Effect of sandalwood oil on inhibition of reactive oxygen species generation and lipopolysaccharideinduced inflammation through down-regulation of the nuclear factor-κB signaling pathways

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.

Section: Discussionmentioning

confidence: 99%

KLF7 promotes LPS induced apoptosis, inflammation, and oxidative stress in H9c2 cells by activating NF-κB pathway

Hu¹,

Zhou²,

Xu³

et al. 2022

“…Thus, we supposed that DUB3 may regulate EZH2 to affect cancer progression. Nuclear factor-kappaB (NF-κB) is a transcription factor that induces signal transduction between nucleus and cytoplasm in many cell types [13]. Hypoxia-inducible factor-1α (HIF-1α) is a subunit of HIF-1 transcriptional factor [14].…”

Section: Introductionmentioning

confidence: 99%

DUB3 contributes to colorectal cancer cell migration and angiogenesis via NF-κB/HIF-1α

Yang¹,

Hui²,

Bai³

et al. 2022

Colorectal cancer (CRC) is a common malignancy with poor prognosis. This study aimed to explore the role of deubiquitinase 3 (DUB3) in CRC cell migration and angiogenesis as well as its molecular mechanism. HCT116 cells were transfected with DUB3 or EZH2 siRNA, or vectors overexpressing EZH2/HIF-1α. CCK8 and colony formation assay were used to assess cell proliferation; wound healing assay and Transwell assay were performed to determine cell migration and invasion; angiogenesis in CRC was detected using tube formation assay; WB was used to measure the protein levels of DUB3, EZH2, p65, p-p65, and HIF-1α. DUB3 downregulation inhibited proliferation, migration, invasion, and angiogenesis in CRC cells. Moreover, DUB3 could positively regulate NF-κB/HIF-1α pathway through EZH2. Overexpression of HIF-1α reversed the effects of DUB3 knockdown on CRC cell proliferation, migration, invasion, and angiogenesis. DUB3 contributes to CRC metastasis and angiogenesis by regulating NF-κB/HIF-1α pathway via EZH2, which may indicate a novel insight for the pathogenesis of CRC.

“…At present, the main treatment of these diseases is limited to dental/surgical repair, antibiotics, and nonsurgical mechanical debridement [3]. Lipopolysaccharide (LPS) is a main component of the outer membrane of Gram-negative bacteria, which can cause inflammation [4,5]. In vivo assays showed that LPS promotes the osteoclastic activity by upregulating the expression of Receptor Activator for Nuclear Factor-κB Ligand (RANKL) [6].…”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide promotes the osteoclastogenesis through the autophagic degradationof TNF receptor-associated factor 3

Hu¹,

Zeng²,

Song³

et al. 2022

Lipopolysaccharide (LPS) is a pro-osteoclastogenic factor and autophagic activator. TNF receptorassociated factor (TRAF) 3, an anti-osteoclastogenic factor, can be degraded by autophagic activation. The effect of LPS on the level of TRAF3 during the osteoclastogenesis keeps vague. In this study, we investigated the roles of LPS in the expression patterns of TRAF3 in vivo and in vitro. Combined with the application of autophagic pharmacological inhibitors, we observed the significance of LPS-regulated autophagy in TRAF3 protein level. Moreover, we explored the effects of TRAF3 on LPS-induced osteoclastogenesis using gain-of-function and loss-of-function assays in vitro.Our study showed that LPS could reduce the protein level of TRAF3 in osteoclast precursors (OCPs) in vitro and in vivo, while no affecting the mRNA expression of TRAF3. In addition, TRAF3 overexpression reversed LPS-induced osteoclastogenesis. Importantly, LPS-inhibited TRAF3 protein level was recovered by autophagic inhibition with chloroquine or bafilomycin. Furthermore, LPS-induced osteoclastogenesis was suppressed by chloroquine, which was reversed by TRAF3 silencing. In conclusion, LPS can promote the autophagic degradation of TRAF3, which serves as an indispensable underlying mechanism in LPS-induced osteoclastogenesis.