T-2毒素,毒性最强的A型单端孢菌,广泛存在于谷物和动物饲料中,导致家禽生长迟缓和组织损伤。鹅对T-2毒素比鸡鸭更敏感。尽管据报道,T-2毒素会导致鸡的胫骨生长板(TGP)软骨发育不良,T-2毒素对鹅胫骨的损伤尚未得到充分证实。本研究旨在探讨T-2毒素对胫骨骨发育的不良影响,骨质量,软骨细胞分化,和骨骼代谢。这里,将48只1日龄的扬州雄鹅随机分为4组,每天用浓度为0、0.5、1.0和2.0mg/kg体重的T-2毒素灌胃21天,分别。小鹅体重和大小的发育是通过称重和在暴露于不同浓度的T-2毒素后进行身体测量来确定的。通过影像学检查确定胫骨发育和骨特征的变化,表型测量,骨质量和成分分析。TGP软骨细胞分化和骨代谢的特点是细胞形态,组织基因特异性表达,和血清标志物水平。结果表明,T-2毒素治疗导致较低的体重,volume,长度,中间宽度,和胫骨中围呈剂量依赖性(p<0.05)。此外,骨断裂强度降低,骨矿物质密度,和灰分的含量,Ca,在T-2毒素攻击的鹅中观察到胫骨中的P(p<0.05)。此外,T-2毒素不仅降低了TGP的高度(p<0.05),而且还诱导TGP软骨细胞以减少的数量和模糊的边界混乱。不出所料,凋亡相关基因(CASP9和CASP3)在T-2毒素攻击的软骨细胞中显著上调,呈剂量依赖性,而细胞分化和成熟相关基因(BMP6、BMP7、SOX9和RUNX2)下调(p<0.05)。考虑到骨代谢,T-2毒素剂量依赖性地显著诱导胫骨成骨细胞数量减少和破骨细胞数量增加,成骨相关基因和酶的模式被抑制,破骨细胞相关基因和酶的模式增加(p<0.05)。同样,血清钙和磷浓度和甲状旁腺激素,降钙素,在T-2毒素暴露下,1,25-二羟基胆钙化醇水平降低(p<0.05)。总之,2.0mg/kgT-2毒素显著抑制胫骨重量,长度,宽度,和周长,以及降低的骨断裂强度,密度,和成分(灰分,钙,和磷)与对照组和低剂量组相比,在21天龄的鹅中。由于细胞凋亡,TGP中软骨细胞的分化被2.0mg/kgT-2毒素延迟。此外,2.0mg/kgT-2毒素促进骨吸收并抑制细胞形态的成骨。基因表达,和荷尔蒙调制模式。因此,T-2毒素显著抑制胫骨生长和发育,具有剂量依赖性,伴随着骨骼几何参数和属性的降低,软骨细胞分化受阻,和不平衡的骨代谢。
T-2 toxin, the most toxic type A trichothecene, is widely present in grain and animal feed, causing growth retardation and tissue damage in poultry. Geese are more sensitive to T-2 toxin than chickens and ducks. Although T-2 toxin has been reported to cause tibial growth plate (TGP) chondrodysplasia in chickens, tibial damage caused by T-2 toxin in geese has not been fully demonstrated. This study aims to investigate the adverse effects of T-2 toxin on tibial bone development, bone quality, chondrocyte differentiation, and bone metabolism. Here, forty-eight one-day-old male Yangzhou goslings were randomly divided into four groups and daily gavaged with T-2 toxin at concentrations of 0, 0.5, 1.0, and 2.0 mg/kg body weight for 21 days, respectively. The development of gosling body weight and size was determined by weighing and taking body measurements after exposure to different concentrations of T-2 toxin. Changes in tibial development and bone characteristics were determined by radiographic examination, phenotypic measurements, and bone quality and composition analyses. Chondrocyte differentiation in TGP and bone metabolism was characterized by cell morphology, tissue gene-specific expression, and serum marker levels. Results showed that T-2 toxin treatment resulted in a lower weight, volume, length, middle width, and middle circumference of the tibia in a dose-dependent manner (p < 0.05). Moreover, decreased bone-breaking strength, bone mineral density, and contents of ash, Ca, and P in the tibia were observed in T-2 toxin-challenged goslings (p < 0.05). In addition, T-2 toxin not only reduced TGP height (p < 0.05) but also induced TGP chondrocytes to be disorganized with reduced numbers and indistinct borders. As expected, the apoptosis-related genes (CASP9 and CASP3) were significantly up-regulated in chondrocytes challenged by T-2 toxin with a dose dependence, while cell differentiation and maturation-related genes (BMP6, BMP7, SOX9, and RUNX2) were down-regulated (p < 0.05). Considering bone metabolism, T-2 toxin dose-dependently and significantly induced a decreased number of osteoblasts and an increased number of osteoclasts in the tibia, with inhibited patterns of osteogenesis-related genes and enzymes and increased patterns of osteoclast-related genes and enzymes (p < 0.05). Similarly, the serum Ca and P concentrations and parathyroid hormone, calcitonin, and 1, 25-dihydroxycholecalciferol levels decreased under T-2 toxin exposure (p < 0.05). In summary, 2.0 mg/kg T-2 toxin significantly inhibited tibia weight, length, width, and circumference, as well as decreased bone-breaking strength, density, and composition (ash, calcium, and phosphorus) in 21-day-old goslings compared to the control and lower dose groups. Chondrocyte differentiation in TGP was delayed by 2.0 mg/kg T-2 toxin owing to cell apoptosis. In addition, 2.0 mg/kg T-2 toxin promoted bone resorption and inhibited osteogenesis in cellular morphology, gene expression, and hormonal modulation patterns. Thus, T-2 toxin significantly inhibited tibial growth and development with a dose dependence, accompanied by decreased bone geometry parameters and properties, hindered chondrocyte differentiation, and imbalanced bone metabolism.