Sinomenine retards LPS-elicited inflammation via down-regulating CCAT1 in HaCaT cells

The initiation of pressure ulcers is accompanied by inflammation. Sinomenine emerges as a potential anti-inflammation agent. The aim of this study was to corroborate its anti-inflammatory property in skin keratinocyte HaCaT cells. Long non-coding RNA colon cancer associated transcript-1 (CCAT1)-associated mechanisms were also investigated.

HaCaT cells were stimulated with lipopolysaccharide (LPS) for 6 h after sinomenine pre-administration. Transfection was carried out to induce CCAT1 overexpression or silence it in HaCaT cells. Viability and apoptosis of HaCaT cells were determined by MMT and observed using flow cytometry, respectively. Protein expression was quantified using Western blot or ELISA. CCAT1 was measured by qRT-PCR.

LPS notably decreased cell viability and exaggerated apoptosis with the cleavage of caspase-3/-9. The secretion of inflammatory factors was promoted. Sinomenine pre-administration maintained cell viability, blocked apoptosis and relieved inflammation with the decrease in cleaved caspase-3/-9 and inflammatory factors. LPS-induced phosphorylation of p65, IκBα and p38MAPK and overexpression of CCAT1 were precluded by sinomenine. CCAT1 overexpression, which per se induced inflammatory lesions, negated the positive effects of sinomenine with the restored phosphorylation of p65, IκBα, and p38MAPK.

Sinomenine played a protective role against LPS-induced inflammation. The anti-inflammatory activity of sinomenine might be mediated by CCAT1 down-regulation.