Context
Pinus densiflora
Siebold & Zucc. (Pinaceae) needle extracts ameliorate oxidative stress, but research into their anti-inflammatory effects is limited.
Objective
To investigate antioxidant and anti-inflammatory effects of a
Pinus densiflora
needles (PINE) ethanol extract
in vitro
and
in vivo
.
Materials and methods
We measured levels of reactive oxygen species (ROS), superoxide dismutase (SOD) and inflammatory mediators in lipopolysaccharide (LPS)-stimulated RAW264.7 cells at various PINE concentrations (25, 50 and 100 μg/mL; but 6.25, 12.5 and 25 μg/mL for interleukin-1β and prostaglandin E
2
(PGE
2
)). Thirty ICR mice were randomized to six groups: vehicle, control, PINE pre-treatment (0.1, 0.3 and 1 mg/left ear for 10 min followed by arachidonic acid treatment for 30 min) and dexamethasone. The posttreatment ear thickness and myeloperoxidase (MPO) activity were measured.
Results
PINE 100 μg/mL significantly decreased ROS (IC
50
, 70.93 μg/mL,
p
< 0.01), SOD (IC
50
, 30.99 μg/mL,
p
< 0.05), malondialdehyde (
p
< 0.01), nitric oxide (NO) (IC
50
, 27.44 μg/mL,
p
< 0.01) and tumour necrosis factor-alpha (
p
< 0.05) levels. Interleukin-1β (
p
< 0.05) and PGE
2
(
p
< 0.01) release decreased significantly with 25 μg/mL PINE. PINE 1 mg/ear inhibited LPS-stimulated expression of cyclooxygenase-2 and inducible NO synthase in RAW264.7 macrophages and significantly inhibited ear oedema (36.73–15.04% compared to the control,
p
< 0.01) and MPO activity (167.94–105.59%,
p
< 0.05).
Discussion and conclusions
PINE exerts antioxidant and anti-inflammatory effects by inhibiting the production of inflammatory mediators. Identified flavonoids such as taxifolin and quercetin glucoside can be attributed to effect of PINE.