ArticleInternational journal of molecular sciences2019
Astragaloside IV Alleviates Ammonia-Induced Apoptosis and Oxidative Stress in Bovine Mammary Epithelial Cells.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 39 citations in OpenAlex.
- Review
- Transcriptomic exploration combined with experimental validation: uncovering the potential value of biomarkers related to ammonia-induced cell death in hepatic ischemia-reperfusion injury.European journal of medical research · 2025Article
- EGCG Alleviates HFood science & nutrition · 2025Article
- Astragaloside IV attenuates glucocorticoid-induced osteoclastogenesis and bone loss via the MAPK/NF-κB pathway.BMC complementary medicine and therapies · 2025Article
- Plant Secondary Metabolites as Modulators of Mitochondrial Health: An Overview of Their Anti-Oxidant, Anti-Apoptotic, and Mitophagic Mechanisms.International journal of molecular sciences · 2025Review
- Targeting Nrf2/KEAP1 signaling pathway using bioactive compounds to combat mastitis.Frontiers in immunology · 2025Review
- Biomineralized MnOPharmaceutics · 2024Article
- Sirtuin 5 alleviates apoptosis and autophagy stimulated by ammonium chloride in bovine mammary epithelial cells.Experimental and therapeutic medicine · 2024Article
- Astragaloside IV protects against autoimmune myasthenia gravis in rats via regulation of mitophagy and apoptosis.Molecular medicine reports · 2024Article
- Astragaloside IV protects LO2 cells from oxidative damage caused by radiation-induced bystander effect through Akt/Nrf2 pathway.Toxicology research · 2023Article
- Astragaloside-IV alleviates high glucose-induced ferroptosis in retinal pigment epithelial cells by disrupting the expression of miR-138-5p/Sirt1/Nrf2.Bioengineered · 2022Article
- Nrf2-ARE Signaling Partially Attenuates Lipopolysaccharide-Induced Mammary Lesions via Regulation of Oxidative and Organelle Stresses but Not Inflammatory Response in Mice.Oxidative medicine and cellular longevity · 2021Article
- 2-Methyl Nonyl Ketone FromFrontiers in chemistry · 2021Article
- Therapeutic effects of astragaloside IV andPeerJ · 2021Article
- PDE9 Inhibitor PF-04447943 Attenuates DSS-Induced Colitis by Suppressing Oxidative Stress, Inflammation, and Regulating T-Cell Polarization.Frontiers in pharmacology · 2021Article
- Jianpiyifei II Granules Suppress Apoptosis of Bronchial Epithelial Cells in Chronic Obstructive Pulmonary DiseaseFrontiers in pharmacology · 2020Article
- Sanqi Oral Solution Ameliorates Renal Ischemia/Reperfusion Injury via Reducing Apoptosis and Enhancing Autophagy: Involvement of ERK/mTOR Pathways.Frontiers in pharmacology · 2020Article
- Astragaloside IV Protects Against Oxidative Stress in Calf Small Intestine Epithelial Cells via NFE2L2-Antioxidant Response Element Signaling.International journal of molecular sciences · 2019Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Ammonia is one of the major toxic components of metabolites in blood and tissues of high-producing dairy cows and could affect the health of bovine mammary glands. Bovine mammary epithelial cells are sensitive to oxidative stress induced by intensive cell metabolism. In our previous study, we found that ammonia could induce oxidative stress, apoptosis and inflammatory responses in bovine mammary epithelial cells. In the present study, the cytoprotective effects of astragaloside IV against ammonia in vitro were explored. The results demonstrated that pretreatment of MAC-T cells with astragaloside IV could potently suppress the increase in the level of intracellular reactive oxygen species (ROS) and the rate of cell apoptosis, inhibit the ammonia-induced inflammatory responses, and rescue the decrease of cell viability. Astragaloside IV prevented ammonia-induced endoplasmic reticulum stress. Astragaloside IV also significantly suppressed the levels of BAX, caspase 3 and p53 phosphorylation in ammonia-induced MAC-T cells. Nuclear factor erythroid 2-related factor 2(Nrf2) was essential for cytoprotective effects of astragaloside IV in MAC-T cells, as knockdown of Nrf2 dramatically abolished the prosurvival effects of astragaloside IV on treated cells. Furthermore, the PI3K/AKT and ERK/MAPK pathways were responsible for the induction of Nrf2 by astragaloside IV. In conclusion, astragaloside IV played a beneficial role against ammonia-induced damage of MAC-T cells. This provides a cue for future study to use astragaloside IV as a protective and curative agent against ammonia exposure of mammary glands in dairy cows.
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