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- Title
KLF7 promotes LPS induced apoptosis, inflammation, and oxidative stress in H9c2 cells by activating NF-κB pathway.
- Authors
Guoyong Hu; Minjie Zhou; Lina Xu; Donglian Wang
- Abstract
This study aimed to investigate and explore the molecular mechanisms of Krüppel-like factor 7 (KLF7) on apoptosis, inflammation, and oxidative stress in H9c2 cells. In the study, the protein expression of KLF7 in H9c2 cells were ascertained by western blot after lipopolysaccharide (LPS) treatment and small interfering RNA (siRNA) transfection. The results confirmed that the expression levels of the protein KLF7 were dramatically increased after LPS treatment and decreased after siRNA transfection. Then, the viability of the LPS treated and siRNA transfected H9c2 cells was tested by cell counting kit-8 (CCK8) assay and enzyme-linked immunosorbent assay (ELISA). The results indicated that down-regulation of KLF7 inhibited LPS-induced injury of H9c2 cells. Flow cytometry assays were applied to test the apoptosis of H9c2 cells, and cell apoptosis-associated proteins in H9c2 cells were also examined by western blot. The results showed that down-regulation of KLF7 inhibited LPS-induced apoptosis of H9c2 cells. The inflammation and oxidative stress related factors, subsequently tested by quantitative polymerase chain reaction (q-PCR) and ELISA, supported the inhibition of LPS-induced oxidative stress in H9c2 cells by the down-regulation of KLF7. Finally, the western blot assays were employed to determine the expression of NF-κB p65 and IκBα after LPS treatment and siRNA transfection. These findings proved that KLF7 promotes LPS-induced apoptosis, inflammation, and oxidative stress in H9c2 cells via activating NF-κB pathway, which hinted that KLF7 knockdown could be a potential therapeutic approach for the treatment of sepsis.
- Subjects
OXIDATIVE stress; ENZYME-linked immunosorbent assay; APOPTOSIS; KRUPPEL-like factors; SMALL interfering RNA; POLYMERASE chain reaction
- Publication
ScienceAsia, 2022, Vol 48, Issue 5, p642
- ISSN
1513-1874
- Publication type
Article
- DOI
10.2306/scienceasia1513-1874.2022.092