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.
Highlights
T-2 toxin is produced by Fusarium piriformis, and it is one of the most toxic A trichothecenes.Myotoxins are widely distributed in grains and agricultural products and have many toxic effects on humans and animals [1]
Pretreatment with low and high doses of Betulinic acid (BA) significantly increased the percentage of viable sperm compared with the T-2 toxin group, and the medium dose of BA had a higher percentage of sperm survival than the T-2 toxin group; the difference in sperm survival for the VE group was obvious (Figure 1B)
Compared with the T-2 group, BA pretreatment significantly reduced the ratios of p-Janus kinase 2 (JAK2)/JAK2 and p-signal transducers and activators of transcription 3 (STAT3)/STAT3. These results indicate that BA could alleviate apoptosis of testicular cells and testis injury induced by the T-2 toxin through the JAK2/STAT3 signaling pathway (Figure 4)
Summary
T-2 toxin is produced by Fusarium piriformis, and it is one of the most toxic A trichothecenes. Myotoxins are widely distributed in grains and agricultural products and have many toxic effects on humans and animals [1]. T-2 toxin can cause toxicity of cells in the digestive system, immune system, and reproductive system, and it has teratogenic, carcinogenic, and mutagenic effects [3]. Accidental consumption of T-2-toxin-contaminated grain or feed can cause chronic and acute poisoning, which manifests as loss of appetite, vomiting, diarrhea, bloody stool, and so on [4]. It has been reported that T-2 toxin is associated with alimentary toxic aleukia [5].
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