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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.
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.
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