.8 points, respectively) at 4 W.kg. To conclude, acute pre-exercise supplementation with HRW reduced blood lactate at higher exercise intensities, improved exercise-induced perception of effort, and ventilatory efficiency.

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Purging and the body in the therapeutic use of ayahuasca.

PMID: 

Soc Sci Med. 2019 Aug 31 ;239:112532. Epub 2019 Aug 31. PMID: 31494522

Abstract Title: 

Purging and the body in the therapeutic use of ayahuasca.

Abstract: 

Ayahuasca is a psychoactive plant mixture used in ceremonial contexts throughout Western Amazonia. Its use has expanded globally in recent decades and become popular among westerners who travel to the Peruvian Amazon in increasing numbers to experience its reportedly healing effects. Through a review of relevant literature on Amazonian shamanism, combined with the authors' ethnographic data from shamanic tourism contexts of the Peruvian Amazon and neo-shamanic networks in Australia (collected between 2003 and 2015 – with a total of 227 people interviewed or surveyed, including healers and participants), we demonstrate that purging has been integral to the therapeutic use of ayahuasca across and beyond Amazonia. Therapeutic approaches to ayahuasca point to combined modulations of the gut and the mind, and the bodily and the social, that are expressed through discourse about healing and the body. Relating ethnographic evidence to recent scientific studies that connect the gut to emotional health, we do not approach the gut as merely biological ground on which cultural meanings are imposed, but rather as simultaneously physical and cultural. Based upon our analysis, we argue that ayahuasca purging should not be dismissed as a drug side effect or irrational belief but reconsidered for its potential therapeutic effects.

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Ayahuasca’s antidepressant effects covary with behavioural activation as well as mindfulness.

PMID: 

J Psychoactive Drugs. 2019 Sep 30:1-8. Epub 2019 Sep 30. PMID: 31570056

Abstract Title: 

Ayahuasca's Antidepressant Effects Covary with Behavioral Activation as Well as Mindfulness.

Abstract: 

Ayahuasca, a plant-based hallucinogen that serves as a spiritual medicine in South America, has improved depression in at least one placebo-controlled clinical trial. Case studies suggest that dramatic behavioral changes often follow the Ayahuasca ceremony, but most explanations of antidepressant effects focus on changes in mindfulness. This study investigated whether both mindfulness and behavioral activation might contribute to these anti-depressant effects. We surveyed individuals (N = 152) about their changes in depressive symptoms, behavioral activation, and mindfulness after an Ayahuasca experience. Mindfulness was strongly associated with reduced depression severity (= – .670,

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Protective effect of ginsenoside Rg1 on attenuating anti-GBM glomerular nephritis by activating NRF2 signalling.

PMID: 

Artif Cells Nanomed Biotechnol. 2019 Dec ;47(1):2972-2979. PMID: 31322005

Abstract Title: 

Protective effect of ginsenoside Rg1 on attenuating anti-GBM glomerular nephritis by activating NRF2 signalling.

Abstract: 

Ginsenoside Rg1 exerts a beneficial effect in many kidney diseases. But little work has been done to confirm whether ginsenoside Rg1 could also exert a protective effect on anti-glomerular basement membrane (anti-GBM) glomerular nephritis (GN). We aimed to explore the role of ginsenoside Rg1 in attenuating anti-GBM GN in vitro and in vivo and investigate the mechanism under its action.Interleukin-1β (IL-1β) treated podocytes were used as a cell model. A total of 20 mice were used to build the Anti-GBM GN mice model. Real-time PCR analysis (RT-PCR), Western blot analysis and ELISA assay were conducted to detect related indicators in this study. The statistical analysis was performed using GraphPad Prism software 6.0.Ginsenoside Rg1 attenuates IL-1β-induced inflammation and apoptosis in podocytes. NRF2 expression can be inhibited by IL-1β, whereas reversed by ginsenoside Rg1. NRF2 inhibitor ML385 can significantly reverse the effects of ginsenoside Rg1 on inflammation and apoptosis induced by IL-1β, and block the inhibitory effect of ginsenoside Rg1 on IL-1β activated MAPK pathway. In addition, ginsenoside Rg1 could improve anti-GBM GN injury.Ginsenoside Rg1 inhibits the anti-GBM GN damage through regulating NRF2 pathwayand. Our findings provide new insight and mechanism of ginsenoside Rg1 to prevent anti-GBM GN.

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Carvacrol inhibits cadmium toxicity through combating against caspase dependent/independent apoptosis in PC12 cells.

PMID: 

Food Chem Toxicol. 2019 Sep 25:110835. Epub 2019 Sep 25. PMID: 31562949

Abstract Title: 

Carvacrol inhibits cadmium toxicity through combating against caspase dependent/independent apoptosis in PC12 cells.

Abstract: 

Carvacrol is a monoterpenic phenol found in essential oils, is considered a safe food additive, and possesses various therapeutic properties. Numerous studies have also deciphered the protective role of carvacrol on various cytotoxicities. We clarify the effects of carvacrol on cadmium-induced apoptosis in PC12 cells. Carvacrol while co-exposed with cadmium for 48 h raised PC12 cell viability in comparison to only cadmium exposed group. The co-exposure increased the cellular glutathione levels and promoted the expression of glutathione reductase. The magnitude of DNA fragmentation caused by cadmiumwas also ameliorated by carvacrol. Flow cytometry exhibited the apoptosis rate augmented by cadmium was reduced by carvacrol. Western blotting revealed that cadmium and carvacrol co-exposure alleviated the cadmium-induced down-regulations of mammalian target of rapamycin (mTOR), protein kinase B (Akt), nuclear factor kappa-light-chain-enhancer of activated B cells (NFКB), extracellular signal-regulated kinase-1 (ERK-1) and nuclear factor erythroid 2-related factor 2 (Nrf2) expressions. The co-exposure also reversed action of cadmium by suppressing the cleavage of caspase 3 and reducing the cytosolic levels of cytochrome c and apoptosis inducing factor (AIF). Moreover, carvacrol upon co-exposure significantly increased the intracellular metallothionein content. In conclusion, carvacrol strongly reduced cadmium-triggered oxidative stress and caspase-dependent and caspase-independent apoptosis in PC12 cells.

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Carvacrol attenuates diabetic cardiomyopathy.

PMID: 

Front Pharmacol. 2019 ;10:998. Epub 2019 Sep 12. PMID: 31572181

Abstract Title: 

Carvacrol Attenuates Diabetic Cardiomyopathy by Modulating the PI3K/AKT/GLUT4 Pathway in Diabetic Mice.

Abstract: 

Diabetic cardiomyopathy (DCM), a common complication of diabetes mellitus, eventually leads to heart failure. Carvacrol is a food additive with diverse bioactivities. We aimed to study the protective effects and mechanisms of carvacrol in DCM.We used a streptozotocin-induced andmouse model of types 1 and 2 diabetes mellitus (T1DM and T2DM), respectively. Both study groups received daily intraperitoneal injections of carvacrol for 6 weeks. Cardiac remodeling was evaluated by histological analysis. We determined gene expression of cardiac remodeling markers (and) by quantitative real-time PCR and cardiac function by echocardiography. Changes of PI3K/AKT signaling were determined with Western blotting. GLUT4 translocation was evaluated by Western blotting and immunofluorescence staining.Compared with control mice, both T1DM and T2DM mice showed cardiac remodeling and left ventricular dysfunction. Carvacrol significantly reduced blood glucose levels and suppressed cardiac remodeling in mice with T1DM and T2DM. At the end of the treatment period, both T1DM and T2DM mice showed lesser cardiac hypertrophy,andmRNA expressions, and cardiac fibrosis, compared to mice administered only the vehicle. Moreover, carvacrol significantly restored PI3K/AKT signaling, which was impaired in mice with T1DM and T2DM. Carvacrol increased levels of phosphorylated PI3K, PDK1, AKT, and AS160 and inhibited PTEN phosphorylation in mice with T1DM and T2DM. Carvacrol treatment promoted GLUT4 membrane translocation in mice with T1DM and T2DM. Metformin was used as the positive drug control in T2DM mice, and carvacrol showed comparable effects to that of metformin on cardiac remodeling and modulation of signaling pathways.Carvacrol protected against DCM in mice with T1DM and T2DM by restoring PI3K/AKT signaling-mediated GLUT4 membrane translocation and is a potential treatment of DCM.

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