Detection of F-actin in SCF-induced RPMCs with or without KMP6 and hesperidin.

<p>RPMCs (3×10⁴) were treated with KMP6 (1 mg/ml) or hesperidin (0.01 mg/ml) for 1 h and then stimulated with SCF (50 ng/ml) for 1 h. Confocal images of RPMCs were stained with NBD-phallacidin. F-actin was visualized using a conforcal laser scanning microscope (A). RPMCs treated with SCF exhibited a high fluorescent intensity (B). Results are representative of three independent experiments with duplicated samples. * <i>P</i><0.05, when compared with the medium alone; ** <i>P</i><0.05, when compared with SCF. Blank, unstimualted cells.</p

Inhibitory effect of KMP6 and hesperidin on SCF-induced p38 activation.

<p>RPMCs (3×10⁶) were treated with KMP6 (1 mg/ml), HS-PS (2 mg/ml), hesperidin (0.01 mg/ml), dexamethasone (100 nM), or SB203580 (20 µM) for 1 h and then stimulated with SCF (50 ng/ml) for 10 min. Total protein was prepared and analyzed for phosphorylated p38 MAPK by Western blotting as described in the experimental procedures (A). Phosphorylated p-38 levels were quantitated by densitometry (B). Results are representative of three independent experiments with duplicated samples. * <i>P</i><0.05, when compared with the medium alone; ** <i>P</i><0.05, when compared with SCF. DEX, dexamethasone; SB, SB203580.</p

Docking scores of the ranked poses for complexes between different components and the c-kit protein.

<p>Docking scores of the ranked poses for complexes between different components and the c-kit protein.</p

Inhibitory effect of KMP6 and hesperidin on SCF-induced morphological alteration.

<p>RPMCs (3×10⁴) were treated with KMP6 (1 mg/ml), HS-PS (2 mg/ml), hesperidin (0.01 mg/ml), or dexamethasone (100 nM) for 1 h and then stimulated with SCF (50 ng/ml) for 4 days. Results are representative of three independent experiments with duplicated samples (A). Morphological alteration was assessed by counting the number of RMPCs for 4 days (B). Each datum represents the mean ± S.E.M. of duplicate determinations from three separate experiments. * <i>P</i><0.05, when compared with the medium alone; ** <i>P</i><0.05, when compared with SCF. Blank, unstimulated cells; DEX, dexamethasone.</p

Anti-allergic inflammatory effect of vanillic acid through regulating thymic stromal lymphopoietin secretion from activated mast cells

<p>Vanillic acid, which is well known as a benzoic acid derivative, has been used as a flavouring agent. Currently, we ascertained the therapeutic potential action of vanillic acid on allergic inflammatory reaction in human mast cell line, HMC-1. Treatment with vanillic acid resulted in a significant decrease in levels of thymic stromal lymphopoietin and pro-inflammatory cytokines compared to phorbol 12-myristate 13-acetate and calcium ionophore A23187 (PMACI)-treated HMC-1 cells. In PMACI-stimulated cells, treatment with vanillic acid also dramatically inhibited activities of caspase-1 and nuclear factor-kB (p65). Furthermore, treatment with vanillic acid suppressed phosphorylation of mitogen-activated protein kinases in PMACI-treated HMC-1 cells. Taken together, these findings suggest that vanillic acid has a beneficial effect on allergic inflammatory disorders.</p

Euscaphic acid relieves fatigue by enhancing anti-oxidative and anti-inflammatory effects

Oxidative stress and inflammation are involved in chronic fatigue. Euscaphic acid (EA) is an active compound of Eriobotrya japonica (Loquat) and has anti-oxidative effect. The goal of present study is to prove whether EA could relieve fatigue through enhancing anti-oxidant and anti-inflammatory effects in in vitro/in vivo models. EA notably improved activity of superoxide dismutase (SOD) and catalase (CAT), while EA reduced levels of malondiadehyde (MDA) and inflammatory cytokines without cytotoxicity in H2O2-stimulated in myoblast cell line, C2C12 cells. EA significantly reduced levels of fatigue-causing factors such as lactate dehydrogenase (LDH) and creatin kinase (CK), while EA significantly incresed levels of anti-fatigue-related factor, glycogen compared to the H2O2-stimulated C2C12 cells. In treadmill stress test (TST), EA significantly enhanced activities of SOD and CAT as well as exhaustive time and decreased levels of MDA and inflammatory cytokines. After TST, levels of free fatty acid, citrate synthase, and muscle glycogen were notably enhanced by oral administration of EA, but EA decreased levels of lactate, LDH, cortisol, aspartate aminotransferase, alanine transaminase, CK, glucose, and blood urea nitrogen compared to the control group. Furthermore, in forced swimming test, EA significantly increased levels of anti-fatigue-related factors and decreased excessive accumulations of fatigue-causing factors. Therefore, the results indicate that potent anti-fatigue effect of EA can be achieved via the improvement of anti-oxidative and anti-inflammatory properties, and this study will provide scientific data for EA to be developed as a novel and efficient component in anti-fatigue health functional food.</p