Abstract：
OBJECTIVE: Given estrogen\'s recognized regulatory influence on diverse metabolic and immune functions, this study sought to explore its potential impact on fibrosis and elucidate the underlying metabolic regulations.
METHODS: Female mice underwent ovary removal surgery, followed by carbon tetrachloride (CCl4) administration to induce liver injury. Biochemical index analysis and histopathological examination were then conducted. The expression levels of alpha-smooth muscle actin (α-SMA), transforming growth factor-β (TGF-β), and collagen type 1 alpha 1 chain (COL1A1) were assessed using western blotting to further elucidate the extent of liver injury. Finally, metabolite extraction and metabolomic analysis were performed to evaluate metabolic changes.
RESULTS: Ovary removal exacerbated CCl4-induced liver damage, while estrogen supplementation provided protection against hepatic changes resulting from OVX. Furthermore, estrogen mitigated liver injury induced by CCl4 treatment in vivo. Estrogen supplementation significantly restored liver damage induced by OVX and CCl4. Comparative analysis revealed significant alterations in pathways including aminoacyl-tRNA biosynthesis, glycine, serine, and threonine metabolism, lysine degradation, and taurine and hypotaurine metabolism in estrogen treatment.
CONCLUSIONS: Estrogen supplementation alleviates liver injury induced by OVX and CCl4, highlighting its protective effects against fibrosis and associated metabolic alterations.
METHODS: Female mice underwent ovary removal surgery, followed by carbon tetrachloride (CCl4) administration to induce liver injury. Biochemical index analysis and histopathological examination were then conducted. The expression levels of alpha-smooth muscle actin (α-SMA), transforming growth factor-β (TGF-β), and collagen type 1 alpha 1 chain (COL1A1) were assessed using western blotting to further elucidate the extent of liver injury. Finally, metabolite extraction and metabolomic analysis were performed to evaluate metabolic changes.
RESULTS: Ovary removal exacerbated CCl4-induced liver damage, while estrogen supplementation provided protection against hepatic changes resulting from OVX. Furthermore, estrogen mitigated liver injury induced by CCl4 treatment in vivo. Estrogen supplementation significantly restored liver damage induced by OVX and CCl4. Comparative analysis revealed significant alterations in pathways including aminoacyl-tRNA biosynthesis, glycine, serine, and threonine metabolism, lysine degradation, and taurine and hypotaurine metabolism in estrogen treatment.
CONCLUSIONS: Estrogen supplementation alleviates liver injury induced by OVX and CCl4, highlighting its protective effects against fibrosis and associated metabolic alterations.
摘要：
目的：鉴于雌激素对多种代谢和免疫功能的公认调节作用，本研究旨在探讨其对纤维化的潜在影响,并阐明其潜在的代谢规律.
方法：雌性小鼠接受卵巢切除手术，然后用四氯化碳(CCl4)给药诱导肝损伤。然后进行生化指标分析和组织病理学检查。α-平滑肌肌动蛋白(α-SMA)的表达水平,转化生长因子-β（TGF-β），和1型胶原α1链（COL1A1）使用蛋白质印迹法进行评估，以进一步阐明肝损伤的程度。最后,进行代谢物提取和代谢组学分析以评估代谢变化.
结果：卵巢切除加重了CCl4诱导的肝损伤，而补充雌激素可防止OVX引起的肝脏变化。此外，雌激素在体内减轻CCl4治疗引起的肝损伤。补充雌激素可显着恢复OVX和CCl4引起的肝损伤。比较分析显示，包括氨酰基-tRNA生物合成在内的途径发生了显着变化，甘氨酸,丝氨酸,苏氨酸代谢，赖氨酸降解，以及牛磺酸和亚牛磺酸在雌激素治疗中的代谢。
结论：补充雌激素减轻了OVX和CCl4诱导的肝损伤，突出了其对纤维化和相关代谢改变的保护作用。
方法：雌性小鼠接受卵巢切除手术，然后用四氯化碳(CCl4)给药诱导肝损伤。然后进行生化指标分析和组织病理学检查。α-平滑肌肌动蛋白(α-SMA)的表达水平,转化生长因子-β（TGF-β），和1型胶原α1链（COL1A1）使用蛋白质印迹法进行评估，以进一步阐明肝损伤的程度。最后,进行代谢物提取和代谢组学分析以评估代谢变化.
结果：卵巢切除加重了CCl4诱导的肝损伤，而补充雌激素可防止OVX引起的肝脏变化。此外，雌激素在体内减轻CCl4治疗引起的肝损伤。补充雌激素可显着恢复OVX和CCl4引起的肝损伤。比较分析显示，包括氨酰基-tRNA生物合成在内的途径发生了显着变化，甘氨酸,丝氨酸,苏氨酸代谢，赖氨酸降解，以及牛磺酸和亚牛磺酸在雌激素治疗中的代谢。
结论：补充雌激素减轻了OVX和CCl4诱导的肝损伤，突出了其对纤维化和相关代谢改变的保护作用。
