Extract of Pinus densiflora needles suppresses acute inflammation by regulating inflammatory mediators in RAW264.7 macrophages and mice

Abstract

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.

Anti-Amnesia-like Effect of Pinus densiflora Extract by Improving Apoptosis and Neuroinflammation on Trimethyltin-Induced ICR Mice

“…It was confirmed that the expression levels of neuroinflammatory factors in response to TMT-induced tau hyperphosphorylation were improved in all brain tissues due to KRPBE treatment. Similar to these results, P. densiflora needle extract had an anti-inflammatory effect by down-regulating inflammatory mediators such as IL-1β, TNF-α, COX-2, and PGE 2 in LPS-induced RAW 264.7 macrophages and arachidonic acid-induced ICR mouse model [30]. Furthermore, the pine (Pinus morrisonicola Hay.)…”

“…Treatment with KRPBE significantly increased the levels of SOD and reduced GSH, which are representative antioxidant biomarkers in the body, and reduced MDA content through the improvement of the antioxidant system. Moreover, P. densiflora needle ethanol extract was found to have antioxidant and anti-inflammatory effects by suppressing oxidative stress and the production of inflammatory mediators in lipopolysaccharide-induced RAW264.7 macrophages and in the arachidonic acid-induced ICR mouse model [ 30 ]. Pine needle extract significantly attenuated the products of lipid peroxidation in the hippocampus and serum of acute restraint stress mouse models and prevented memory impairment with the regulation of stress hormones, hippocampal excitotoxicity, and oxidative damage [ 31 ].…”

Novel Therapeutic Potentials of Taxifolin for Obesity-Induced Hepatic Steatosis, Fibrogenesis, and Tumorigenesis

“…Taxifolin is also known to suppress proinflammatory cytokine expression in cultured macrophages in vitro and chemically induced liver fibrosis in vivo [ 18 , 39 ]. Several studies suggest the involvement of Nrf-2 (nuclear factor erythroid 2-related factor 2), HO-1 (heme oxygenase 1), and AMPK (AMP-activated protein kinase) as the underlying mechanism of the antioxidative properties of Taxifolin [ 8 , 40 , 41 ]. Given that the NASH pathogenesis is heterogenous and diverse in humans, these pleiotropic effects of Taxifolin may be advantageous for clinical practice.…”

Glucocorticoids in lung cancer: Navigating the balance between immunosuppression and therapeutic efficacy

“…The effects of GCSs on mediators of inflammation and immune responses include: (i) reducing the production of prostaglandin compounds by decreasing the expression of cyclooxygenase II and inhibiting the release of arachidonic acid substrates [ 153 ]; (ii) decreasing the production of numerous cytokines, including TNF-α, cell adhesion molecules, IL-1, IL-3, IL-2, IL-4, IL-6, IL-5, IL-8, and granulocyte-macrophage colony-stimulating factor, largely secondary to the inhibition of gene transcription [ 154 ]; (iii) lowering the concentration of complement components in plasma [ 155 ]; (iv) reducing the production of NO by inducing the production of nitric oxide synthase 2 (NOS2) isoforms [ 156 ]; (v) decreasing the release of histamine and other mediators from basophils and mast cells [ 157 ]; (vi) reducing the production of immunoglobulin G (IgG) [ 158 ]; (vii) increasing the synthesis of anti-inflammatory factors such as IL-10, IL-1 soluble receptor, and clusterin [ 159 ]; (viii) endogenous GCs entering the bloodstream increase in quantity during inflammation and stress events [ 160 ], playing a crucial regulatory role in preventing excessive activation of inflammation and other potent defense responses, which, if left uncontrolled, may lead to a state of dysregulation in the organism [ 161 ].…”