The aim of this study was to investigate the inhibitory effect of
salvianolic acid on inflammatory mediators of rats with
collagen-induced
rheumatoid arthritis (RA). Thirty rats were randomly divided into the normal control group,
collagen-induced arthritis model group (CIA model group) and
drug group (
Salvianolic Acid-CIA group). In the model group, the CIA models were established through
intradermal injection of
collagen emulsion at the toes. At 3 weeks after the model establishment, grouped
drug administration was conducted, of which
salvianolic acid was given by gavage to
Salvianolic Acid-CIA group. The degrees of joint swelling of each group of rats were recorded.
Enzyme-linked
immunosorbent assay (ELISA) was applied to detect the levels of relevant inflammatory mediators, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to measure the
messenger RNA (
mRNA) expression levels of serum
necrosis factor-alpha (TNF-α),
interleukin-6 (IL-6) and
prostaglandin E2 (
PGE2), and
hematoxylin and
eosin staining was utilized to detect the pathological characteristics of the synovial tissues. After the establishment of models, the ankle joint swelling degree of rats in the model group was more obvious compared with that in the normal control group (P<0.01). After 3 weeks of
drug administration, the ankle joint swelling degree of rats in the
Salvianolic Acid-CIA group was alleviated compared with that in the model group (P<0.05). The contents of TNF-α,
IL-6 and
PGE2 in
Salvianolic Acid-CIA group were obviously lower than those in the model group (P<0.01). The
mRNA expression levels of TNF-α,
IL-6 and
PGE2 in the
Salvianolic Acid-CIA group were markedly lower than those in the model group. The
hyperemia of rat synovial tissues in
Salvianolic Acid-CIA group was obviously relieved compared with that in the CIA model group. In conclusion, the models of CIA rats are successfully established, and the results show
salvianolic acid has an inhibitory effect on the RA of CIA model rats and can significantly inhibit the expression levels of relevant inflammatory mediators.