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Regulation of taurine in OTA-induced apoptosis and autophagy

机译:在OTA诱导的细胞凋亡和自噬中牛磺酸的调节

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摘要

Ochratoxin A (OTA), one of the most deleterious mycotoxins, could cause a variety of toxicological effects especially nephrotoxicity in animals and humans. Taurine, a wide-distributed cytoprotective amino acid, plays an important role as a basic factor for maintaining cellular integrity homeostasis. However, the potential effect of taurine in OTA-induced nephrotoxicity remains unknown. In the present study, we demonstrated that OTA treatment at 4.0-8.0 mu M increased apoptosis in PK-15 cells as shown by increased the ratio of apoptosis and protein expression of Bax and cleaved-caspase-3, decreased protein expression of Bcl-2. Meantime, OTA treatment triggered autophagy, as indicated by markedly increased the protein expression of LC3-II and fluorescence intensity of GFP-LC3 dots. Taurine supplementation decreased OTA-induced cytotoxicity and attenuated apoptosis as shown by the decreased Annexin V/PI staining and the decreased expression of apoptosis-related proteins including Bax and caspase-3. Meanwhile, taurine attenuated OTA-induced autophagy by decreased the protein expression of LC3-II and fluorescence intensity of GFP-LC3 dots to maintain cellular homeostasis. In conclusion, taurine treatment could alleviate OTA-induced apoptosis and inhibit the triggered autophagy in PK-15 cells. Our study provides supportive data for the potential roles of taurine in reducing OTA-induced renal toxicity.
机译:Ochratoxin A(OTA)是最有害的霉菌毒素之一,可能导致动物和人类中肾毒性的各种毒理学作用。牛磺酸是一种广泛分布的细胞保护氨基酸,起到保持细胞完整性稳态的基本因素的重要作用。然而,牛磺酸在OTA诱导的肾毒性中的潜在效果仍然未知。在本研究中,我们证明了在40-8.0μm的ota治疗增加了PK-15细胞中的凋亡,如凋亡和切割 - caspase-3的凋亡和蛋白表达的比例增加,蛋白表达降低了Bcl-2的蛋白质表达。同时,OTA治疗触发自噬,如通过显着提高LC3-II的蛋白质表达和GFP-LC3点的荧光强度所示。牛磺酸补充剂降低了OTA诱导的细胞毒性和减毒细胞凋亡,如下降的膜蛋白v / pi染色所示,并降低了包括BAX和Caspase-3的凋亡相关蛋白质的表达。同时,牛磺酸通过降低LC3-II的蛋白表达和GFP-LC3点的荧光强度降低,牛磺酸诱导的自噬,以维持细胞稳态。总之,牛磺酸治疗可以缓解OTA诱导的细胞凋亡并抑制PK-15细胞中的触发自噬。我们的研究提供了牛磺酸潜在作用的支持性数据,以降低卵巢诱导的肾毒性。

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