探讨T-2毒素对人肾小管上皮细胞HK-2体外增殖和凋亡的影响。将体外培养的HK-2细胞,经不同浓度的T-2毒素作用72 h后,分别测定T-2毒素对HK-2细胞增殖抑制率、细胞形态、DNA片段化、细胞凋亡率、细胞周期分布和caspase-3活性的影响。结果表明,T-2 毒素对HK-2细胞具有增殖抑制作用,抑制率随浓度升高而增大,IC50值为49.34 nmol/L。T-2毒素在10~40 nmol/L可剂量依赖性的诱导HK-2细胞凋亡,且20 nmol/L下HK-2细胞即可出现染色质固缩等凋亡细胞的典型特征。同时,10~40 nmol/L,T-2毒素可通过引起G2/M期阻滞影响细胞的周期分布。此外,T-2毒素在10~40 nmol/L下可引起caspase-3活性剂量依赖性增强,与对照组相比,最大可提高1.93倍(P<0.05)。因此,该研究为阐明T-2毒素的肾脏毒性作用机制提供了理论依据。
This study aimed to study the effects of T-2 toxin on proliferation and apoptosis of human renal tubular epithelial cell HK-2. The HK-2 cells were treated with different concentrations of T-2 toxin for 72 h, followed by measuring their proliferation inhibition rate, cell morphology, DNA fragmentation, apoptosis rate, cell cycle distribution, and caspase-3 activity. The results showed that T-2 toxin inhibited HK-2 cell proliferation and the inhibition rate increased with increasing T-2 toxin concentration (IC50 =49.34 nmol/L). Moreover, T-2 toxin induced cell apoptosis of HK-2 cells in a positive dose-dependent manner in the range of 10-40 nmol/L. Additionally, 20 nmol/L T-2 toxin resulted in chromatin condensation and other typical characteristics of apoptotic cells. Furthermore, 10-40 nmol/L T-2 toxin affected the cell cycle distribution by arresting the G2/M phase and dose-dependently increased the caspase-3 activity with maximally 1.93-fold higher than the control (P<0.05). This paper provides a theoretical basis to elucidate the mechanisms of adverse effects of T-2 toxin on the kidneys.
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