Ferrostatin-1 alleviates lipopolysaccharide-induced cardiac dysfunction

Zheng, Xiaojiao; Kong, Bin; Jin, Fu; Qin, Tianyou; Dai, Chang; Shuai, Wei; Huang, He

doi:10.1080/21655979.2021.2001913

Cited by 128 publications

(82 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The HE staining reagent was provided by Solarbio Life Sciences. The pathological changes of the kidney and liver tissues were observed under a light microscope (magnification × 200) [ 16 ].…”

Section: Methodsmentioning

confidence: 99%

Dexpanthenol attenuates inflammatory damage and apoptosis in kidney and liver tissues of septic mice

2022

View full text Add to dashboard Cite

Sepsis is capable of causing systemic infections resulting in multiple organ damage. Dexpanthenol (DXP) has been reported to protect against kidney and liver injury. Therefore, this paper attempts to explore the role of DXP in sepsis-induced kidney and liver injury. A mice model of sepsis was established using the cecal ligation and puncture (CLP) method. The expressions of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and monocyte chemoattractant protein (MCP)-1 in the serum of mice were measured utilizing enzyme linked immunosorbent assay (ELISA). Additionally, the damage of kidney and liver tissues in CLP-induced mice was determined by their respective commercial kits, western blot, and hematoxylin–eosin (HE) staining kits. The apoptosis of kidney and liver tissues in CLP-induced mice was assessed by means of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and western blot. It was observed that DXP decreased the expressions of TNF-α, IL-1β, IL-6, and MCP-1 in the serum of CLP-induced mice, attenuated the functional impairment, pathological damage, inflammation, and cell apoptosis of kidney tissue. Meanwhile, DXP decreased the functional impairment of liver in CLP-induced mice, reduced the levels of inflammatory factors and antioxidant enzymes, attenuated liver pathological damage, and decreased cell apoptosis in liver tissues. In conclusion, DXP attenuates inflammatory damage and apoptosis in kidney and liver organs in a sepsis model.

show abstract

Section: Methodsmentioning

confidence: 99%

Dexpanthenol attenuates inflammatory damage and apoptosis in kidney and liver tissues of septic mice

2022

View full text Add to dashboard Cite

show abstract

“…Currently, many researchers have demonstrated that ferroptosis was associated with sepsis ( Wei et al, 2020 ; Wang et al, 2021 ; Xiao et al, 2021 ). However, it is not common to construct miRNA-mRNA regulatory networks of FRGs in SCM and to predict its biomarkers.…”

Section: Discussionmentioning

confidence: 99%

Identification and Validation of Ferroptosis-Related Biomarkers in Septic Cardiomyopathy via Bioinformatics Analysis

et al. 2022

View full text Add to dashboard Cite

Septic cardiomyopathy (SCM) is a cardiac dysfunction caused by severe sepsis and septic shock that increases the risk of heart failure and death and its molecular mechanism remains unclear. Ferroptosis, a novel form of programmed cell death, has been reported to be present in the heart tissue of patients with sepsis, which demonstrated that ferroptosis may be a potential mechanism of myocardial injury in SCM. Therefore, we explored the role of ferroptosis-related genes (FRGs) in SCM and aimed to identify pivotal ferroptosis-related targets in SCM and potential therapeutic targets involved in the pathological process of SCM. To explore the regulatory mechanisms of ferroptosis in SCM, we identified differentially expressed genes (DEGs) in SCM and FRGs by bioinformatics analysis, and further identified hub genes. And the crucial microRNAs (miRNAs)-FRGs regulatory network was subsequently constructed. Finally, several candidate drugs associated with the hub genes were predicted, and Real-time quantitative reverse Transcription PCR (qRT-PCR) and western blotting analysis were performed to confirm the abnormal expression of hub genes. In this study, we identified several FRGs that may be involved in the pathogenesis of SCM, which helps us further clarify the role of ferroptosis in SCM and deeply understand the molecular mechanisms and potential therapeutic targets of SCM.

show abstract

“…According to the previous study [ 24 ], LEC cells were lysed with radioimmunoprecipitation assay buffer supplemented with protease inhibitors (P0013C; Beyotime). The liquid was aspirated and centrifuged to collect the protein for quantification.…”

Section: Methodsmentioning

confidence: 99%

Toll-like receptor 3 gene regulates cataract-related mechanisms via the Jagged-1/Notch signaling pathway

Xie

Wang

et al. 2022

Bioengineered

View full text Add to dashboard Cite

Epithelial-melancholy transition (EMT) is the main cause of organ fibrosis and a common pathogenetic mechanism in most cataracts. This study aimed to explore the molecular mechanism of Toll-like receptor (TLR)-3 in the occurrence and development of post-cataract EMT and to provide new ideas for the prevention and treatment of posterior capsule opacification (PCO). In the presence or absence of TLR3, the human lens epithelial cell (LEC) line, SRA01/04, was treated with the transforming growth factor (TGF)-β2. Cell counting kit-8 (CCK-8) and Transwell assays were used to analyze the cell proliferation, migration, and invasion. The expression levels of proteins and RNAs were detected by western blotting and quantitative polymerase chain reaction (qPCR) experiments. Functional gain and loss studies showed that TLR3 regulates the proliferation, migration, and invasion of LECs and EMT induced by TGF-β2. Moreover, TLR3 regulates the expression of Jagged-1, Notch-1, and Notch-3 These findings indicate that TLR3 prevents the progression of lens fibrosis by targeting the Jagged-1/Notch signaling pathway to regulate the proliferation, migration, and invasion of LECs, and TGF-β2-induced EMT. Therefore, the TLR3-Jagged-1/Notch signaling axis may be a potential therapeutic target for the treatment of fibrotic cataracts.

show abstract

Ferrostatin-1 alleviates lipopolysaccharide-induced cardiac dysfunction

Cited by 128 publications

References 36 publications

Dexpanthenol attenuates inflammatory damage and apoptosis in kidney and liver tissues of septic mice

Dexpanthenol attenuates inflammatory damage and apoptosis in kidney and liver tissues of septic mice

Identification and Validation of Ferroptosis-Related Biomarkers in Septic Cardiomyopathy via Bioinformatics Analysis

Toll-like receptor 3 gene regulates cataract-related mechanisms via the Jagged-1/Notch signaling pathway

Contact Info

Product

Resources

About