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The pathogenesis of systemic sclerosis (SSC) fibrosis involves the rapid proliferation of skin fibroblasts, and current anti-fibrotic treatments are limited. This study investigated the relationship between ferroptosis and SSC skin fibroblasts. We observed that erastin-induced ferroptosis was suppressed in SSC fibroblasts. RSL3, a direct inhibitor of Glutathione Peroxidase 4 (GPX4), significantly reduced the viability of the fibroblasts, and upregulation of GPX4 in the SSC fibroblasts contributed to ferroptosis resistance. Furthermore, we demonstrated that transferrin receptor 1 (TfR1) was a crucial transporter for iron deposition in the fibroblasts. Collectively, our results highlight that GPX4 inhibition could enhance the sensitivity to ferroptosis by SSC fibroblasts, which showed distinct characteristics of iron metabolism that were not observed in normal fibroblasts in this study. Taken together, these results suggest that targeting ferroptosis could be a therapeutic strategy for the treatment of SSC. [Display omitted] • Upregulation of GPX4 in SSC skin fibroblasts contributed to Erastin resistance. • TfR1 was a crucial transporter for iron deposition in SSC skin fibroblasts. • Downregulation of Ft-H and Ft-L indicated that cellular iron storage was inhibited in SSC fibroblasts. • NRF2 was decreased in SSC fibroblasts. [ABSTRACT FROM AUTHOR]

• C3G could shield apoptosis induced by ZEN, which may be connected with the changes of lncRNA expression profiles in porcine granulosa cells (pGCs). • The DELs were related to cell metabolism and PI3K-AKT signaling pathways. • This study complements our understanding of the genetic basis and molecular mechanisms by which C3G mitigates the toxicity of ZEN in pGCs. Long non-coding RNA (lncRNA), a class of RNA molecules with transcripts longer than 200 nt, is crucial for maintaining animal reproductive function. Zearalenone (ZEN) damaged animal reproduction by targeting ovarian granulosa cells (GCs), especially in pigs. Nonetheless, it is not quite clear that whether Cyanidin-3-O-glucoside (C3G) exert effects on porcine GCs (pGCs) after ZEN exposure by altering lncRNA expression. Here, we sought to gain novel information regarding C3G protect against damages induced by ZEN in pGCs. The pGCs were divided into control (Ctrl), ZEN, ZEN + C3G (Z + C), and C3G groups. Results revealed that C3G effectively increased cell viability and suppressed ZEN-induced apoptosis in pGCs. 87 and 82 differentially expressed lncRNAs (DELs) were identified in ZEN vs. Ctrl and Z + C vs. ZEN group, respectively. Gene Ontology (GO) analysis observed that the DELs were related to cell metabolism and cell-matrix adhesion biological processes. The Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis found that the DELs were associated with the phosphatidylinositide 3-kinases (PI3K)-protein kinase B (AKT) signaling pathway. In brief, we demonstrated that C3G could shield apoptosis induced by ZEN, which may be connected with the changes of lncRNA expression profiles in pGCs. This study complemented our understanding of the genetic basis and molecular mechanisms by which C3G mitigated the toxicity of ZEN in pGCs. [ABSTRACT FROM AUTHOR]

LPS-induced injury in lung epithelial cells is a crucial part of the process of acute lung injury (ALI). The aim of this study is to explore whether Xanthorrhizol, a medicine that has antioxidant and anti-inflammatory activity, could mitigate the injury of lung epithelial cells caused by LPS. Mouse lung epithelial cell line (MLE-12 cells) were treated with LPS in the absence and presence of Xanthorrhizol. As a results, we observed that LPS could induce MLE-12 cells death, mitochondrial dysfunction, oxidative stress and inflammation, and activate MAPK signaling pathways. However, Xanthorrhizol mitigated the injury in MEL-12 caused by LPS by promoting cell viability and MDA, GSH production as well as inhibiting LDH release, mitochondria damage, IL-1β, IL-6 and TNF-α production and the phosphorylation levels of ERK, P38 and JNK. Our results indicated that Xanthorrhizol could protect lung epithelial cells from LPS-induced injury, more likely by inhibiting the phosphorylation of MAPK pathway related proteins. • Xanthorrhizol mitigates LPS-induced death in lung epithelial cells. • Xanthorrhizol alleviates the damage of mitochondria in lung epithelial cells induced by LPS. • Xanthorrhizol diminish oxidative stress and inflammation in lung epithelial cell caused by LPS. • Xanthorrhizol inhibits MAPK pathway activation in LPS-induced lung epithelial cell. [ABSTRACT FROM AUTHOR]