Glabridin exhibits potent inhibitory effects against Toxoplasma gondii in vitro and in vivo.

Parasit Vectors

Laboratory of Parasitic Diseases, College of Veterinary Medicine, Shanxi Agricultural University, Taigu, Shanxi Province, 030801, People's Republic of China.

Published: December 2024

AI Article Synopsis

  • Toxoplasma gondii is a common parasite in warm-blooded animals and humans, with current treatments like pyrimethamine and sulfadiazine having significant limitations, prompting a search for safer, more effective options.
  • This study focused on glabridin, a natural compound from a medicinal plant, finding it to be low in toxicity while effectively inhibiting T. gondii growth and altering its structure.
  • The results showed that glabridin improved survival rates in infected mice and affected T. gondii's metabolism, suggesting a promising new treatment avenue for this parasite.

Article Abstract

Background: Toxoplasma gondii is an obligate protozoan parasite capable of infecting a wide range of warm-blooded animals and humans. Current treatment options, primarily pyrimethamine and sulfadiazine, have limitations, such as high recurrence rates, long treatment durations, and limited effectiveness against T. gondii. There is an unmet need for novel, safe, low-toxicity, and highly effective treatments. This study aimed to evaluate the anti-T. gondii effects of glabridin, a natural compound derived from the roots of a widely used medicinal plant.

Methods: The cytotoxicity of glabridin in Vero cells was assessed using a CCK-8 cell viability assay. Quantitative polymerase chain reaction (qPCR) targeting the Tg-529 gene was developed to quantify T. gondii and assess the inhibitory effects of glabridin on parasite proliferation. Ultrastructural changes in T. gondii after treatment were examined using electron microscopy. The levels of reactive oxygen species (ROS) and mitochondrial membrane potential (ΔΨm) were examined to assess the effects of glabridin on ROS levels and ΔΨm in T. gondii tachyzoites. Additionally, metabolomics and transcriptomics analyses were conducted to investigate the mechanisms underlying glabridin's anti-T. gondii effects.

Results: Glabridin exhibited low toxicity to host cells and effectively inhibited T. gondii invasion and proliferation in vitro in a time-dependent manner. Glabridin-treated tachyzoites exhibited significant structural alterations, along with increased ROS production and a reduction in ΔΨm. Metabolomic analysis indicated that glabridin significantly affected amino acid metabolism pathways in T. gondii. In vivo, glabridin treatment significantly improved survival rates in T. gondii-infected BALB/c mice at a dosage of 100 mg/kg.

Conclusions: This study demonstrates that glabridin has potent anti-T. gondii effects in vitro and in vivo, likely through disruption of amino acid metabolism in the parasite. These findings highlight glabridin's potential as a promising therapeutic agent for toxoplasmosis.

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Source
http://dx.doi.org/10.1186/s13071-024-06610-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11656597PMC

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