Rheumatoid arthritis is primarily associated with
inflammation and increased level of proinflammatory
cytokines which are released by immune cells, macrophages or activation of
arachidonic acid metabolism. The expression of these
cytokines, oxidative
free radicals and the activation of COX-2
enzymes are crucial targets for chronic
inflammation. On the basis of established anti-inflammatory efficacy of
nerolidol, the primary study was further appraised to determine its approach against Freund's complete adjuvant (CFA) rheumatoid model.
Arthritis was induced by inoculation of 0.1 mL CFA injection into the left hind footpad of rats. Anti-arthritic potential of
nerolidol (at 200, 400 and 800 mg/kg doses) was assessed by measuring the paw volume,
body weight, serum analysis, histopathological and radiographs of ankle joints. Expressions of
cytokine's panels such as
IL-10,
IL-4, COX-2,
NF-kB, TNF-α,
IL-6, PGE-2 and IL-1β were determined by real-time qPCR.
Antioxidant enzyme analyses were conducted by measuring the SOD, POD and
catalase activity from serum and equated with arthritic control group.
Nerolidol prevented
body weight loss, stabilized biochemical and haematological homeostasis and significantly reduced the paw volume. Furthermore, X-ray and histopathological assessment of ankle joints showed an improvement in the joint structure of rats treated with
nerolidol. Besides that, overexpression of gene pointers like TNF-α, IL-1β,
IL-6,
NF-kB, PGE-2 and COX-2 in CFA-treated control rats were also reversed with
nerolidol. This anti-arthritic mechanism was further supported by the increased level of
IL-10,
IL-4 and serum
antioxidant activity. The present findings demonstrate that
nerolidol reduced
adjuvant arthritis by downregulating the proinflammatory
cytokines and upregulating the aforementioned anti-inflammatory
cytokines and may be used as a therapeutic substance for the management of human
rheumatoid arthritis.