ArticleJournal of molecular histology2025
Melatonin modulates SHH/GLI3 signaling and placental angiogenesis to counter acrylamide embryotoxicity.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Acrylamide (ACR), a prevalent dietary toxicant formed in thermally processed foods via the Maillard reaction, is known to cross the placental barrier. While ACR-induced reproductive and developmental toxicity has been reported, the protective role of melatonin (MTN) via modulation of the SHH/GLI3 signaling pathway remains unclear. Pregnant Balb/c mice were divided into three groups (n = 6/group): control (distilled water), ACR (50 mg/kg/d), and ACR (50 mg/kg/d) + MTN (10 mg/kg/d), treated orally from gestational day (GD) 3.5 to GD 13.5. Placentas and embryos were collected for analysis. Oxidative stress (MDA levels), VEGF expression, and SHH/GLI3 pathway activity were assessed using immunohistochemistry and qRT-PCR. ACR exposure induced significant embryotoxicity, manifested as a 34% reduction in fetal weight (1.60 ± 0.09 g vs. 1.88 ± 0.14 g in controls, p < 0.001) and a 46.2% reduction in fetal crown-rump length (0.7 ± 0.08 cm vs. 1.1 ± 0.1 cm, p < 0.001). MTN co-treatment significantly ameliorated these growth restrictions. IHC analysis revealed that ACR significantly reduced SHH protein expression in the embryonic intestine and liver (p < 0.01), while it increased GLI3 protein levels (p < 0.01). MTN effectively normalized the expression of both proteins. At the molecular level, ACR downregulated SHH expression (p < 0.001) and upregulated GLI3 (p < 0.01), which were reversed by MTN. ACR exposure significantly increased oxidative stress (105% increase in placental MDA, p < 0.001) and reduced placental VEGF expression by 69.3% (p < 0.0001), both of which were significantly mitigated by MTN co-treatment. These integrated findings demonstrate that MTN exerts potent antioxidative and cytoprotective effects by mitigating ACR-induced oxidative stress, restoring SHH/GLI3 protein and gene expression, preserving VEGF-mediated placental angiogenesis, and preventing morphological defects. Our results underscore MTN's therapeutic potential in counteracting ACR-induced teratogenicity and supporting healthy organogenesis.
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