Research articles
ScienceAsia 48 (2022):ID 642-649 |doi:
10.2306/scienceasia1513-1874.2022.092
KLF7 promotes LPS induced apoptosis, inflammation, and
oxidative stress in H9c2 cells by activating NF-κB pathway
Guoyong Hua, Minjie Zhoua,* , Lina Xub, Donglian Wanga
ABSTRACT: This study aimed to investigate and explore the molecular mechanisms of Kr?ppel-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-?B p65 and I?B? 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-?B pathway, which hinted that KLF7 knockdown could be a potential therapeutic approach
for the treatment of sepsis.
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| a |
Department of Emergency Medicine, Shanghai Jiao Tong University Affiliated Sixth People?s Hospital,
Shanghai 201306 China
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| b |
Department of Infectious Medicine, Shanghai Jiao Tong University Affiliated Sixth People?s Hospital,
Shanghai 201306 China |
* Corresponding author, E-mail: Mj_Zhou1635@163.com
Received 10 Jan 2022, Accepted 7 Apr 2022
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