Anti-malarial effect of 1-(N-acetyl-6-aminohexyl)-3-hydroxy-2-methylpyridin-4-one and green tea extract on erythrocyte-stage Plasmodium berghei in mice

Objective: To examine the efficacy of 1-(N-acetyl-6-aminohexyl)-3-hydroxy-2-methylpyridin-4-one (CM1) iron chelator and green tea extract (GTE) as anti-malarial activity in Plasmodium berghei (P. berghei) infected mice. Methods: The CM1 (0–100 mg/kg/day) and GTE (0–100 mg (−)-epigallocatechin 3-gall...

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Bibliographic Details
Published in:Asian Pacific Journal of Tropical Biomedicine
Main Authors: Phitsinee Thipubon, Wachiraporn Tipsuwan, Chairat Uthaipibull, Sineenart Santitherakul, Somdet Srichairatanakool
Format: Article in Journal/Newspaper
Language:English
Published: Wolters Kluwer Medknow Publications 2015
Subjects:
Plasmodium
Antimalarial drug
Green tea
Iron chelator
Hydroxypyridinone
Arctic medicine. Tropical medicine
RC955-962
Biology (General)
QH301-705.5
Arctic
Online Access:https://doi.org/10.1016/j.apjtb.2015.07.021
https://doaj.org/article/900063ef37764dea8d0a1eb5c7f8af2e
Description
Summary:Objective: To examine the efficacy of 1-(N-acetyl-6-aminohexyl)-3-hydroxy-2-methylpyridin-4-one (CM1) iron chelator and green tea extract (GTE) as anti-malarial activity in Plasmodium berghei (P. berghei) infected mice. Methods: The CM1 (0–100 mg/kg/day) and GTE (0–100 mg (−)-epigallocatechin 3-gallate equivalent/kg/day) were orally administered to P. berghei infected mice for consecutive 4 days. Parasitized red blood cells (PRBC) were enumerated by using Giemsa staining microscopic method. Results: CM1 lowered percentage of PRBC in dose-dependent manner with an ED50 value of 56.91 mg/kg, when compared with pyrimethamine (PYR) (ED50 = 0.76 mg/kg). GTE treatment did not show any inhibition of the malaria parasite growth. In combined treatment, CM1 along with 0.6 mg/kg PYR significantly inhibited the growth of P. berghei in mice while GTE did not enhance the PYR anti-malarial activity. Conclusions: CM1 would be effective per se and synergize with PYR in inhibiting growth of murine malaria parasites, possibly by limiting iron supply from plasma transferrin and host PRBC cytoplasm, and chelating catalytic iron cstitutive in parasites’ mitochondrial cytochromes and cytoplasmic ribonucleotide reductase. CM1 would be a promising adjuvant to enhance PYR anti-malarial activity and minimize the drug resistance.

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