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白藜芦醇减轻伏马菌素B1诱导的支持细胞毒性。

Resveratrol Alleviates Fumonisin B1-Induced Cytotoxicity in Sertoli Cells.

作者信息

Yu Song, Zou Lianpeng, Zhao Jiawei, Zhu Yiping

机构信息

Division of Chemical Toxicity and Safety Assessment, Shanghai Institutes of Preventive Medicine, Shanghai 200336, China.

出版信息

Foods. 2024 Nov 26;13(23):3810. doi: 10.3390/foods13233810.

Abstract

Fumonisin B1 is a common food contaminant that has been found to adversely affect the reproductive system, especially Sertoli cells. However, the potential mitigation of FB1-induced cytotoxicity in Sertoli cells has not been fully elaborated. Resveratrol is a natural substance with anti-inflammatory, antioxidant, and anti-tumor properties. Herein, the protective effects of resveratrol against FB1-induced cytotoxicity in Sertoli cells were examined in this work. The mouse Sertoli cell line (TM4) was used as a research model. These results indicated that FB1 (40 μM and 80 μM) significantly reduces cell viability, disrupts the cell barrier, and induces an inflammatory response in TM4 cells. To our surprise, resveratrol (15 μM) showed an ability to reverse adverse effects induced by FB1 (40 μM). Furthermore, resveratrol could alleviate the FB1-induced apoptosis, decrease ROS level, and promote the antioxidant enzymes (CAT and SOD2) expression in FB1-treated TM4 cells. The addition of resveratrol could mitigate FB1-induced promoted phosphorylation of JNK and upregulation of c-jun expression. Interestingly, resveratrol was also able to mitigate the cytotoxicity of FB2 (40 μM), FB3 (40 μM), and an FB1-FB2-FB3 (40 μM-40 μM-40 μM) combination group on TM4 cells. In summary, this research displayed that resveratrol may alleviate fumonisin B1-induced cytotoxicity in Sertoli cells via inhibiting oxidative stress-mediated JNK/c-jun signaling pathway-induced apoptosis. This study provides new insights into the prevention and treatment of FB1-induced testicular toxicity and highlights the potential application value of resveratrol.

摘要

伏马菌素B1是一种常见的食品污染物,已被发现会对生殖系统产生不利影响,尤其是对支持细胞。然而,伏马菌素B1诱导支持细胞产生细胞毒性的潜在缓解作用尚未得到充分阐述。白藜芦醇是一种具有抗炎、抗氧化和抗肿瘤特性的天然物质。在本研究中,检测了白藜芦醇对伏马菌素B1诱导的支持细胞毒性的保护作用。使用小鼠支持细胞系(TM4)作为研究模型。这些结果表明,伏马菌素B1(40μM和80μM)显著降低细胞活力,破坏细胞屏障,并在TM4细胞中诱导炎症反应。令我们惊讶的是,白藜芦醇(15μM)显示出能够逆转伏马菌素B1(40μM)诱导的不利影响。此外,白藜芦醇可以减轻伏马菌素B1诱导的细胞凋亡,降低活性氧水平,并促进伏马菌素B1处理的TM4细胞中抗氧化酶(CAT和SOD2)的表达。添加白藜芦醇可以减轻伏马菌素B1诱导的JNK磷酸化增加和c-jun表达上调。有趣的是,白藜芦醇还能够减轻伏马菌素B2(40μM)、伏马菌素B3(40μM)以及伏马菌素B1-伏马菌素B2-伏马菌素B3(40μM-40μM-40μM)组合组对TM4细胞的细胞毒性。总之,本研究表明白藜芦醇可能通过抑制氧化应激介导的JNK/c-jun信号通路诱导的细胞凋亡来减轻伏马菌素B1诱导的支持细胞毒性。本研究为伏马菌素B1诱导的睾丸毒性的预防和治疗提供了新的见解,并突出了白藜芦醇的潜在应用价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0754/11640369/37c3197189b2/foods-13-03810-g001.jpg

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