Dataset Information

Curcumin Attenuates Liver Fibrosis and Inflammation by Modulating Slamf8-Mediated TNF/NF-κB Signaling

ABSTRACT: Liver fibrosis (LF) is characterized by inflammation and fibrosis following liver injury. Curcumin has anti-inflammatory, antioxidant, and cytoprotective properties, with benefits in managing liver diseases. However, the specific mechanisms underlying these effects remain obscure. This work aims to probe into the potential mechanism of curcumin treating LF.We used CCL4 to construct a liver fibrosis model and treated with low, medium, and high concentrations of curcumin. Subsequently, we collected liver tissues and performed RNA sequencing to identify potential targets and associated signaling pathways affected by curcumin treatment. The results showed that curcumin significantly reduced liver damage in mice induced with carbon tetrachloride. RNA sequencing results indicated that Slamf8 was a likely target and the Slamf8 expression was notably decreased in the curcumin group. According to in vivo and vitro results, curcumin inhibited the TNF/NF-κB pathway via Slamf8 modulation, reducing release of pro-inflammatory cytokines (IL-6, IL-17A, MCP-1). Curcumin also suppressed the expression of LF-associated proteins, including α-SMA, COL1A1 and FN. In summary, curcumin exerts potent anti-fibrotic and anti-inflammatory effects by modulating Slamf8 to influence the TNF/NF-κB pathway, thus protecting the liver.

ORGANISM(S): Mus musculus

PROVIDER: GSE299517 | GEO | 2026/06/11

REPOSITORIES: GEO

ACCESS DATA

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Project description:Long non-coding RNAs (lncRNAs) are transcripts of more than 200 nucleotides that are not translated into functional proteins. Cellular lncRNAs have been shown to act as regulators by interacting with target nucleic acids or proteins and modulating their activities. We investigated the role of RNA1.2, which is one of four major lncRNAs expressed by human cytomegalovirus (HCMV), by comparing the properties of parental virus in vitro with those of deletion mutants lacking either most of the RNA1.2 gene or only the TATA element of the promoter. In comparison with parental virus, these mutants exhibited no growth defects and minimal differences in viral gene expression in human fibroblasts. In contrast, 76 cellular genes were consistently up- or down-regulated by the mutants at both the RNA and protein levels at 72 hours after infection. Differential expression of the gene most highly upregulated by the mutants (Tumor protein p63-regulated gene 1-like protein; TPRG1L) was confirmed at both levels by RT-PCR and immunoblotting. Consistent with the known ability of TPRG1L to upregulate IL-6 expression via NF-κB stimulation, RNA1.2 mutant-infected fibroblasts were observed to upregulate IL-6 in addition to TPRG1L. Comparable surface expression of TNF receptors and responsiveness to TNF-α in cells infected by the parental and mutant viruses indicated that activation of signaling by TNF-α is not involved in upregulation of IL-6 by the mutants. In contrast, inhibition of NF-κB activity and knockdown of TPRG1L expression reduced the extracellular release of IL-6 by RNA1.2 mutant-infected cells, thus demonstrating that upregulation of TPRG1L activates NF-κB. The levels of CCL2 and CXCL1 transcripts were also increased in RNA1.2 mutant-infected cells, further demonstrating the presence of active NF-κB signalling. These results suggest that RNA1.2 plays a role in manipulating intrinsic NF-B-dependent cytokine and chemokine release during HCMV infection , thereby impacting downstream immune responses.

Dataset Information

Curcumin Attenuates Liver Fibrosis and Inflammation by Modulating Slamf8-Mediated TNF/NF-κB Signaling

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets