Osteoarthritis (OA) is a joint disease characterized by inflammation and cartilage
degradation. Accumulating evidence has demonstrated that luteolin, a natural flavonoid,
has anti-inflammatory and anticatabolic effects. The present study aimed to assess
the protective effect of luteolin on interleukin (IL)-1β-stimulated rat chondrocytes
and a monosodium iodoacetate (MIA)-induced model of OA. Rat chondrocytes were pretreated
with luteolin (0, 25, 50, and 100 μM for 12 h) prior to stimulation with IL-1β (10 ng/ml
for 24 h). Nitric oxide (NO) production was determined using the Griess method. Production
of prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), and matrix metalloproteinase-2,
-8, and -9 (MMP-2, MMP-8 and MMP-9) was measured by an enzyme-linked immunosorbent
assay (ELISA). Protein levels of inducible nitric oxide synthase (iNOS), cyclooxygenase-2
(COX-2), MMP-1, MMP-3, MMP-13, p65, p-p65, IκB, and p-IκB were determined by Western
blotting. The OA rats received luteolin (10 mg/kg/day) by gavage in vivo. Morphological
and ultrastructural scanning electron microscopy (SEM) observations were performed
to assess the severity of OA at 45 days following MIA injection. Collagen II protein
expression was determined by immunohistochemistry. In this study, luteolin considerably
reduced the IL-1β-induced production of NO, PGE2, TNF-α, MMP-2, MMP-8 and MMP-9 and
the expression of COX-2, iNOS, MMP-1, MMP-3 and MMP-13. Luteolin reversed the degradation
of collagen II induced by IL-1β. Luteolin also significantly inhibited IL-1β-induced
phosphorylation of NF-κB in vitro. Luteolin treatment prevented cartilage destruction
and enhanced collagen II expression in OA rats in vivo. Overall, our findings suggest
that luteolin may be a useful therapeutic agent for patients with OA.