ArticleInflammation2020
GFI-1 Protects Against Lipopolysaccharide-Induced Inflammatory Responses and Apoptosis by Inhibition of the NF-κB/TNF-α Pathway in H9c2 Cells.
Article in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- E3 Ubiquitin Ligase FBXO32 Promotes LPS-Induced Cardiac Injury by Regulating ANXA1/PI3K/AKT Signaling.Inflammation · 2025Article
- Growth factor independence 1 ameliorates osteoarthritis by inhibiting chondrocyte ferroptosis via inactivation of MAPK signaling pathway.Journal of orthopaedic translation · 2025Article
- Establishment of a Novel in vitro Model of Sepsis-Induced Myocardial Injury Using Septic Serum: A Comprehensive Comparative Study.Journal of inflammation research · 2025Article
- Article
- FOXO1 regulates NLRP3 inflammasome proteins in LPS-induced cardiotoxicity.American journal of translational research · 2023Article
- Article
- Tannic acid alleviates lipopolysaccharide‑induced H9C2 cell apoptosis by suppressing reactive oxygen species‑mediated endoplasmic reticulum stress.Molecular medicine reports · 2021Article
- Detecting Critical Functional Ingredients Group and Mechanism of Xuebijing Injection in Treating Sepsis.Frontiers in pharmacology · 2021Article
- Screening of the Hepatotoxic Components inMolecules (Basel, Switzerland) · 2019Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Growth factor independence 1 (Gfi-1) has been widely studied for its anti-inflammatory and anti-apoptotic effects. However, whether Gfi-1 has similar effects on H9c2 cardiomyocytes has not yet been reported. In this study, we explored the effect of Gfi-1 on lipopolysaccharide (LPS)-induced inflammatory responses and apoptosis in H9c2 cells. We found that LPS induced the increased expression of TNF-α and IL-6 in the LPS group. After transfection of the Gfi-1 overexpression plasmid, the expression of TNF-α and IL-6 decreased significantly in the LPS + Gfi-1 group. Gfi-1 clearly blocked LPS-induced NF-κB, TNF-α, TNFR1, cleaved-caspase-3 and cleaved-caspase-8 expression and increased Gfi-1 and Bcl-xL expression in H9c2 cells. Similarly, compared with the LPS group, Gfi-1 significantly decreased the expression of cleaved-caspase3/8 and increased the expression of Bcl-xL in the LPS + Gfi-1 group, as verified by immunocytochemical analysis. Furthermore, Gfi-1 markedly inhibited LPS-induced H9c2 cardiomyocyte apoptosis in the LPS + Gfi-1 group, as determined by TEM, TUNEL and flow cytometry. Taken together, these results demonstrate that Gfi-1 may have protective effects against LPS-induced inflammatory responses and apoptosis in H9c2 cells. Gfi-1 may be a novel molecule for treating septic cardiomyopathy.
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