curcumin and indoleacetic-acid

curcumin has been researched along with indoleacetic-acid* in 3 studies

Trials

1 trial(s) available for curcumin and indoleacetic-acid

ArticleYear
Can curcumin supplementation reduce plasma levels of gut-derived uremic toxins in hemodialysis patients? A pilot randomized, double-blind, controlled study.
    International urology and nephrology, 2021, Volume: 53, Issue:6

    Gut dysbiosis is common in patients with chronic kidney disease (CKD) and is closely related to inflammatory processes. Some nutritional strategies, such as bioactive compounds present in curcumin, have been proposed as an option to modulate the gut microbiota and decrease the production of uremic toxins such as indoxyl sulfate (IS), p-cresyl sulfate (pCS) and indole-3 acetic acid (IAA).. To evaluate the effects of curcumin supplementation on uremic toxins plasma levels produced by gut microbiota in patients with CKD on hemodialysis (HD).. The oral supplementation of curcumin for three months seems to reduce p-CS plasma levels in HD patients, suggesting a gut microbiota modulation.

    Topics: Adult; Aged; Cresols; Curcumin; Dietary Supplements; Double-Blind Method; Female; Gastrointestinal Microbiome; Humans; Indican; Indoleacetic Acids; Male; Middle Aged; Pilot Projects; Renal Dialysis; Sulfuric Acid Esters; Toxins, Biological; Uremia

2021

Other Studies

2 other study(ies) available for curcumin and indoleacetic-acid

ArticleYear
Fungal endophytes of turmeric (Curcuma longa L.) and their biocontrol potential against pathogens Pythium aphanidermatum and Rhizoctonia solani.
    World journal of microbiology & biotechnology, 2018, Mar-14, Volume: 34, Issue:3

    Endophytic fungi have been isolated from the healthy turmeric (Curcuma longa L.) rhizomes from South India. Thirty-one endophytes were identified based on morphological and ITS-rDNA sequence analysis. The isolated endophytes were screened for antagonistic activity against Pythium aphanidermatum (Edson) Fitzp., and Rhizoctonia solani Kuhn., causing rhizome rot and leaf blight diseases in turmeric respectively. Results revealed that only six endophytes showed > 70% suppression of test pathogens in antagonistic dual culture assays. The endophyte T. harzianum TharDOB-31 showed significant in vitro mycelial growth inhibition of P. aphanidermatum (76.0%) and R. solani (76.9%) when tested by dual culture method. The SEM studies of interaction zone showed morphological abnormalities like parasitism, shriveling, breakage and lysis of hyphae of the pathogens by endophyte TharDOB-31. Selected endophytic isolates recorded multiple plant growth promoting traits in in vitro studies. The rhizome bacterization followed by soil application of endophyte TharDOB-31 showed lowest Percent Disease Incidence of rhizome rot and leaf blight, 13.8 and 11.6% respectively. The treatment of TharDOB-31 exhibited significant increase in plant height (85 cm) and fresh rhizome yield/plant (425 g) in comparison with untreated control under greenhouse condition. The confocal microscopy validates the colonization of the TharDOB-31 in turmeric rhizomes. The secondary metabolites in ethyl acetate extract of TharDOB-31 were found to contain higher number of antifungal compounds by high resolution liquid chromatograph mass spectrometer analysis. Thereby, endophyte T. harzianum isolate can be exploited as a potential biocontrol agent for suppressing rhizome rot and leaf blight diseases in turmeric.

    Topics: Antibiosis; Antifungal Agents; Biological Control Agents; Curcuma; DNA, Fungal; DNA, Ribosomal; Endophytes; Fungi; Hydrogen Cyanide; India; Indoleacetic Acids; Microbial Sensitivity Tests; Plant Development; Plant Diseases; Plant Leaves; Pythium; Rhizoctonia; Rhizome; Secondary Metabolism

2018
Rapid burst of H2O2 by plant growth regulators increases intracellular Ca2+ amounts and modulates CD4+ T cell activation.
    International immunopharmacology, 2010, Volume: 10, Issue:11

    The identification of small molecules that affect T cell activation is an important area of research. Three molecules that regulate plant growth and differentiation, but not their structurally similar analogs, were identified to enhance primary mouse CD4(+) T cell activation in conjunction with soluble anti-CD3 stimulation: Indoleacetic acid (natural plant auxin), 1-Napthaleneacetic acid (synthetic plant auxin) and 2,4-Dichlorophenoxyacetic acid (synthetic plant auxin and herbicide). These effects are distinct in comparison to Curcumin, the well known phenolic immunomodulator, which lowers T cell activation. An investigation into the mechanisms of action of the three plant growth regulators revealed a rapid induction of reactive oxygen species (ROS), mainly comprising H(2)O(2). In addition, these three molecules synergize with soluble anti-CD3 signaling to enhance intracellular Ca(2+) concentrations [Ca(2+)](i), leading to greater T cell activation, e.g. induction of CD25 and IL-2. Enhanced production of TNFα and IFNγ by CD4(+) T cells is also observed upon plant growth regulator treatment with soluble anti-CD3. Interestingly, maximal IL-2 production and CD4(+) T cell cycle progression are observed upon activation with soluble anti-CD3 and phorbol 12-myristate 13-acetate (PMA), a phorbol ester. Additionally, stimulation with PMA and Ionomcyin (a Ca(2+) ionophore), which activates T cells by circumventing the TCR, and plant growth regulators also demonstrated the role of the strength of signal (SOS): T cell cycle progression is enhanced with gentle activation conditions but decreased with strong activation conditions. This study demonstrates the direct effects of three plant growth regulators on CD4(+) T cell activation and cycling.

    Topics: 2,4-Dichlorophenoxyacetic Acid; Animals; Calcium; CD3 Complex; CD4-Positive T-Lymphocytes; Cell Cycle; Curcumin; Female; Hydrogen Peroxide; Indoleacetic Acids; Interferon-gamma; Interleukin-2; Ionomycin; Lymphocyte Activation; Male; Mice; Mice, Inbred C57BL; Naphthaleneacetic Acids; Plant Growth Regulators; Receptors, Antigen, T-Cell; Signal Transduction; Tetradecanoylphorbol Acetate; Tumor Necrosis Factor-alpha

2010