Abstract
To investigate the anti-inflammatory effects of high-density lipoprotein (HDL) in mice with rheumatoid arthritis (RA) induced by collagen. Male DBA/1 mice (8-week-old) were divided into three groups: control (treated with saline), collagen-induced arthritis (CIA), and CIA + HDL. CIA was induced with bovine type II collagen, and after the injection of bovine type II collagen, the CIA + HDL group received an injection of HDL on day 28 followed by HDL injections four times every 3 days. Mice were weighed, the paws were scored, and paw thickness was measured beginning on day 21. Additionally, the levels of tumor necrosis factor-alpha (TNF-α) and IL-6 were measured by ELISA kits, tissue sections of paws were stained with hematoxylin and eosin, and the inflammatory signaling pathway was analyzed by western blotting. We found that the production of pro-inflammatory cytokines TNF-α and IL-6 in mice which received HDL decreased 45.14 and 35.02%, respectively. And we also found that HDL could significantly decrease the level of anti-type-II-collagen IgG2a and inhibit the neutrophil infiltration and cell proliferation and protect the ankle joint from type II collage-induced injury. Western blot analysis indicated that HDL could also inhibit the activation of the NF-κB, MAPK, and ERK signaling pathways in RA mice. HDL can inhibit the inflammation induced by bovine type II collagen and the development of RA.
Highlights
In 1993, Levine et al reported that the increase in the plasma levels of tumor necrosis factor-alpha (TNF-α), as well as the mortality rates caused by endotoxin, were reduced in transgenic mice in which plasma levels of high-density lipoproteins (HDLs) were twofold higher than normal [1]
Changes in the body weights of the mice in each group showed that the collagen-induced arthritis (CIA) model group and the CIA + HDL treatment group began to decrease on day 28
We found that HDL suppressed CIA development and protected against morphological and anatomical joint destruction
Summary
In 1993, Levine et al reported that the increase in the plasma levels of tumor necrosis factor-alpha (TNF-α), as well as the mortality rates caused by endotoxin (lipopolysaccharide), were reduced in transgenic mice in which plasma levels of high-density lipoproteins (HDLs) were twofold higher than normal [1]. HDL has been shown to reduce monocyte CD11b expression and migration along a monocyte chemotactic protein-1 gradient. Rheumatoid arthritis (RA) is a systemic inflammatory autoimmune disease that causes joint destruction, as evidenced by radiological findings, such as joint space narrowing and bone erosion, which are related to functional disability. Both B cells and T cells aggregate in the synovium of inflamed joints and mediate the pathogenesis of RA. In this study, we used an RA mouse model to investigate the anti-inflammatory effect of HDL on collagen-induced arthritis (CIA) in mice
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