ArticleFrontiers in pharmacology2018
Xiaoaiping Induces Developmental Toxicity in Zebrafish Embryos Through Activation of ER Stress, Apoptosis and the Wnt Pathway.
Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 68 citations in OpenAlex.
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- Curcumin's Radioprotective Effects on Zebrafish Embryos.Antioxidants (Basel, Switzerland) · 2024Article
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- Developmental toxicity and programming alterations of multiple organs in offspring induced by medication during pregnancy.Acta pharmaceutica Sinica. B · 2023Review
- RETRACTED: Environmental Impact of Pharmaceutical Pollutants: Synergistic Toxicity of Ivermectin and Cypermethrin.Toxics · 2022Article
- RETRACTED: Combined Effects of Potassium Perchlorate and a Neonicotinoid on Zebrafish Larvae (Toxics · 2022Article
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- RETRACTED: Combined Toxicity of Xenobiotics Bisphenol A and Heavy Metals on Zebrafish Embryos (Toxics · 2021Article
- In Vivo Evaluation ofPharmaceuticals (Basel, Switzerland) · 2021Article
- Study of the Potential Hepatoprotective Effect of Myo-Inositol and Its Influence on Zebrafish Development.Nutrients · 2021Article
- Clozapine Induced Developmental and Cardiac Toxicity on Zebrafish Embryos by Elevating Oxidative Stress.Cardiovascular toxicology · 2021Article
- lncRNA Ttc3-209 Promotes the Apoptosis of Retinal Ganglion Cells in Retinal Ischemia Reperfusion Injury by Targeting the miR-484/Wnt8a Axis.Investigative ophthalmology & visual science · 2021Article
- Zebrafish as a Successful Animal Model for Screening Toxicity of Medicinal Plants.Plants (Basel, Switzerland) · 2020Review
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Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the study was to determine the developmental toxicity of the traditional Chinese medicine Xiaoaiping (XAP) and to investigate its underlying mechanism of action. Zebrafish embryos were incubated with 0.4, 0.8, 1.2, and 1.6 mg/mL XAP. Endpoints such as mortality, hatching rate, malformation, body length, morphology score, swimming behavior, histological changes, reactive oxygen species (ROS) production, total superoxide dismutase (T-SOD) activity, and the mRNA expression of genes related to oxidative stress, endoplasmic reticulum (ER) stress, apoptosis, and the Wnt pathway were evaluated. Our results demonstrated that XAP exposure increased mortality and malformation and reduced the hatching rate. XAP resulted in severe malformation, including swim bladder deficiency, yolk retention, pericardial edema, and tail curvature. Histopathological analysis showed that XAP induced liver, heart and muscle injury. High doses (≥1.2 mg/mL) of XAP notably decreased the locomotor capacity of zebrafish. ROS generation was remarkably increased and T-SOD activity was decreased, confirming that oxidative stress was induced by XAP. The mRNA expression levels of ER stress-related genes (
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.