Coenzyme Q10 (CoQ10) is a biosynthesized quinone with 10 isoprene side chains in humans. To investigate the anti-inflammatory and wound healing effect of CoQ10, we performed in vivo and in vitro experiments. In vivo studies, there were 3 groups; Naive (without skin incision), Control (with skin incision) and CoQ10 (100 mg/kg treatment with skin incision). Collagen-like polymer (CLP) level of CoQ10 group was increased significantly compared to the control group (p<0.05). Also, CoQ10 group showed significant inhibition on myeloperoxidase (MPO) and PLA(2) level compared to the control group (p<0.05). These data show that CoQ10 may have an anti-inflammatory and a wound healing effect. CoQ10 showed significant antioxidant activity in vivo on malondialdehyde (MDA) and superoxide dismutase (SOD) levels compared to the control group (p<0.05). Although CoQ10 did not show antioxidant activity in cell free system of DPPH radical scavenge, it had a potent antioxidant activity in cell culture system of both silica- and zymosan-induced reactive oxygen species generation using Raw 264.7 cells. This result may be associated with the conversion of CoQ10 to the reduced form (CoQ10H(2)) in the presence of some kinds of intracellular reducing agents. In conclusion, it is considered that CoQ10 appears to have a cutaneous healing effect in vivo, which may be related to the secondary action of CoQ10.

Previously, we reported that dibenzylbutyrolactone lignans (DBLLs) from the fruit of Forsythia koreana NAKAI (Oleaceae) has anti-inflammatory, antioxidant, and anti-asthmatic effects. In this study, to clarify the antiinflammatory mechanisms of DBLL, we evaluated the effects of DBLLs on lipopolysaccharide-stimulated inducible nitric oxide synthetase (iNOS) and cyclooxygenase-2 (COX-2) expressions, nitric oxide (NO) and prostaglandin E 2 (PGE 2 ) productions, nuclear factor-kB (NF-kB) and mitogen-activated protein kinase (MAPK) activations, inhibitor of kB (IkB) and inhibitor of kB kinase (IKK) phosphorylations in cytosolic proteins, and cytotoxicity in Raw264.7 cells. DBLLs potently suppressed both the enzyme expression and DNA-binding activity of NF-kB. Arctiin, arctigenin (1.0 mM) and matairesinol (10 mM) inhibited the expression of iNOS by 37.71؎ 2.86%, 32.51؎4.28%, and 27.44؎2.65%, respectively, and arctiin, arctigenin (0.1 mM) and matairesinol (1.0 mM) inhibited COX-2 expression by 37.93؎7.81%, 26.70؎4.61% and 29.37؎5.21%, respectively. The inhibitory effects of DBLLs on NO and PGE 2 productions were the same patterns as those seen for the reductions in iNOS and COX-2 expression, respectively. Arctiin, arctigenin (1.0 mM) and matairesinol (10 mM) significantly (pϽ0.05) inhibited NF-kB DNA binding by 44.85؎6.67%, 44.16؎6.61%, and 44.79؎5.62%, respectively, and arctiin (0.1 mM) and arctigenin (1.0 mM) significantly (pϽ0.05) inhibited the phosphorylation of IkB by 20.58؎3.86% and 25.99؎6.18%, respectively. Furthermore, arctiin, matairesinol (1.0 mM) and arctigenin (10 mM) inhibited the phosphorylation of IKK by 38.80؎6.64%, 38.33؎6.65%, and 38.57؎8.14%, respectively. In addition, DBLLs potently inhibited the lipopolysaccharide (LPS)-induced activation of MAPKs (SAPK/c-Jun NH 2 -terminal kinase (JNK), p38, and extracellular signal receptor-activated kinase (ERK)1/2). Overall, arctiin was the most effective; its effect was nearly the same as that of 10 mM helenalin. These findings suggest that treatment with non-toxic DBLLs inhibits not only NF-kB and NF-kB-regulated protein activation, but also potently inhibits the activations of specific MAPKs.

No abstract

The root of Aralia cordata is a traditional medicine for the treatment of inflammation, fever, pain, and spasm in the various diseases in Korea. We isolated a dibenzylbutyrolactone diterpene acid, 7-oxosandaracopimaric acid (OSA), from the ether fraction of Aralia cordata MeOH extract, and studied the effect of OSA on phenylquinone (PQ)-induced writhing syndrome and PQ-induced capillary permeability increase, compound 48/80-induced histamine release by peritoneal mast cells, cycloxygenase (COX) activities, and silica-induced RAW 264.7 cell reactive oxygen species production. OSA (30 mg/kg, p.o.) significantly (p < 0.05) inhibited PQ-induced writhes by 25.8% and the PQ-induced capillary permeability increase levels by 33.13% as compared with PQ control. Furthermore, OSA (10 mM) inhibited COX-1 by 22.82 +/- 1.94%, and COX-2 by 15.86 +/- 1.35%, respectively, to the same extent as indomethacin at the same concentration (10 mM). And OSA (3.0 mM) significantly (p < 0.05) inhibited compound 48/80-induced histamine release from rat mast cells, and its activity was similar to that of celebrex (1 mM), but no piracetam (0.1 mM) inhibited them. OSA did not inhibit ROS production in RAW 264.7 cells. These results indicated that OSA has analgesic and anti-inflammatory effects due to its inhibitory effects on capillary permeability, COX activities, and histamine release.

The antioxidant effect of CoQ10 on N-nitrosodiethylamine (NDEA)-induced oxidative stress was investigated in mice. Food intake and body weight were similar in both CoQ10 and control groups during the 3-week experimental period. NDEA significantly increased the activities of typical marker enzymes of liver function (AST, ALT and ALP) both in control and CoQ10 groups. However, the increase of plasma aminotransferase activity was significantly reduced in the CoQ10 group. Lipid peroxidation in various tissues, such as heart, lung, liver, kidney, spleen and plasma, was significantly increased by NDEA, but this increase was significantly reduced by 100 mg/kg of CoQ10. Superoxide dismutase activity increased significantly upon NDEA-induced oxidative stress in both the control and CoQ10 groups with the effect being less in the CoQ10 group. Catalase activity decreased significantly in both the control and CoQ10 groups treated with NDEA, again with the effect being less in the CoQ10 group. The lesser effect on superoxide dismutase and catalase in the NDEA-treated CoQ10 group is indicative of the protective effect CoQ10. Thus, CoQ10 can offer useful protection against NDEA-induced oxidative stress.