Abstract：
BACKGROUND: Injury systemically disrupts the homeostatic balance and can cause organ failure. LF mediates both iron-dependent and iron-independent mechanisms, and the role of LF in regulating iron homeostasis is vital in terms of metabolism.
OBJECTIVE: In this study, we evaluated the organ-level effect and gene expression change of bLf in the cutaneous repair process.
METHODS: An excisional full-thickness skin defect (FTSD) wound model was created in male Sprague Dawley rats (180-250 g) (n = 48) fed a high-fat diet (HFD) and the PHGPx, SLC7A11 and SLC40A1 genes and iron metabolism were evaluated. The animals were randomly divided into 6 groups: 1- Control, 2- bLf (200 mg/kg/day, oral), 3- FTSD (12 mm in diameter, dorsal), 4- HFD + bLf, 5- HFD + FTSD, 6- HFD + FTSD + bLf. Histologically, iron accumulation was demonstrated by Prussian blue staining in the liver, kidney, and intestinal tissues. Gene expression analysis was performed with qPCR.
RESULTS: Histologically, iron accumulation was demonstrated by Prussian blue staining in the liver, kidney, and intestinal tissues. Prussian blue reactions were detected in the kidney. PHPGx and SLC7A11 genes in kidney and liver tissue were statistically significant (P < 0.05) except for the SLC40A1 gene (P > 0.05). Expression changes of the three genes were not statistically significant in analyses of rat intestinal tissue (P = 0.057).
CONCLUSIONS: In the organ-level ferroptotic damage mechanism triggered by wound formation. BLf controls the expression of three genes and manages iron deposition in these three tissues. In addition, it suppressed the increase in iron that would drive the cell to ferroptosis and anemia caused by inflammation, thereby eliminating iron deposition in the tissues.
OBJECTIVE: In this study, we evaluated the organ-level effect and gene expression change of bLf in the cutaneous repair process.
METHODS: An excisional full-thickness skin defect (FTSD) wound model was created in male Sprague Dawley rats (180-250 g) (n = 48) fed a high-fat diet (HFD) and the PHGPx, SLC7A11 and SLC40A1 genes and iron metabolism were evaluated. The animals were randomly divided into 6 groups: 1- Control, 2- bLf (200 mg/kg/day, oral), 3- FTSD (12 mm in diameter, dorsal), 4- HFD + bLf, 5- HFD + FTSD, 6- HFD + FTSD + bLf. Histologically, iron accumulation was demonstrated by Prussian blue staining in the liver, kidney, and intestinal tissues. Gene expression analysis was performed with qPCR.
RESULTS: Histologically, iron accumulation was demonstrated by Prussian blue staining in the liver, kidney, and intestinal tissues. Prussian blue reactions were detected in the kidney. PHPGx and SLC7A11 genes in kidney and liver tissue were statistically significant (P < 0.05) except for the SLC40A1 gene (P > 0.05). Expression changes of the three genes were not statistically significant in analyses of rat intestinal tissue (P = 0.057).
CONCLUSIONS: In the organ-level ferroptotic damage mechanism triggered by wound formation. BLf controls the expression of three genes and manages iron deposition in these three tissues. In addition, it suppressed the increase in iron that would drive the cell to ferroptosis and anemia caused by inflammation, thereby eliminating iron deposition in the tissues.
摘要：
背景：损伤会系统性地破坏体内平衡并导致器官衰竭。LF介导铁依赖和铁独立机制，LF在调节铁稳态中的作用在代谢方面至关重要。
目的：在本研究中，我们评估了bLf在皮肤修复过程中的器官水平作用和基因表达变化。
方法：在饲喂高脂饮食（HFD）和PHGPx的雄性SpragueDawley大鼠（180-250g）（n=48）中创建了切除的全层皮肤缺损（FTSD）伤口模型，评价SLC7A11和SLC40A1基因与铁代谢的关系。将动物随机分为6组：1-对照组，2-bLf（200mg/kg/天，oral),3-FTSD（直径12毫米，背侧)，4-HFD+BLf,5-HFD+FTSD,6-HFD+FTSD+bLf。组织学上,肝脏中的普鲁士蓝染色证明了铁的积累，肾,和肠道组织。用qPCR进行基因表达分析。
结果：组织学，肝脏中的普鲁士蓝染色证明了铁的积累，肾,和肠道组织。在肾脏中检测到普鲁士蓝反应。除SLC40A1基因(P>0.05)外,PHPGx和SLC7A11基因在肾和肝组织中均有统计学意义(P<0.05)。在大鼠肠组织分析中，这三个基因的表达变化无统计学意义（P=0.057）。
结论：在由伤口形成引发的器官水平的铁损伤机制中。BLf控制三个基因的表达并管理这三个组织中的铁沉积。此外,它抑制了铁的增加，铁的增加会促使细胞发生铁凋亡和炎症引起的贫血，从而消除组织中的铁沉积。
目的：在本研究中，我们评估了bLf在皮肤修复过程中的器官水平作用和基因表达变化。
方法：在饲喂高脂饮食（HFD）和PHGPx的雄性SpragueDawley大鼠（180-250g）（n=48）中创建了切除的全层皮肤缺损（FTSD）伤口模型，评价SLC7A11和SLC40A1基因与铁代谢的关系。将动物随机分为6组：1-对照组，2-bLf（200mg/kg/天，oral),3-FTSD（直径12毫米，背侧)，4-HFD+BLf,5-HFD+FTSD,6-HFD+FTSD+bLf。组织学上,肝脏中的普鲁士蓝染色证明了铁的积累，肾,和肠道组织。用qPCR进行基因表达分析。
结果：组织学，肝脏中的普鲁士蓝染色证明了铁的积累，肾,和肠道组织。在肾脏中检测到普鲁士蓝反应。除SLC40A1基因(P>0.05)外,PHPGx和SLC7A11基因在肾和肝组织中均有统计学意义(P<0.05)。在大鼠肠组织分析中，这三个基因的表达变化无统计学意义（P=0.057）。
结论：在由伤口形成引发的器官水平的铁损伤机制中。BLf控制三个基因的表达并管理这三个组织中的铁沉积。此外,它抑制了铁的增加，铁的增加会促使细胞发生铁凋亡和炎症引起的贫血，从而消除组织中的铁沉积。
