In vitro Antifungal Activity and Mechanism of Action of Tea Polyphenols and Tea Saponin against Rhizopus stolonifer

2015 ◽  
Vol 25 (4) ◽  
pp. 269-276 ◽  
Author(s):  
Xiaodong Jiang ◽  
Kejue Feng ◽  
Xiaoping Yang
Keyword(s):  
Cell Membrane ◽  
Oxidative Damage ◽  
Mechanism Of Action ◽  
Soluble Sugar ◽  
Tea Polyphenols ◽  
Cell Membrane Permeability ◽  
Dependent Manner ◽  
Rhizopus Stolonifer ◽  
Tea Saponin

The in vitro antifungal activities and mechanism of action of tea polyphenols (TP), tea saponin (TS) and their combination were evaluated against <i>Rhizopus stolonifer</i>. The results showed that both TP and TS inhibited the mycelial growth in a dose-dependent manner, and their combination at the ratio of 7:3 exhibited synergistic antifungal interaction. We also observed that the treatment of TP or TS significantly induced the production of H<sub>2</sub>O<sub>2</sub> and resulted in membrane lipid peroxidation, thus leading to an increase in cell membrane permeability and the leakage of K<sup>+</sup>, soluble protein and soluble sugar. Moreover, combining them for treatment increased the induction of H<sub>2</sub>O<sub>2</sub> production and oxidative damage. Scanning electron microscopic observations also showed the damage to the hyphal cell structure. It was concluded that TP, TS and their combination inhibit the growth of <i>R. stolonifer</i> through the induction of H<sub>2</sub>O<sub>2</sub> production, leading to cell membrane oxidative damage and intracellular constituent leakage. These findings suggest that TP and TS can potentially be used as an alternative to control postharvest fruit diseases caused by <i>R. stolonifer.</i>

scholarly journals Mn Inhibits GSH Synthesis via Downregulation of Neuronal EAAC1 and Astrocytic xCT to Cause Oxidative Damage in the Striatum of Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-15 ◽  
Author(s):  
Xinxin Yang ◽  
Haibo Yang ◽  
Fengdi Wu ◽  
Zhipeng Qi ◽  
Jiashuo Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Dependent Manner ◽  
Protein Levels ◽  
Key Factor ◽  
Protein Sulfhydryl ◽  
Mrna And Protein Expression ◽  
The Brain

Excessive manganese (Mn) can accumulate in the striatum of the brain following overexposure. Oxidative stress is a well-recognized mechanism in Mn-induced neurotoxicity. It has been proven that glutathione (GSH) depletion is a key factor in oxidative damage during Mn exposure. However, no study has focused on the dysfunction of GSH synthesis-induced oxidative stress in the brain during Mn exposure. The objective of the present study was to explore the mechanism of Mn disruption of GSH synthesis via EAAC1 and xCT in vitro and in vivo. Primary neurons and astrocytes were cultured and treated with different doses of Mn to observe the state of cells and levels of GSH and reactive oxygen species (ROS) and measure mRNA and protein expression of EAAC1 and xCT. Mice were randomly divided into seven groups, which received saline, 12.5, 25, and 50 mg/kg MnCl2, 500 mg/kg AAH (EAAC1 inhibitor) + 50 mg/kg MnCl2, 75 mg/kg SSZ (xCT inhibitor) + 50 mg/kg MnCl2, and 100 mg/kg NAC (GSH rescuer) + 50 mg/kg MnCl2 once daily for two weeks. Then, levels of EAAC1, xCT, ROS, GSH, malondialdehyde (MDA), protein sulfhydryl, carbonyl, 8-hydroxy-2-deoxyguanosine (8-OHdG), and morphological and ultrastructural features in the striatum of mice were measured. Mn reduced protein levels, mRNA expression, and immunofluorescence intensity of EAAC1 and xCT. Mn also decreased the level of GSH, sulfhydryl, and increased ROS, MDA, 8-OHdG, and carbonyl in a dose-dependent manner. Injury-related pathological and ultrastructure changes in the striatum of mice were significantly present. In conclusion, excessive exposure to Mn disrupts GSH synthesis through inhibition of EAAC1 and xCT to trigger oxidative damage in the striatum.

Inhibitory activity of isoniazid and ethionamide against Cryptococcus biofilms

2015 ◽  
Vol 61 (11) ◽  
pp. 827-836 ◽  
Author(s):  
Rossana de Aguiar Cordeiro ◽  
Rosana Serpa ◽  
Francisca Jakelyne de Farias Marques ◽  
Charlline Vládia Silva de Melo ◽  
Antonio José de Jesus Evangelista ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Biofilm Formation ◽  
Inhibitory Effect ◽  
Cell Membrane Permeability ◽  
Planktonic Cells ◽  
Fungal Cell ◽  
Antituberculosis Drugs ◽  
Opportunistic Mycoses ◽  
Cryptococcus Spp

In recent years, the search for drugs to treat systemic and opportunistic mycoses has attracted great interest from the scientific community. This study evaluated the in vitro inhibitory effect of the antituberculosis drugs isoniazid and ethionamide alone and combined with itraconazole and fluconazole against biofilms of Cryptococcus neoformans and Cryptococcus gattii. Antimicrobials were tested at defined concentrations after susceptibility assays with Cryptococcus planktonic cells. In addition, we investigated the synergistic interaction of antituberculosis drugs and azole derivatives against Cryptococcus planktonic cells, as well as the influence of isoniazid and ethionamide on ergosterol content and cell membrane permeability. Isoniazid and ethionamide inhibited both biofilm formation and viability of mature biofilms. Combinations formed by antituberculosis drugs and azoles proved synergic against both planktonic and sessile cells, showing an ability to reduce Cryptococcus biofilms by approximately 50%. Furthermore, isoniazid and ethionamide reduced the content of ergosterol in Cryptococcus spp. planktonic cells and destabilized or permeabilized the fungal cell membrane, leading to leakage of macromolecules. Owing to the paucity of drugs able to inhibit Cryptococcus biofilms, we believe that the results presented here might be of interest in the designing of new antifungal compounds.

scholarly journals The Effects of Taurine on Permethrininduced Cytogenetic and Oxidative Damage in Cultured Human Lymphocytes

2012 ◽  
Vol 63 (1) ◽  
pp. 27-34 ◽  
Author(s):  
Hasan Turkez ◽  
Elanur Aydin
Keyword(s):  
Oxidative Damage ◽  
Textile Industry ◽  
Human Lymphocytes ◽  
Sister Chromatid Exchanges ◽  
Dependent Manner ◽  
Beneficial Effects ◽  
Oxidative Damages ◽  
Total Oxidative Stress ◽  
Oxidative Effects

The Effects of Taurine on Permethrininduced Cytogenetic and Oxidative Damage in Cultured Human LymphocytesPermethrin (PM) is a common pyrethroid pesticide used to control pests in agriculture, forestry, horticulture, health care, homes, and textile industry. It is confirmed as a strong mutagen in animals and humans. Taurine (TA) is an amino acid found in mammalian tissues that protects the cell against DNA damage. In this study, we investigated whether supplementation of human lymphocyte cultures with TA (in the concentrations of 25 μg mL-1, 50 μg mL-1and 100 μg mL-1) provided any protection against PM toxicity applied in the concentration of 200 μg mL-1. Genotoxicity was assessed using the micronucleus (MN) and sister chromatid exchanges (SCE) tests. In addition, we measured the total antioxidant capacity (TAC) and total oxidative stress (TOS) levels in the plasma to determine oxidative effects. PM increased SCE and MN levels and altered TAC and TOS levels. TA alone did not affect SCE and MN levels compared to controls, regardless of the concentration applied. In addition, it increased TAC levels without changing TOS levels. Moreover, it significantly buffered the negative cytogenetic and oxidative effects induced by PM in a clear dose-dependent manner. In conclusion, this study is the first to evidence the beneficial effects of TA against PM-induced DNA and oxidative damagesin vitro.

scholarly journals Ellagic Acid Inhibits Trichophyton rubrum Growth via Affecting Ergosterol Biosynthesis and Apoptotic Induction

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Zhi-Jian Li ◽  
Amima Abula ◽  
Abudumijiti Abulizi ◽  
Chun Wang ◽  
Qin Dou ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Ellagic Acid ◽  
Cell Apoptosis ◽  
Trichophyton Rubrum ◽  
Ergosterol Biosynthesis ◽  
Dependent Manner ◽  
Biosynthesis Pathway ◽  
Gene Expressions ◽  
Fungal Cell

Background. Trichophyton rubrum, among other dermatophytes, is a major causative agent for superficial dermatomycoses like onychomycosis and tinea pedis, especially among pediatric and geriatric populations. Ellagic acid (EA) and shikonin (SK) have been reported to have many bioactivities, including antifungal activity. However, the mechanism of EA and SK on Trichophyton rubrum has not yet been reported. Objectives. The purposes of this study were to evaluate the antifungal activities of EA and SK against Trichophyton rubrum and to illuminate the underlying action mechanisms. Methods. The effect of EA (64, 128, and 256 μg/mL) and SK (8, 4, and 2 μg/mL) on Trichophyton rubrum was investigated with different doses via detecting cell viability, ultrastructure with using a scanning electron microscope (SEM), cell apoptosis and necrosis by using the flow cytometry instrument technique (FCIT), and the ergosterol biosynthesis pathway-related fungal cell membrane key gene expressions in vitro. Results. SEM detection revealed that the T. rubrum cell surface was shrivelled, folded, and showed deformation and expansion, visible surface peeling, and broken hyphae, and cell contents overflowed after being treated with EA and SK; the cell apoptosis rate was significantly increased in dose-dependent manner after T. rubrum was treated with EA and SK; the qPCR results showed that mRNA expression of MEP4 and SUB1 was downregulated in EA- and SK-treated groups. Conclusions. Overall, our results revealed the underlying antifungal mechanism of EA and SK, which may be related to the destruction of the fungal cell membrane and inhibition of C14 demethylase and the catalytic rate of squalene cyclooxidase in the ergosterol biosynthesis pathway via downregulation of MEP4 and SUB1, suggesting that EA and SK have the potential to be developed further as a natural antifungal agent for clinical use.

scholarly journals Effects of triphenyltetradecylphosphonium bromide and tributylhexadecylphosphonium bromide on cellular permeability in patients with hereditary cellular membrane hyperpermeability

2014 ◽  
Vol 95 (1) ◽  
pp. 59-62
Author(s):  
O V Orlova ◽  
V N Oslopov ◽  
S A Sidullina
Keyword(s):  
Cell Membrane ◽  
Membrane Permeability ◽  
Erythrocyte Membrane ◽  
Biologically Active ◽  
Cell Membrane Permeability ◽  
Speed Increase ◽  
Antifungal Action ◽  
Antibacterial And Antifungal ◽  
Genetically Determined

Aim. Comparative analysis of effects of novel biologically active agents: triphenyltetradecylphosphonium bromide and tributylhexadecylphosphonium bromide on cell membrane permeability for sodium by determination of of Na +-Li +-countertransport speed in erythrocyte membrane at patients with genetically determined high membrane permeability for sodium. Methods. Blood samples of 8 healthy volunteers who were classified as persons belonging to IV population quartile according to Na +-Li +-counter-transport speed in erythrocyte membrane, i.e. persons with high membrane permeability, were studied. Effects of different concentrations of triphenyltetradecylphosphonium bromide and tributylhexadecylphosphonium bromide (known by antibacterial and antifungal action) on Na +-Li +-counter-transport speed in erythrocyte membrane in vitro according to the method proposed by M. Canessa et al. Results. Effect of triphenyltetradecylphosphonium bromide (С 14) and tributylhexadecylphosphonium bromide (С 16) on cell membrane permeability for sodium depends on the genetically determined baseline cell membrane state. С 14reduced the erythrocyte membrane permeability for sodium in studied patients belonging to IV quartile of Na +-Li +-counter-transport speed if administered in a concentration of 0.05 μm. C 16increased membrane permeability for sodium in the same group if administered in concentrations of 0.001 and 0.005 μm. Thus, tributylhexadecylphosphonium bromide is better suitable for designing a drug with antibacterial and antifungal action for patients belonging to IV quartile of Na +-Li +-counter-transport speed, if Na +-Li +-counter-transport speed reduction is wanted. If Na +-Li +-counter-transport speed increase is wanted, triphenyltetradecylphosphonium bromide is better suitable. Conclusion. Cand Csubstances affect cell membrane permeability for sodium in patients with genetically determined high membrane permeability for sodium.

Involvement of calmodulin in mediating inhibitory action of intracellular Ca2+ on renin secretion

1986 ◽  
Vol 251 (6) ◽  
pp. F1055-F1062 ◽  
Author(s):  
C. S. Park ◽  
T. W. Honeyman ◽  
E. S. Chung ◽  
J. S. Lee ◽  
D. H. Sigmon ◽  
...  
Keyword(s):  
Renin Secretion ◽  
Cell Membrane Permeability ◽  
Dependent Manner ◽  
Calmodulin Antagonists ◽  
Structural Analogue ◽  
Concentration Dependent Manner ◽  
Calmodulin Antagonist ◽  
High K ◽  
Cortical Slices

This study sought to elucidate further the cellular mechanism(s) involved in the control of renin secretion by Ca2+. The rate of renin secretion in vitro by rabbit and dog renal cortical slices was inversely related to medium Ca2+ concentration. The inverse relationship was observed only when the cell membrane permeability to Ca2+ was increased by K+ depolarization, suggesting that the Ca2+ concentration in the juxtaglomerular cell modulates renin secretion. From this relationship, renin secretion appears to turn on at intracellular Ca2+ concentrations between 10(-8) and 10(-7) M. Calmidazolium, a potent calmodulin antagonist, markedly stimulated basal renin secretion in a concentration-dependent manner. Pretreatment of slices with calmidazolium blocked the inhibition of renin secretion by high-K+ medium. Calmidazolium and several other calmodulin antagonists (W-7, W-13, and trifluoperazine) partly or fully reversed the inhibition of renin secretion previously inhibited by high-K+ medium in the order of their potencies as calmodulin antagonists. Indeed, W-5, a biologically inactive structural analogue of W-7, was without effect. These results support the hypothesis that renin secretion is inversely related to intracellular Ca2+ and that Ca2+ inhibits renin secretion by a calmodulin-dependent process.

scholarly journals Role of High-Mobility Group Box 1 Protein and Poly(ADP-Ribose) Polymerase 1 Degradation in Chlamydia trachomatis-Induced Cytopathicity

2010 ◽  
Vol 78 (7) ◽  
pp. 3288-3297 ◽  
Author(s):  
Hangxing Yu ◽  
Katja Schwarzer ◽  
Martin Förster ◽  
Olaf Kniemeyer ◽  
Vera Forsbach-Birk ◽  
...  
Keyword(s):  
Chlamydia Trachomatis ◽  
Cell Membrane ◽  
Hela Cells ◽  
High Mobility ◽  
Host Cells ◽  
High Mobility Group ◽  
Cell Membrane Permeability ◽  
Dependent Manner ◽  
Infected Cells ◽  
Parp 1

ABSTRACT As intracellular bacteria, chlamydiae block the apoptotic pathways of their host cells. However, the infection of epithelial cells causes the loss of cell membrane integrity and can result in nonapoptotic death. Normally, cells undergoing necrosis release high-mobility group box 1 protein (HMGB1) that acts as an important proinflammatory mediator. Here, we show that in Chlamydia trachomatis-infected HeLa cells HMGB1 is not translocated from the nucleus to the cytosol and not released from injured cells in increased amounts. At 48 h after infection, degradation of HMGB1 was observed. In infected cells, poly(ADP-ribose) polymerase 1 (PARP-1), a DNA repair enzyme that also regulates HMGB1 translocation, was found to be cleaved into fragments that correspond to a necrosislike pattern of PARP-1 degradation. Cell-free cleavage assays and immunoprecipitation using purified proteolytic fractions from infected cells demonstrated that the chlamydial-protease-like activity factor (CPAF) is responsible for the cleavage of both HMGB1 and PARP-1. Proteolytic cleavage of PARP-1 was accompanied by a significant decrease in the enzymatic activity in a time-dependent manner. The loss of PARP-1 function obviously affects the viability of Chlamydia-infected cells because silencing of PARP-1 in uninfected HeLa cells with specific small interfering RNA results in increased cell membrane permeability. Our findings suggest that the Chlamydia-specific protease CPAF interferes with necrotic cell death pathways. By the degradation of HMGB1 and PARP-1, the pathogen may have evolved a strategy to reduce the inflammatory response to membrane-damaged cells in vivo.

Exploring the effect of Polyphyllin I on hepatitis B virus-related liver cancer through network pharmacology and in vitro experiments

2021 ◽  
Vol 24 ◽  
Author(s):  
Shuxian Yu ◽  
Wenhui Gao ◽  
Puhua Zeng ◽  
Chenglong Chen ◽  
Zhuo Liu ◽  
...  
Keyword(s):  
Molecular Docking ◽  
Liver Cancer ◽  
Mechanism Of Action ◽  
Active Ingredient ◽  
Vehicle Group ◽  
Network Pharmacology ◽  
Dependent Manner ◽  
In Vitro Experiments ◽  
Concentration Dependent Manner

Aim and Objective: To investigate the effect of Polyphyllin I (PPI) on HBV-related liver cancer through network pharmacology and in vitro experiments, and to explore its mechanism of action. Materials and Methods: Use bioinformatics software to predict the active ingredient target of PPI and the disease target of liver cancer, and perform active ingredient-disease target analysis. The results of network pharmacology through molecular docking and in vitro experiments can be further verified. The HepG2 receptor cells (HepG2. 2. 15) were transfected with HBV plasmid for observation, with the human liver cancer HepG2 being used as the control. Results: Bioinformatics analysis found that PPI had totally 161 protein targets, and the predicted target and liver cancer targets were combined to obtain 13 intersection targets. The results of molecular docking demonstrated that PPI had good affinity with STAT3, PTP1B, IL2, and BCL2L1. The results of the in vitro experiments indicated that the PPI inhibited cell proliferation and metastasis in a concentration-dependent manner (P<0.01). Compared with the vehicle group, the PPI group of 1.5, 3, and 6 μmol/L can promote the apoptosis of liver cancer to different degrees (P<0.01). Conclusion: The present study revealed the mechanism of PPI against liver cancer through network pharmacology and in vitro experiments. Its mechanism of action is related to the inhibition of PPI on the proliferation of HBV-related liver cancer through promoting the apoptosis of liver cancer cells. Additionally, in vitro experiments have also verified that PPI can promote the apoptosis of HepG2 and HepG2.2.15 cells.

Sign in / Sign up

Export Citation Format

Share Document