ArticleBiomolecules2019
Betulinic Acid Attenuates T-2-Toxin-Induced Testis Oxidative Damage Through Regulation of the JAK2/STAT3 Signaling Pathway in Mice.
Article in Biomolecules, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- MicroRNAs as diagnostic biomarkers in diabetes male infertility: a systematic review.Molecular biology reports · 2024Pooled it
- Lycopene Alleviates T-2 Toxin-Induced Testosterone Synthesis Disorder by Inhibiting ROS/p38/TORC2/CREB Axis.Antioxidants (Basel, Switzerland) · 2026Article
- The JAK/STAT pathway: a pivotal therapeutic target in disease and advances in natural product modulation.Molecular diversity · 2026Review
- Beta-caryophyllene mitigates high fat diet-induced testicular dysfunctions by targeting JNK/ERK-1 and JAK-1/STAT-3 pathways in rats.Scientific reports · 2026Article
- Yixinshu attenuates myocardial infarction via SHP1/JAK2/STAT3-mediated regulation of mitochondrial function and apoptosis.Chinese medicine · 2026Article
- T-2 Toxin Neurotoxicity: Molecular Mechanisms and Emerging Chemoprotective Strategies.Antioxidants (Basel, Switzerland) · 2026Review
- Zinc Alleviates Oxidative Stress Injury of the Testis Induced by Zearalenone through Sirt3-Foxo3 Pathway in Mice.Biological trace element research · 2026Article
- An exhaustive examination of the research progress in identifying potential JAK inhibitors from natural products: a comprehensive overview.Chinese medicine · 2025Review
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- Effective protective agents against the organ toxicity of T-2 toxin and corresponding detoxification mechanisms: A narrative review.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2024Review
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- T-2 toxin-induced intestinal damage with dysregulation of metabolism, redox homeostasis, inflammation, and apoptosis in chicks.Archives of toxicology · 2023Article
- The research development of STAT3 in hepatic ischemia-reperfusion injury.Frontiers in immunology · 2023Review
- Recent Advances Regarding the Molecular Mechanisms of Triterpenic Acids: A Review (Part II).International journal of molecular sciences · 2022Review
- Quercetin ameliorates testosterone secretion disorder by inhibiting endoplasmic reticulum stress through the miR-1306-5p/HSD17B7 axis in diabetic rats.Bosnian journal of basic medical sciences · 2022Article
- JAK Inhibition Prevents DNA Damage and Apoptosis in Testicular Ischemia-Reperfusion Injury via Modulation of the ATM/ATR/Chk Pathway.International journal of molecular sciences · 2021Article
- Protective effect of selenomethionine on T-2 toxin-induced liver injury in New Zealand rabbits.BMC veterinary research · 2021Article
- Betulinic Acid Alleviates Spleen Oxidative Damage Induced by Acute Intraperitoneal Exposure to T-2 Toxin by Activating Nrf2 and Inhibiting MAPK Signaling Pathways.Antioxidants (Basel, Switzerland) · 2021Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T-2 toxin is one of the most toxic type A trichothecene mycotoxins in nature, and it exhibits reproductive toxicity. Betulinic acid (BA) is a natural pentacyclic triterpene compound found in species of Betula, and it has been reported to have antioxidant activity. The aim of the present study was to investigate the protective effect of BA on T-2-toxin-induced testicular injury in mice and explore its molecular mechanism. Sixty adult male mice were randomly divided into groups. The mice were pretreated orally with BA (0.25, 0.5, and 1.0 mg/kg) daily for 14 days, and the T-2 toxin (4 mg/kg body weight) was administered via intraperitoneal injection to induce oxidative stress after the last administration of BA. BA pretreatment significantly increased the secreted levels of testosterone and sperm motility. Moreover, BA pretreatment significantly increased the total antioxidant capacity (T-AOC), the activity of SOD and CAT, and the content of GSH, and it reduced the content of MDA. Furthermore, BA relieved testicular injury and reduced the number of apoptotic cells, and it significantly decreased the protein expression of Janus kinase 2 (JAK2), signal transducers and activators of transcription 3 (STAT3), caspsae-3, and Bcl-2-associated X protein (Bax). BA also increased the expression of B-cell lymphoma-2 (Bcl-2). We suggest that BA reduced the oxidative damage induced by T-2 toxin, and that these protective effects may be partially mediated by the JAK2/STAT3 signaling pathway.
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