scholarly journals The Role of Acetate in the Antagonization of Oxalate: A Potential Causative Molecule for Heart Disease and Cancer Death

2020 ◽  
Vol 15 (3) ◽  
pp. 1934578X2091369 ◽  
Author(s):  
Shanshan An ◽  
Xiaoxia Li ◽  
Man Tang ◽  
Meng Xing ◽  
Ying Zhang ◽  
...  
Keyword(s):  
Annexin V ◽  
Fluorescein Isothiocyanate ◽  
Underlying Mechanism ◽  
Sodium Oxalate ◽  
Protective Effects ◽  
Anticancer Effects ◽  
Propidium Iodide Staining ◽  
Strong Acids ◽  
Insight Into

Previous reports demonstrated the anticancer effects and the protective effects on cardiovascular diseases of vinegar products. The molecular mechanism underlying these phenomena is not well elucidated. It was proposed that carcinogenesis is triggered by the formation of local strong acids such as HCl. Cancer cells may overproduce weak or moderate organic acids such as oxalate to antagonize strong acids, and calcium oxalate may cause organ failure and death. This study aimed at elucidating the underlying mechanism on the antagonism of apoptosis by acetate on oxalate. Quantitation of cell apoptosis of HEK293T cells in the presence of sodium oxalate and compounds with similar structures to oxalate was conducted by using Annexin V-fluorescein isothiocyanate/propidium iodide staining via flow cytometry. The data indicate that acetate could attenuate the proapoptotic functions of oxalate. This study yields insight into the anticancer and antidisease functions of vinegar products and opens up a new path in the use of weak acetic acid in the prevention and treatment of cancer.

Role of metabolism in K-induced tension changes in guinea pig taenia coli

1965 ◽  
Vol 208 (6) ◽  
pp. 1203-1205 ◽  
Author(s):  
M. Pfaffman ◽  
N. Urakawa ◽  
W. C. Holland
Keyword(s):  
Guinea Pig ◽  
Active Transport ◽  
Underlying Mechanism ◽  
Taenia Coli ◽  
Na Transport ◽  
Phasic Response ◽  
Metabolic Intermediates ◽  
Substrate Removal ◽  
Insight Into

Further insight into the underlying mechanism(s) of the K-induced phasic and tonic contractions of the taenia coli of the guinea pig was obtained by examining the effects of various metabolic intermediates, inhibitors of metabolism and active transport, on these responses. Evidence is presented to support the thesis that the tonic response is dependent on the aerobic breakdown of carbohydrates and is abolished by substrate removal, a decrease of temperature, DNP, lithium, and ouabain. These same factors have little or no effect on the phasic response. From the evidence presented, it is concluded that the phasic response is a passive process, whereas the tonic contracture is an active one depending on metabolism and possibly linked to active Na transport.

scholarly journals Sildenafil (Viagra) Protective Effects on Neuroinflammation: The Role of iNOS/NO System in an Inflammatory Demyelination Model

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Catarina Raposo ◽  
Ana Karolina de Santana Nunes ◽  
Rayana Leal de Almeida Luna ◽  
Shyrlene Meiry da Rocha Araújo ◽  
Maria Alice da Cruz-Höfling ◽  
...  
Keyword(s):  
Neuroprotective Effect ◽  
Underlying Mechanism ◽  
Protective Effects ◽  
Wild Type ◽  
Glutathione S Transferase ◽  
Cox 2 ◽  
Inflammatory Regulation ◽  
Inos Inhibition ◽  
Inflammatory Effect

We recently demonstrated that sildenafil reduces the expression of cytokines, COX-2, and GFAP in a demyelinating model induced in wild-type (WT) mice. Herein, the understandings of the neuroprotective effect of sildenafil and the mediation of iNOS/NO system on inflammatory demyelination induced by cuprizone were investigated. The cerebella of iNOS−/−mice were examined after four weeks of treatment with cuprizone alone or combined with sildenafil. Cuprizone increased GFAP, Iba-1, TNF-α, COX-2, IL-1β, and IFN-γexpression, decreased expression of glutathione S-transferase pi (GSTpi), and damaged myelin in iNOS−/−mice. Sildenafil reduced Iba-1, IFN-γ, and IL-1βlevels but had no effect on the expression of GFAP, TNF-α, and COX-2 compared to the cuprizone group. Sildenafil elevated GSTpi levels and improved the myelin structure/ultrastructure. iNOS−/−mice suffered from severe inflammation following treatment with cuprizone, while WT mice had milder inflammation, as found in the previous study. It is possible that inflammatory regulation through iNOS-feedback is absent in iNOS−/−mice, making them more susceptible to inflammation. Sildenafil has at least a partial anti-inflammatory effect through iNOS inhibition, as its effect on iNOS−/−mice was limited. Further studies are required to explain the underlying mechanism of the sildenafil effects.

scholarly journals miR-135b Plays a Neuroprotective Role by Targeting GSK3β in MPP+-Intoxicated SH-SY5Y Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Jianlei Zhang ◽  
Wei Liu ◽  
Yabo Wang ◽  
Shengnan Zhao ◽  
Na Chang
Keyword(s):  
Cell Proliferation ◽  
Glycogen Synthase ◽  
Underlying Mechanism ◽  
Protective Role ◽  
Luciferase Reporter ◽  
Dependent Manner ◽  
Protective Effects ◽  
Inflammatory Cytokine Production ◽  
Protein Levels

miR-135a-5p was reported to play a crucial role in the protective effects of hydrogen sulfide against Parkinson’s disease (PD) by targeting rho-associated protein kinase 2 (ROCK2). However, the role of another member of miR-135 family (miR-135b) and the underlying mechanism in PD are still unclear. qRT-PCR and western blot showed that miR-135 was downregulated and glycogen synthase kinase 3β (GSK3β) was upregulated at mRNA and protein levels in MPP+-intoxicated SH-SY5Y cells in a dose- and time-dependent manner. MTT, TUNEL, and ELISA assays revealed that miR-135b overexpression significantly promoted cell proliferation and inhibited apoptosis and production of TNF-α and IL-1β in SH-SY5Y cells in the presence of MPP+. Luciferase reporter assay demonstrated that GSK3β was a direct target of miR-135b. Moreover, sodium nitroprusside (SNP), a GSK3β activator, dramatically reversed the effects of miR-135b upregulation on cell proliferation, apoptosis, and inflammatory cytokine production in MPP+-intoxicated SH-SY5Y cells. Taken together, miR-135b exerts a protective role via promotion of proliferation and suppression of apoptosis and neuroinflammation by targeting GSK3β in MPP+-intoxicated SH-SY5Y cells, providing a potential therapeutic target for the treatment of PD.

scholarly journals Bifidobacterium infantis Metabolizes 2′Fucosyllactose-Derived and Free Fucose Through a Common Catabolic Pathway Resulting in 1,2-Propanediol Secretion

2020 ◽  
Vol 7 ◽  
Author(s):  
Liv R. Dedon ◽  
Ezgi Özcan ◽  
Asha Rani ◽  
David A. Sela
Keyword(s):  
Gut Microbiome ◽  
Bifidobacterium Longum ◽  
Underlying Mechanism ◽  
Catabolic Pathway ◽  
Oligosaccharide Structure ◽  
Infant Gut Microbiome ◽  
Microbe Interactions ◽  
The Impact ◽  
Insight Into

Human milk oligosaccharides (HMOs) enrich beneficial bifidobacteria in the infant gut microbiome which produce molecules that impact development and physiology. 2′fucosyllactose (2′FL) is a highly abundant fucosylated HMO which is utilized by Bifidobacterium longum subsp. infantis, despite limited scientific understanding of the underlying mechanism. Moreover, there is not a current consensus on whether free fucose could be metabolized when not incorporated in a larger oligosaccharide structure. Based on metabolic and genomic analyses, we hypothesize that B. infantis catabolizes both free fucose and fucosyl oligosaccharide residues to produce 1,2-propanediol (1,2-PD). Accordingly, systems-level approaches including transcriptomics and proteomics support this metabolic path. Co-fermentation of fucose and limiting lactose or glucose was found to promote significantly higher biomass and 1,2-PD concentrations than individual substrates, suggesting a synergistic effect. In addition, and during growth on 2′FL, B. infantis achieves significantly higher biomass corresponding to increased 1,2-PD. These findings support a singular fucose catabolic pathway in B. infantis that is active on both free and HMO-derived fucose and intimately linked with central metabolism. The impact of fucose and 2′FL metabolism on B. infantis physiology provides insight into the role of fucosylated HMOs in influencing host- and microbe-microbe interactions within the infant gut microbiome.

Influence of simulated ischemia on apoptosis induction by oxidative stress in adult cardiomyocytes of rats

2000 ◽  
Vol 278 (1) ◽  
pp. H94-H99 ◽  
Author(s):  
J. Inserte ◽  
G. Taimor ◽  
B. Hofstaetter ◽  
D. Garcia-Dorado ◽  
H. M. Piper
Keyword(s):  
Oxidative Stress ◽  
Ischemia Reperfusion ◽  
Annexin V ◽  
Fluorescein Isothiocyanate ◽  
Adult Rats ◽  
Partial Protection ◽  
Adult Cardiomyocytes ◽  
Propidium Iodide Staining ◽  
Induction Of Apoptosis ◽  
Induced Apoptosis

Oxidative stress may cause apoptosis of cardiomyocytes in ischemic-reperfused myocardium. We investigated whether ischemia-reperfusion modifies the susceptibility of cardiomyocyte induction of apoptosis by oxidative stress. Ischemia was simulated by incubating isolated cardiomyocytes from adult rats in an anoxic, glucose-free medium, pH 6.4, for 3 h. Annexin V-fluorescein isothiocyanate/propidium iodide staining and the detection of DNA laddering were used as apoptotic markers. H2O2(7.5 μmol/l) induced apoptosis in 20.1 ± 1.8% of cells under normoxic conditions but only 14.4 ± 1.6% ( n = 6, P < 0.05) after ischemia-reoxygenation. This partial protection of ischemic-reoxygenated cells was observed despite a reduction in their cellular glutathione content, from 11.4 ± 1.9 in normoxic controls to 2.9 ± 0.8 nmol/mg protein ( n = 3, P < 0.05). Elevation of end-ischemic glutathione contents by pretreatment with 1 mmol/l N-acetylcysteine entirely protected ischemic-reoxygenated cells against induction of apoptosis by H2O2. In conclusion, ischemia-reperfusion can protect cardiomyocytes against induction of apoptosis by exogenous oxidative stress. This endogenous protective effect is most clearly demonstrated when control and postischemic cardiomyocytes are compared at similar glutathione levels.

scholarly journals Irisin alleviates obesity-related spermatogenesis dysfunction via the regulation of the AMPKα signalling pathway

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Yang Mu ◽  
Huang-Guan Dai ◽  
Ling-Bo Luo ◽  
Jing Yang
Keyword(s):  
Oxidative Stress ◽  
Sperm Count ◽  
Underlying Mechanism ◽  
Signalling Pathway ◽  
Protective Effects ◽  
Exercise Induced ◽  
Amp Activated Protein Kinase

Abstract Background Infertility is a common complication in obese men. Oxidative stress and testicular apoptosis play critical roles in obesity-induced spermatogenesis dysfunction. It has been reported that irisin, an exercise-induced myokine, may attenuate oxidative damage and testicular apoptosis in several diseases; however, its role in obesity-induced spermatogenesis dysfunction remains unclear. The purpose of this study was to investigate the role and underlying mechanism of irisin in obesity-induced dysfunction of spermatogenesis. Methods Male mice were fed a high-fat diet (HFD) for 24 weeks to establish a model of obesity-induced spermatogenesis dysfunction. To explore the effects of irisin, mice were subcutaneously infused with recombinant irisin for 8 weeks beginning at 16 weeks after starting a HFD. To confirm the role of AMP-activated protein kinase α (AMPKα), AMPKα-deficient mice were used. Results The data showed decreased serum irisin levels in obese patients, which was negatively correlated with sperm count and progressive motility. Irisin was downregulated in the plasma and testes of obese mice. Supplementation with irisin protected against HFD-induced spermatogenesis dysfunction and increased testosterone levels in mice. HFD-induced oxidative stress, endoplasmic reticulum (ER) stress and testicular apoptosis were largely attenuated by irisin treatment. Mechanistically, we identified that irisin activated the AMPKα signalling pathway. With AMPKα depletion, we found that the protective effects of irisin on spermatogenesis dysfunction were abolished in vivo and in vitro. Conclusions In conclusion, we found that irisin alleviated obesity-related spermatogenesis dysfunction via activation of the AMPKα signalling pathway. Based on these findings, we hypothesized that irisin is a potential therapeutic agent against obesity-related spermatogenesis dysfunction.

scholarly journals MiR-22 Inhibition Alleviates Cardiac Dysfunction in Doxorubicin-Induced Cardiomyopathy by Targeting the sirt1/PGC-1α Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Runze Wang ◽  
Yuerong Xu ◽  
Xiaolin Niu ◽  
Yexian Fang ◽  
Dong Guo ◽  
...  
Keyword(s):  
Cardiac Dysfunction ◽  
Poor Prognosis ◽  
Cardiac Fibrosis ◽  
Underlying Mechanism ◽  
Protective Effects ◽  
Loss Of Function ◽  
Life Threatening

Doxorubicin (DOX) cardiotoxicity is a life-threatening side effect that leads to a poor prognosis in patients receiving chemotherapy. We investigated the role of miR-22 in doxorubicin-induced cardiomyopathy and the underlying mechanism in vivo and in vitro. Specifically, we designed loss-of-function and gain-of-function experiments to identify the role of miR-22 in doxorubicin-induced cardiomyopathy. Our data suggested that inhibiting miR-22 alleviated cardiac fibrosis and cardiac dysfunction induced by doxorubicin. In addition, inhibiting miR-22 mitigated mitochondrial dysfunction through the sirt1/PGC-1α pathway. Knocking out miR-22 enhanced mitochondrial biogenesis, as evidenced by increased PGC-1α, TFAM, and NRF-1 expression in vivo. Furthermore, knocking out miR-22 rescued mitophagy, which was confirmed by increased expression of PINK1 and parkin and by the colocalization of LC3 and mitochondria. These protective effects were abolished by overexpressing miR-22. In conclusion, miR-22 may represent a new target to alleviate cardiac dysfunction in doxorubicin-induced cardiomyopathy and improve prognosis in patients receiving chemotherapy.

scholarly journals Solving the Puzzle: What Is the Role of Progestogens in Neovascularization?

Biomolecules ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 1686
Author(s):  
Zhi Xia ◽  
Jian Xiao ◽  
Qiong Chen
Keyword(s):  
Progesterone Receptor ◽  
Sex Steroids ◽  
Underlying Mechanism ◽  
Physiological Changes ◽  
Exact Role ◽  
The Past ◽  
Naturally Occurring ◽  
Pathological Conditions ◽  
Insight Into

Ovarian sex steroids can modulate new vessel formation and development, and the clarification of the underlying mechanism will provide insight into neovascularization-related physiological changes and pathological conditions. Unlike estrogen, which mainly promotes neovascularization through activating classic post-receptor signaling pathways, progesterone (P4) regulates a variety of downstream factors with angiogenic or antiangiogenic effects, exerting various influences on neovascularization. Furthermore, diverse progestins, the synthetic progesterone receptor (PR) agonists structurally related to P4, have been used in numerous studies, which could contribute to unequal actions. As a result, there have been many conflicting observations in the past, making it difficult for researchers to define the exact role of progestogens (PR agonists including naturally occurring P4 and synthetic progestins). This review summarizes available evidence for progestogen-mediated neovascularization under physiological and pathological circumstances, and attempts to elaborate their functional characteristics and regulatory patterns from a comprehensive perspective.

Role of Salicylic Acid in Heavy Metal Stress Tolerance: Insight into Underlying Mechanism

2017 ◽  
pp. 123-144 ◽  
Author(s):  
Sukhmeen Kaur Kohli ◽  
Neha Handa ◽  
Ravdeep Kaur ◽  
Vinod Kumar ◽  
Kanika Khanna ◽  
...  
Keyword(s):  
Heavy Metal ◽  
Salicylic Acid ◽  
Stress Tolerance ◽  
Heavy Metal Stress ◽  
Underlying Mechanism ◽  
Metal Stress ◽  
Insight Into

scholarly journals In-store interactive advertising screens: the effect of interactivity on impulse buying explained by self-agency

2021 ◽  
Vol ahead-of-print (ahead-of-print) ◽  
Author(s):  
Anne Moes ◽  
Marieke Fransen ◽  
Bob Fennis ◽  
Tibert Verhagen ◽  
Harry van Vliet
Keyword(s):  
Field Experiments ◽  
Underlying Mechanism ◽  
Impulse Buying ◽  
Content Type ◽  
Mediating Role ◽  
Interactive Advertising ◽  
Impulse Purchases ◽  
Mediating Factor ◽  
Insight Into

PurposePhysical stores are increasingly dependent on impulse visits and the impulse purchases of passers-by. Interactive advertising screens in store windows could help retailers increase impulse-visit urges and impulse-buying urges. However, the effects of interactive screens in physical surroundings have not been studied before. Therefore, this study aimed to examine the effect of interactive screens on impulse urges and gain insight into the underlying mechanism that explains the possible effect.Design/methodology/approachAn interactive screen was placed in a store window. Using three field experiments, we studied the effect of interactivity-level (high vs low) on the impulse-visit and impulse-buying urges of passers-by, and the mediating role of self-agency in these effects.FindingsHighly interactive (compared to less interactive) advertising screens in store windows positively affect impulse-visit and impulse-buying urges through self-agency. Retailers can therefore use interactive advertising screens to increase the number of impulse purchases if feelings of self-agency are activated.Originality/valueThis is the first study to examine the extent to which interactive screens in a store window enhance the impulse-visit and impulse-buying urges of passers-by and the mediating factor of these effects. By conducting three field experiments, we achieved a high external validity and managed to share very reliable results owing to the replication of the findings.

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