A comparison study of effects of Echinacea extract and levamisole on phenytoin-induced cleft palate in mice

Mahabady, M. Khaksary; Ranjbar, R; Arzi, Ardeshir; Papahn, A A; Najafzadeh, Hossein

doi:10.1016/j.yrtph.2006.06.005

Cited by 11 publications

(3 citation statements)

References 14 publications

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“…1A). PHE is known to inhibit cell proliferation through induction of apoptosis and cell cycle arrest in mice and cell line (Czeizel, 1976;Hu et al, 2011;Khaksary Mahabady et al, 2006;Martinelli et al, 2020). We investigated the involvement of apoptosis and cell cycle by treatment with PHE in HEPM cells.…”

Section: Resultsmentioning

confidence: 99%

Involvement of <i>microRNA-4680-3p</i> against phenytoin-induced cell proliferation inhibition in human palate cells

Tsukiboshi,

Horita,

Mikami

et al. 2024

J. Toxicol. Sci.

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Cleft palate (CP) is one of the most common birth defects and is caused by a combination of genetic and/or environmental factors. Environmental factors such as pharmaceutical exposure in pregnant women are known to induce CP. Recently, microRNA (miRNA) was found to be affected by environmental factors. The aim of the present study was to investigate the involvement of miRNA against phenytoin (PHE)-induced inhibition of proliferation in human embryonic palatal mesenchymal (HEPM) cells. We demonstrated that PHE inhibited HEPM cell proliferation in a dose-dependent manner. We found that treatment with PHE downregulated cyclin-D1 and cyclin-E expressions in HEPM cells. Furthermore, PHE increased miR-4680-3p expression and decreased two downstream genes (ERBB2 and JADE1). Importantly, an miR-4680-3p-specific inhibitor restored HEPM cell proliferation and altered expression of ERBB2 and JADE1 in cells treated with PHE. These results suggest that PHE suppresses cell proliferation via modulation of miR-4680-3p expression.

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Section: Resultsmentioning

confidence: 99%

Involvement of <i>microRNA-4680-3p</i> against phenytoin-induced cell proliferation inhibition in human palate cells

Tsukiboshi,

Horita,

Mikami

et al. 2024

J. Toxicol. Sci.

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“…Studies found that E. purpurea could stimulate immune system of mice more than levamisole and had better prophylactic effect against the teratogenic effect of phenytoin as evidenced by lower incidence of phenytoin-induced cleft palate, but it was not signifi cant (Mahabady et al 2006 ). Cleft palate incidence was 16, 5.3 and 3.2 % in fetuses of mice that received only phenytoin, phenytoin with levamisole, and phenytoin with Echinacea extract, respectively.…”

Section: Anti-teratogenic Activitymentioning

confidence: 99%

Echinacea purpurea

Lim¹

2013

Edible Medicinal and Non-Medicinal Plants

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“…Failure of the neural tube to close during development results in exencephaly, anencephaly, and spina bifida. Nonspecific stimulation of maternal immune system in mice reduces a wide variety of fetal malformations induced by various physical and chemical agents, and also diseases such as diabetes mellitus (Nomura et al., ; Toder et al., ; Holladay et al., ; Prater et al., ; Punareewattana and Holladay ; Laudermilch et al., ; Khaksary et al., ; Latorre et al., ; Hrubec et al., ). Maternal immune stimulation with IFNγ reduces the incidence of valproic acid (VA) induced NTDs in late gestational fetuses (Hrubec et al., ).…”

Section: Introductionmentioning

confidence: 99%

Reduction in Valproic Acid–Induced Neural Tube Defects by Maternal Immune Stimulation: Role of Apoptosis

Mallela

Hrubec

2012

Birth Defects Research Pt B

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Teratogenic deregulation of apoptosis during development is a possible mechanism for birth defects. Administration of valproic acid (VA) during first trimester of pregnancy causes neural tube defects (NTDs). Nonspecific stimulation of the mother’s immune system has been shown to reduce various teratogen-induced fetal malformations including NTDs in rodents. This present study investigated the role of reduced apoptosis by maternal immune stimulation in prevention of VA-induced NTDs in CD-1 mice. Prevention of VA-induced NTDs by nonspecific maternal immune stimulation using IFNγ was employed to evaluate the role of reduced apoptosis by IFNγ in this protective mechanism. Apoptosis was quantified using flow cytometry. Terminal Transferase dUTP Nick End Labeling assay was used to localize the apoptosis. Increased apoptosis, suggesting involvement in VA teratogenicity, was observed along the neural tube in both normal and abnormal embryos from VA-exposed dams. Increased apoptosis in normal VA-exposed embryos suggests that VA may alter other cellular processes such as cell proliferation and differentiation in addition to apoptosis. Apoptotic levels in embryos with closed neural tubes from IFNγ + VA dams were similar to controls indicating resistance to VA-induced apoptosis and protection against teratogenicity of VA. In IFNγ + VA exposed embryos with open neural tubes, maternal immune stimulation failed to regulate apoptosis resulting in an NTD. Overall, these results suggest that VA alters several biological processes including apoptosis in the developing embryos to induce fetal malformations. Resistance to VA-induced apoptosis in embryos resulting from maternal immune stimulation may be involved in protective mechanism.

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A comparison study of effects of Echinacea extract and levamisole on phenytoin-induced cleft palate in mice

Cited by 11 publications

References 14 publications

Involvement of <i>microRNA-4680-3p</i> against phenytoin-induced cell proliferation inhibition in human palate cells

Involvement of <i>microRNA-4680-3p</i> against phenytoin-induced cell proliferation inhibition in human palate cells

Echinacea purpurea

Reduction in Valproic Acid–Induced Neural Tube Defects by Maternal Immune Stimulation: Role of Apoptosis

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