| First Author | Shi Y | Year | 2020 |
| Journal | Mol Med Rep | Volume | 22 |
| Issue | 4 | Pages | 3117-3126 |
| PubMed ID | 32945469 | Mgi Jnum | J:305707 |
| Mgi Id | MGI:6705292 | Doi | 10.3892/mmr.2020.11426 |
| Citation | Shi Y, et al. (2020) Increased expression levels of inflammatory cytokines and adhesion molecules in lipopolysaccharideinduced acute inflammatory apoM/ mice. Mol Med Rep 22(4):3117-3126 |
| abstractText | Apolipoprotein M (apoM) may serve a protective role in the development of inflammation. Nuclear factorkappaB (NFkappaB) and its downstream factors (including a number of inflammatory cytokines and adhesion molecules) are essential for the regulation of inflammatory processes. In the present study, the importance of apoM in lipopolysaccharide (LPS)induced acute inflammation and its potential underlying mechanisms, were investigated using an apoMknockout mouse model. The levels of inducible nitric oxide synthase (iNOS), NFkappaB, interleukin (IL)1beta, intercellular adhesion molecule 1 (ICAM1) and vascular cell adhesion protein 1 (VCAM1) were detected using reverse transcriptionquantitative PCR and western blotting. The serum levels of IL6 and IL10 were detected using Luminex technology. The results demonstrated that the protein levels of iNOS, NFkappaB, IL1beta, ICAM1 and VCAM1 were significantly increased in apoM/ mice compared with those in apoM+/+ mice. In addition, twoway ANOVA revealed that the interaction between apoM and LPS had a statistically significant effect on a number of factors, including the mRNA expression levels of hepatic iNOS, NFkappaB, IL1beta, ICAM1 and VCAM1. Notably, the effects of apoM and 10 mg/kg LPS on the levels of IL6 and IL10 were the opposite of those induced by 5 mg/kg LPS, which could be associated with the dual anti and proinflammatory effects of IL6 and IL10. Collectively, the results of the present study revealed that apoM is an important regulator of inflammatory cytokine and adhesion molecule production in LPSinduced inflammation, which may consequently be associated with the severity of inflammation. These findings indicated that the antiinflammatory effects of apoM may partly result from the inhibition of the NFkappaB pathway. |
