Abstract：
BACKGROUND: Cadmium (Cd) is a strong toxic agent and causes serious damage to testicular tissues. Chrysin (CHR) is a natural flavonoid with many effective properties, especially antioxidant, anti-inflammatory and anti-apoptotic properties. The current study describes new evidence for the ameliorative effects of CHR on oxidative stress, apoptosis, autophagy and inflammation pathways in Cd-induced testicular tissue toxicity.
METHODS: Thirty-five male Wistar rats were divided into five groups, control, Cd, CHR, Cd + CHR25, and Cd + CHR50. Cd was administered alone at a dose of 25 mg/kg body weight or in combination with CHR 25 mg/kg and CHR 50 mg/kg for 7 days. Cd and CHR were administered orally. Biochemical, molecular, and histological methods were used to investigate inflammation, apoptosis, autophagy, and oxidant pathways in testicular tissue.
RESULTS: Cd increased lipid peroxidation, JAK-2/STAT-3 levels, inflammation-related NF-κB, TNF-α, IL-1β, IL-6, COX-2, and iNOS levels, AKT-2, FOXO1, Bax, Apaf-1 and Caspase-3 levels, autophagic Beclin-1, LC3A and LC3B. The Cd also caused a decrease in the activities of antioxidant enzymes and GSH levels, antiapoptotic Bcl-2 levels. CHR, on the other hand, had the opposite effect of all these Cd-induced changes.
CONCLUSIONS: Overall, the data of this study indicate that testicular damage associated with Cd toxicity could be ameliorated by CHR administration.
METHODS: Thirty-five male Wistar rats were divided into five groups, control, Cd, CHR, Cd + CHR25, and Cd + CHR50. Cd was administered alone at a dose of 25 mg/kg body weight or in combination with CHR 25 mg/kg and CHR 50 mg/kg for 7 days. Cd and CHR were administered orally. Biochemical, molecular, and histological methods were used to investigate inflammation, apoptosis, autophagy, and oxidant pathways in testicular tissue.
RESULTS: Cd increased lipid peroxidation, JAK-2/STAT-3 levels, inflammation-related NF-κB, TNF-α, IL-1β, IL-6, COX-2, and iNOS levels, AKT-2, FOXO1, Bax, Apaf-1 and Caspase-3 levels, autophagic Beclin-1, LC3A and LC3B. The Cd also caused a decrease in the activities of antioxidant enzymes and GSH levels, antiapoptotic Bcl-2 levels. CHR, on the other hand, had the opposite effect of all these Cd-induced changes.
CONCLUSIONS: Overall, the data of this study indicate that testicular damage associated with Cd toxicity could be ameliorated by CHR administration.
摘要：
背景：镉（Cd）是一种强毒性剂，对睾丸组织造成严重损害。白菊素（CHR）是一种具有许多有效特性的天然类黄酮，尤其是抗氧化剂，抗炎和抗凋亡特性。当前的研究描述了CHR对氧化应激的改善作用的新证据，凋亡，自噬和炎症通路在镉致睾丸组织毒性中的作用.
方法:35只雄性Wistar大鼠分为5组,control,Cd,CHR,Cd+CHR25和Cd+CHR50。Cd以25mg/kg体重的剂量单独施用或与CHR25mg/kg和CHR50mg/kg组合施用7天。口服Cd和CHR。生物化学,分子，和组织学方法用于研究炎症，凋亡，自噬,和睾丸组织中的氧化途径。
结果：Cd增加脂质过氧化，JAK-2/STAT-3水平，炎症相关NF-κB，TNF-α,IL-1β,IL-6、COX-2和iNOS水平，AKT-2,FOXO1,Bax,Apaf-1和Caspase-3水平，自噬Beclin-1，LC3A和LC3B。Cd还引起抗氧化酶活性和GSH水平的降低，抗凋亡Bcl-2水平。CHR,另一方面,与所有这些Cd诱导的变化相反。
结论：总体而言，这项研究的数据表明，与Cd毒性相关的睾丸损伤可以通过CHR管理来改善。
方法:35只雄性Wistar大鼠分为5组,control,Cd,CHR,Cd+CHR25和Cd+CHR50。Cd以25mg/kg体重的剂量单独施用或与CHR25mg/kg和CHR50mg/kg组合施用7天。口服Cd和CHR。生物化学,分子，和组织学方法用于研究炎症，凋亡，自噬,和睾丸组织中的氧化途径。
结果：Cd增加脂质过氧化，JAK-2/STAT-3水平，炎症相关NF-κB，TNF-α,IL-1β,IL-6、COX-2和iNOS水平，AKT-2,FOXO1,Bax,Apaf-1和Caspase-3水平，自噬Beclin-1，LC3A和LC3B。Cd还引起抗氧化酶活性和GSH水平的降低，抗凋亡Bcl-2水平。CHR,另一方面,与所有这些Cd诱导的变化相反。
结论：总体而言，这项研究的数据表明，与Cd毒性相关的睾丸损伤可以通过CHR管理来改善。
