Treatment with Commelina communis Extract Exerts Anti-inflammatory Effects in Murine Macrophages via Modulation of the Nuclear Factor-κB Pathway.

The incidence of severe inflammatory diseases caused by chronic inflammation has increased owing to unprecedented changes brought about by industrialization. In this study, we aimed to assess the effect of treatment of lipopolysaccharide- (LPS-) induced murine macrophages with Commelina communis Linne extract (CCE) on synthesis of nitric oxide (NO), hypersecretion of proinflammatory cytokines, intranuclear transition of the p65 subunit of nuclear factor- (NF-) κB, and degradation of the NF-κB inhibitor IκBα. Notably, CCE treatment did not affect cell viability even at a final concentration of 1.5 mg/mL. At a high concentration of CCE, the LPS-induced high levels of NO, tumor necrosis factor-α, interleukin- (IL-) 1ß, and IL-6 were decreased via downregulation of inducible NO synthase and proinflammatory cytokine mRNA expression. Furthermore, phosphorylation of IκBα was significantly decreased upon CCE treatment, and the intranuclear transition of NF-κB p65 triggered by LPS was inhibited at a high concentration of CCE. Polyphenols and flavonoids, secondary metabolites in CCE that regulate the NF-κB pathway, may be responsible for its anti-inflammatory activity. We suggest that CCE has anti-inflammatory effects related to suppression of the NF-κB pathway and can be used to treat chronic inflammation.

Korean National Oral Health Survey Data on the Symmetry of Primary Dentition Surface Caries.

OBJECTIVES: This study evaluated the intraoral symmetry of dental caries in primary teeth as part of a study of caries patterns in primary dentition. STUDY DESIGN: The data for 4,800 5-year-old and 4,379 8-year-old children in this study were from the 2012 Korean national oral health survey. Pearson correlation coefficients of the decayed and filled surface (dfs) values ranged from 0.436 (lower primary canines) to 0.835 (upper primary central incisors) for the right and left primary teeth and from 0.084 (right primary central incisor) to 0.457 (left primary second molar) for the upper and lower primary dentition (P< 0.01). RESULTS: The upper and lower dfs values differed significantly (P< 0.05) when the right and left primary second molars were excluded. The left or right primary data without caries ranged from 56.4% (lower of first and second primary molars) to 99.7% (lower primary central incisors). The bilateral caries among cases with one or more in the right or left primary teeth ranged from 25.0% (lower lateral primary incisor) to 72.7% (upper primary central incisors). CONCLUSIONS: These results suggested that dental caries in primary teeth show bilateral symmetry and differences in the degree of symmetry according to the teeth set or surface set of the homologous teeth.

Emodin suppresses inflammatory responses and joint destruction in collagen-induced arthritic mice.

OBJECTIVE: Emodin (3-methyl-1,6,8-trihydroxyanthraquinone) is one of the active components present in the root and rhizome of Rheum palmatum. It has been shown to contain biological activity (antitumour, antibacterial, diuretic and vasorelaxant effects). However, the mechanisms underlying the anti-arthritic effect of emodin have not been elucidated. Here we investigated whether emodin treatment would modulate the severity of the disease in an experimental arthritis model. METHODS: We evaluated the effects of emodin on CIA mice in vivo. RESULTS: The pathological processes of RA are mediated by a number of cytokines and MMPs. Expression of these proinflammatory mediators is controlled by nuclear factor-κB (NF-κB). This study was performed to explore the effect of emodin on control of the NF-κB activation pathway and to investigate whether emodin has anti-inflammatory effects in CIA mice in vivo. Emodin inhibited the nuclear translocation and DNA binding of NF-κB subunits, which were correlated with its inhibitory effect on cytoplasmic IκBα degradation in CIA mice. These events further suppressed chemokine production and MMP expression. In addition, emodin inhibited the osteoclast differentiation induced by M-CSF and receptor activation of NF-κB ligand in bone marrow macrophages. CONCLUSION: These findings suggest that emodin exerts anti-inflammatory effects in CIA mice through inhibition of the NF-κB pathway and therefore may have therapeutic value for the treatment of RA.

Curcumin inhibits UVB-induced matrix metalloproteinase-1/3 expression by suppressing the MAPK-p38/JNK pathways in human dermal fibroblasts.

Curcumin (diferuloylmethane) is a polyphenol derived from turmeric (Curcuma longa), which is commonly used as a spice. Recent studies have shown that curcumin has a wide range of pharmacological activities, including anticarcinogenic, antioxidant, anti-inflammatory and antiangiogenic activities. However, the antiphotoageing effects of curcumin have yet to be characterized. In this study, we investigated the inhibitory effects of curcumin on matrix metalloproteinase (MMP)-1 and MMP-3 expression in human dermal fibroblast cells. Western blot analysis revealed that curcumin inhibited ultraviolet (UV) B-induced MMP-1 and MMP-3 expression. Furthermore, curcumin significantly blocked UVB-induced reactive oxygen species generation in fibroblasts. Curcumin treatment significantly blocked the UVB-induced activation of nuclear factor (NF)-κB and activator protein (AP)-1. Additionally, curcumin strongly repressed the UVB-induced phosphorylation of p38 and c-Jun N-terminal kinase. Curcumin prevented UVB-induced MMP expression through mitogen-activated protein kinase/NF-κB inhibition and AP-1 activation. In conclusion, curcumin may be useful for preventing and treating skin photoageing.

Dihydroavenanthramide D prevents UV-irradiated generation of reactive oxygen species and expression of matrix metalloproteinase-1 and -3 in human dermal fibroblasts.

Ultraviolet B (UVB) radiation induces photoageing by upregulating the expression of matrix metalloproteinases (MMPs) in human skin cells. Dihydroavenanthramide D (DHAvD) is a synthetic analog to naturally occurring avenanthramide, which is the active component in oats. Although anti-inflammatory, anti-atherosclerotic and antioxidant effects have been reported, the antiphotoageing effects of DHAvD are yet to be understood. In this study, we investigated the inhibitory effects of DHAvD on UVB-induced production of reactive oxygen species (ROS) and expression of MMPs, and its molecular mechanism in UVB-irradiated human dermal fibroblasts. Western blot and real-time PCR analyses revealed that DHAvD inhibited UVB-induced MMP-1 and MMP-3 expression. It also significantly blocked UVB-induced ROS generation in fibroblasts. Additionally, DHAvD attenuated UVB-induced phosphorylation of MAPKs, activation of NF-κB and AP-1. DHAvD regulates UVB-irradiated MMP expression by inhibiting ROS-mediated MAPK/NF-κB and AP-1 activation. DHAvD may be a useful candidate for preventing UV light-induced skin photoageing.

Downregulation of Matriptase Inhibits Porphyromonas gingivalis Lipopolysaccharide-Induced Matrix Metalloproteinase-1 and Proinflammatory Cytokines by Suppressing the TLR4/NF-κB Signaling Pathways in Human Gingival Fibroblasts.

Matriptases are cell surface proteolytic enzymes belonging to the type II transmembrane serine protease family that mediate inflammatory skin disorders and cancer progression. Matriptases may affect the development of periodontitis via protease-activated receptor-2 activity. However, the cellular mechanism by which matriptases are involved in periodontitis is unknown. In this study, we examined the antiperiodontitis effects of matriptase on Porphyromonas gingivalis-derived lipopolysaccharide (PG-LPS)-stimulated human gingival fibroblasts (HGFs). Matriptase small interfering RNA-transfected HGFs were treated with PG-LPS. The mRNA and protein levels of proinflammatory cytokines and matrix metalloproteinase 1 (MMP-1) were evaluated using the quantitative real-time polymerase chain reaction (qRT-PCR) and an enzyme-linked immunosorbent assay (ELISA), respectively. Western blot analyses were performed to measure the levels of Toll-like receptor 4 (TLR4)/interleukin-1 (IL-1) receptor-associated kinase (IRAK)/transforming growth factor ß-activated kinase 1 (TAK1), p65, and p50 in PG-LPS-stimulated HGFs. Matriptase downregulation inhibited LPS-induced proinflammatory cytokine expression, including the expression of IL-6, IL-8, tumor necrosis factor-α (TNF-α), and IL-Iß. Moreover, matriptase downregulation inhibited PG-LPS-stimulated MMP-1 expression. Additionally, we confirmed that the mechanism underlying the effects of matriptase downregulation involves the suppression of PG-LPS-induced IRAK1/TAK1 and NF-κB. These results suggest that downregulation of matriptase PG-LPS-induced MMP-1 and proinflammatory cytokine expression via TLR4-mediated IRAK1/TAK1 and NF-κB signaling pathways in HGFs.

Evodiae fructus Extract Inhibits Interleukin-1ß-Induced MMP-1, MMP-3, and Inflammatory Cytokine Expression by Suppressing the Activation of MAPK and STAT-3 in Human Gingival Fibroblasts In Vitro.

Periodontitis is a Gram-negative bacterial infectious disease. Numerous inflammatory cytokines, including interleukin-1ß (IL-1ß), regulate periodontitis pathophysiology and cause periodontal tissue destruction. In human gingival fibroblasts (HGFs), IL-1ß stimulates the production of matrix metalloproteinases (MMPs) and proinflammatory cytokines via various mechanisms. Several transcription factors, such as signal transducer and activator of transcription 3 (STAT-3), activator protein 1 (AP-1), and nuclear factor-κB (NF-κB), regulate gene expression. Mitogen-activated protein kinases (MAPKs) regulate these transcription factors. However, the MAPK/STAT-3 activation signal in HGFs is unknown. We investigated the potential inhibitory effects of the extract of Evodiae fructus (EFE), the dried, ripe fruit of Evodia rutaecarpa, on MMP and proinflammatory cytokine expression in IL-1ß-stimulated HGFs. EFE inhibited the expression of MMP-1, MMP-3, and proinflammatory cytokines (TNF-α, IL-6, and IL-8) in IL-1ß-stimulated HGFs through the inhibition of IL-1ß-induced MAPK/STAT-3 activation. Also, these results suggest that the EFE may be a useful for the bioactive material for oral care.

Aqueous extract of Chrysanthemum morifolium Ramat. inhibits RANKL-induced osteoclast differentiation by suppressing the c-fos/NFATc1 pathway.

OBJECTIVE: The flower of chrysanthemum, used worldwide as a medicinal and edible product, has shown various bioactivities, such as anti-inflammatory, antioxidant, anti-tumorigenic, and hepatoprotective activities, as well as cardiovascular protection. However, the effect of Chrysanthemum morifolium Ramat. on the regulation of osteoclast differentiation has not yet been reported. In this study, we aimed to investigate the inhibitory effect of Chrysanthemum morifolium Ramat. water extract (CME) on RANKL-induced osteoclast differentiation in mouse bone marrow-derived macrophages (BMMs). STUDY DESIGN: Bone marrow-derived macrophages (BMMs) isolated from the C57BL/6 J mice. The viability of BMMs was detected with MTT assays. Inhibitory effects of CME on osteoclast differentiation and bone resorption was measured by TRAP staining and Pit assay. Osteoclast differentiation-associated gene expression were assessed by Real-time quantitative polymerase chain reaction. Intracellular signaling molecules was assessed by western blot. RESULTS: CME significantly inhibited osteoclast differentiation in BMMs without cytotoxicity, besides inhibiting MAPK/c-fos and PLCγ2/CREB activation. The inhibitory effects of CME on differentiation-related signaling molecules resulted in significant repression of NFATc1 expression, which is a key transcription factor in osteoclast differentiation, fusion, and activation. CONCLUSION: Our results confirmed the inhibition of RANKL-induced PLCγ2/CREB/c-fos/NFATc1 activation by CME during osteoclast differentiation. The findings collectively suggested CME as a traditional therapeutic agent for osteoporosis, RA, and periodontitis.

Pueraria thunbergiana inhibits cisplatin-induced damage of HEI-OC1 auditory cells through scavenging free radicals.

The radix of Pueraria thunbergiana (P. thunbergiana) is traditionally prescribed to attenuate the clinical manifestation of inner ear dysfunction and various clinical situations including fevers, gastrointestinal disorders, skin problems, migraine headaches, lowering cholesterol, and treating chronic alcoholism in oriental medicine. In the present study, we examined the protective effect of ethanol extract of the radix of P. thunbergiana (RPT) on cisplatin-induced damage of HEI-OC1 auditory hair cells. When the cells were cultured in the medium containing 5-100 microg/mL of RPT, RPT showed protective effect against the cisplatin-induced HEI-OC1 cell damage. We also measured the effects of RPT on lipid peroxidation of cisplatin-treated cells as well as scavenging activities against superoxide radical, hydroxyl radical, hydrogen peroxide, and DPPH radical. RPT reduced cisplatin-induced lipid peroxidation in a dose-dependent manner. Furthermore, RPT showed strong scavenging activity against superoxide radical, hydroxyl radical, hydrogen peroxide, and DPPH radical. These results indicate that RPT protects cisplatin-induced HEI-OC1 cell damage through inhibition of lipid peroxidation and scavenging activities of free radials.

Weissella cibaria CMU exerts an anti­inflammatory effect by inhibiting Aggregatibacter actinomycetemcomitans­induced NF­κB activation in macrophages.

Periodontitis is a chronic inflammatory disease caused by various periodontal pathogens. Weissella cibaria CMU (oraCMU) is a probiotic that promotes oral health. However, its anti­inflammatory effects against periodontal pathogens have not yet been investigated. The present study evaluated the anti­inflammatory effects of live oraCMU against stimulation with the formalin­inactivated periodontal pathogen Aggregatibacter actinomycetemcomitans in RAW 264.7 macrophages. Cell viability was analyzed by the MTS assay in a dose­dependent manner (at multiplicities of infection of 0.1, 1, 10, 100 and 1,000). Nitric oxide (NO) was monitored using the Griess test. The mRNA expression of proinflammatory cytokines such as interleukin (IL)1ß and IL6 was assessed by reverse transcription­quantitative PCR. Western blotting was used to examine the effects of oraCMU on the phosphorylation of NF­κB inhibitor α (IκBα) and IκBα kinase (IKK), the nuclear translocation of the NF­κB subunit p65 and the expression of inducible NO synthase (iNOS). Live oraCMU had no cytotoxic effects on RAW 264.7 macrophages. In A. actinomycetemcomitans­stimulated RAW 264.7 macrophages, oraCMU reduced NO production by suppressing iNOS expression and downregulating the mRNA expression of proinflammatory cytokines in a dose­dependent manner. IKK phosphorylation and IκBα degradation were dose­dependently inhibited by oraCMU and the nuclear translocation of p65 via the canonical NF­κB pathway was simultaneously reduced. The results indicated that oraCMU possessed anti­inflammatory activity associated with the inhibition of NF­κB signal activation in response to periodontal pathogens. This suggests that oraCMU is a beneficial anti­inflammatory probiotic that can aid in the maintenance of oral health.

Protective effect of ursolic acid from Cornus officinalis on the hydrogen peroxide-induced damage of HEI-OC1 auditory cells.

The fruits of Cornus officinalis have been used in traditional oriental medicine for treatment of inner ear diseases, such as tinnitus and hearing loss. In the present study, we investigated the protective effect of C. officinalis on hydrogen peroxide-induced cytotoxicity in HEI-OC1 auditory cells. The results from bioassay-guided fractionation of methanol extract of C. officinalis fruits showed that ursolic acid is a major active component. Ursolic acid (0.05-2 microg/ml) had protective effect against the HEI-OC1 cell damage and reduced lipid peroxidation in a dose-dependent manner. In addition, pre-treatment with ursolic acid significantly attenuated the decrease of activities of catalase (CAT) and glutathione peroxidase (GPX), but superoxide dismutase (SOD) activity was not significantly affected by ursolic acid. These results indicate that ursolic acid protects hydrogen peroxide-induced HEI-OC1 cell damage through inhibition of lipid peroxidation and induction of antioxidant enzymes, CAT and GPX, and may be one of the active components responsible for these effects of C. officinalis fruits.

Reversine inhibits MMP-3, IL-6 and IL-8 expression through suppression of ROS and JNK/AP-1 activation in interleukin-1ß-stimulated human gingival fibroblasts.

OBJECTIVE: Periodontitis is an inflammatory disease of the supporting tissue around teeth commonly caused by gram-negative bacterial infections. Interleukin (IL)-1ß, a cytokine involved in host immune and inflammatory responses, is known to induce the activation of various intracellular signaling pathways. One of these signaling mechanisms involves the regulation of gene expression by activation of transcription factors (AP-1 and NF-κB). These transcription factors are controlled by mitogen-activated protein kinases (MAPKs), which increase cytokine and matrix metalloproteinase (MMP) expression. We examined the preventive effects of reversine, a 2,6-disubstituted purine derivative, on cytokine and MMP-3 expression in human gingival fibroblasts (HGFs) stimulated with IL-lß. STUDY DESIGN: Western blot analyses were performed to verify the activities of MAPK, p65, p50, and c-Jun and the expression of MMPs in IL-1ß-stimulated HGFs. Cytokine and MMP-3 expression in IL-1ß-stimulated HGFs was measured by real-time quantitative polymerase chain reaction. RESULTS: Reversine decreased the IL-1ß-induced expression of proinflammatory cytokines (IL-6 and IL-8) and MMP-3 in HGFs. Furthermore, the mechanism underlying the effects of reversine involved the suppression of IL-1ß-stimulated MAPK activation and AP-1 activation. CONCLUSION: Reversine inhibits IL-1ß-induced MMP and cytokine expression via inhibition of MAPK/AP-1 activation and ROS generation. Therefore, we suggest that reversine may be an effective therapeutic candidate for preventing periodontitis.

Artemisia princeps Inhibits Growth, Biofilm Formation, and Virulence Factor Expression of Streptococcus mutans.

This study was designed to determine whether the ethanol extract of Artemisia princeps could inhibit the cariogenic activity of Streptococcus mutans. The increase in acid production and biofilm formation by S. mutans were evaluated. The expression levels of virulence factor genes were determined by performing the real-time polymerase chain reaction (PCR). The bactericidal effect was tested by confocal laser scanning microscopy. The A. princeps extract was observed to inhibit the growth of S. mutans at concentrations >0.05 mg/mL (P < .05). After using the safranin staining method, we found that the A. princeps extract had an inhibitory effect against biofilm formation at a concentration of >0.05 mg/mL. These experimental results were similar to that observed with the scanning electron microscopy. The results of the confocal microscopy revealed that the A. princeps extract at high concentrations of 0.4-3.2 mg/mL showed a bactericidal effect in a concentration-dependent manner. According to the results of the real-time PCR analysis, it was observed that the A. princeps extract inhibited the expression of virulence factor genes. These results suggest that A. princeps may inhibit the cariogenic activity of S. mutans, and may be useful as an anticariogenic agent.

Silencing of casein kinase 2 inhibits PKC­induced cell invasion by targeting MMP­9 in MCF­7 cells.

Casein kinase 2 (CK2) is a serine/threonine protein kinase that has been considered to represent an important factor in mammary tumorigenesis. Increased expression of matrix metalloproteinase­9 (MMP­9) via nuclear factor­κB (NF­κB) activation has been demonstrated to promote breast cancer cell invasion. In the present study, the involvement of CK2 in protein kinase C (PKC) induced cell invasion in MCF­7 breast cancer cells was investigated as well as the underlying molecular mechanisms. The mRNA and protein levels of MMP­9 in MCF­7 cells were investigated using reverse transcription­quantitative polymerase chain reaction, western blot analyses and a zymography assay. Cell invasiveness was investigated using a Matrigel invasion assay, and it was revealed that small interfering RNA specific for CK2 suppressed PKC induced cell invasion by regulating MMP­9 expression via activation of the p38 kinase/c­Jun N­terminal kinase/NF­κB pathway. In addition, it was demonstrated that CK2 inhibitors [apigenin (20 µM), emodin (20 µM) or 2­dimethylamino­4,5,6,7­tetrabromo­1H­benzimidazole (2 µM)] suppressed PKC induced cell invasion and MMP­9 expression. The results of the present study suggested that CK2 is an important factor involved in the induction of MCF­7 breast cancer cell invasion by PKC. Therefore, CK2 may represent novel candidates for therapy intended to inhibit invasion in breast cancer.

Saussurea lappa inhibits the growth, acid production, adhesion, and water-insoluble glucan synthesis of Streptococcus mutans.

In the present study, inhibitory effects of the ethanol extract of Saussurea lappa (S. lappa) on the growth, acid production, adhesion, and water-insoluble glucan synthesis of Streptococcus mutans (S. mutans) were examined. The growth and acid production of Streptococcus mutans were inhibited by the presence of ethanol extract of Saussurea lappa (0.5-4 mg/ml) significantly. The ethanol extract of Saussurea lappa (0.25-4 mg/ml) also significantly lowered the adherence of Streptococcus mutans in a dose dependent manner. In water-insoluble glucan synthesis assay, 2-4 mg/ml of the ethanol extract of Saussurea lappa significantly inhibited the formation of water-insoluble glucan. These results suggest that Saussurea lappa may inhibit the caries-inducing properties of Streptococcus mutans. Further studies are necessary to clarify the active constituents of Saussurea lappa responsible for such biomolecular activities.

Anticariogenic properties of the extract of Cyperus rotundus.

Streptococcus mutans (S. mutans) is known as the causative bacteria in the formation of dental plaque and dental caries. The aim of this experiment was to investigate the effects of Cyperus rotundus (C. rotundus) tuber extract on the growth, acid production, adhesion, and water-insoluble glucan synthesis of S. mutans. The growth and acid production were reduced by the extract of C. rotundus in a dose dependent manner. The extract of C. rotundus markedly inhibited the adherence of S. mutans to saliva-coated hydroxyapatite beads (HAs). The adherence was repressed by more than 50% at the concentration of 0.5 mg/ml of the extract and complete inhibition was observed at the concentration of 4 mg/ml of the extract. On the activity of glucosyltransferase (GTFase) which synthesizes water-insoluble glucan from sucrose, the extract of C. rotundus showed more than 10% inhibition at a concentration of 2 mg/ml. These results suggest that C. rotundus may inhibit cariogenic properties of S. mutans. Further studies are necessary to clarify the active constituents of C. rotundus responsible for such biomolecular activities.

Tanshinone IIA inhibits LPS-induced NF-kappaB activation in RAW 264.7 cells: possible involvement of the NIK-IKK, ERK1/2, p38 and JNK pathways.

Nuclear factor kappaB (NF-kappaB) activation by NF-kappaB-inducing kinase (NIK)-IkappaB alpha kinase (IKK) pathway and mitogen-activated protein kinases (MAPKs) pathway are important in inflammation. We recently found that the tanshinone IIA, a diterpene isolated from Salvia miltiorrhiza (S. miltiorrhiza), reduced the production of pro-inflammatory mediators in RAW 264.7 cells stimulated with lipopolysaccharide (LPS). However, little is known about the inhibitory mechanisms of tanshinone IIA on the production of pro-inflammatory mediators. To investigate the inhibitory mechanism, we determined the inhibitory effects of tanshinone IIA on the activation of NF-kappaB and IkappaB alpha phosphorylation, and also examined phosphorylation of NIK and IKK as well as the activation of MAPKs such as p38 MAPK (p38), extracellular signal-regulated kinases 1/2 (ERK1/2), and c-Jun N-terminal kinase (JNK) in RAW 264.7 cells stimulated with LPS. Tanshinone IIA inhibited NF-kappaB-DNA complex, NF-kappaB binding activity, and the phosphorylation of IkappaB alpha in a dose dependent manner. Tanshinone IIA also inhibited the translocation of NF-kappaB from cytosol to nucleus. Moreover, the phosphorylation of NIK and IKK as well as the phosphorylation of p38, ERK1/2, and JNK in the LPS-stimulated RAW 264.7 cells were suppressed by the tanshinone IIA in a dose dependent manner. These results suggest that tanshinone IIA may inhibit LPS-induced IkappaB alpha degradation and NF-kappaB activation via suppression of the NIK-IKK pathway as well as the MAPKs (p38, ERK1/2, and JNK) pathway in RAW 264.7 cells and these properties may provide a potential mechanism that explains the anti-inflammatory activity of tanshinone IIA.

Scoparone inhibits PMA-induced IL-8 and MCP-1 production through suppression of NF-kappaB activation in U937 cells.

Scoparone is a major component of the shoot of Artemisia capillaris (Compositae), which has been used for the treatment of hepatitis and biliary tract infection in oriental countries. In this study, the effects of scoparone on the expression of interleukin-8 (IL-8) and monocyte chemotactic protein-1 (MCP-1) and activation of nuclear factor-kappaB (NF-kappaB) were examined in U937 human monocytes activated with phorbol 12-myristate 13-acetate (PMA). Scoparone (5-100 microM) had no cytotoxic effect in unstimulated cells and concentration-dependently reversed PMA-induced toxicity in the cells stimulated with PMA. Scoparone concentration-dependently reduced the release of IL-8 and MCP-1 protein and expression of IL-8 and MCP-1 mRNA levels induced by PMA. Moreover, scoparone inhibited the levels of NF-kappaB-DNA complex and NF-kappaB activity in the cells stimulated with PMA in a concentration-dependent manner. Scoparone dose-dependently inhibited the phosphorylation of IkappaBalpha and nuclear translocation of NF-kappaB1 p50, RelA p65, and c-Rel p75. These data suggest that scoparone may inhibit the expression of chemokines (IL-8 and MCP-1) in PMA-stimulated U937 cells and a potential mechanism of scoparone may be inhibition of NF-kappaB activation, which is linked to inhibition of NF-kappaB subunits (NF-kappaB1 p50, RelA p65, and c-Rel p75) translocation via suppression of IkappaBalpha phosphorylation.

Protective effect of Rehmannia glutinosa on the cisplatin-induced damage of HEI-OC1 auditory cells through scavenging free radicals.

The steamed root of Rehmannia glutinosa has been used in traditional Oriental Medicine for treatment of inner ear diseases, such as tinnitus and hearing loss. In the present study, we showed that the ethanol extract of steamed roots of Rehmannia glutinosa (SRG) protected HEI-OC1 auditory cells from cisplatin cytotoxicity in a dose-dependent fashion. In addition, to investigate the protection mechanism of SRG on cisplatin cytotoxicity towards HEI-OC1, we measured the effects of SRG on lipid peroxidation of cisplatin treated cells as well as scavenging activities against superoxide radical, hydroxyl radical, hydrogen peroxide, and DPPH radical. SRG (5-100 microg/ml) had protective effect against the cisplatin-induced HEI-OC1 cell damage and reduced lipid peroxidation in a dose-dependent manner. Furthermore, SRG showed strong scavenging activity against superoxide radical, hydroxyl radical, hydrogen peroxide, and DPPH radical. These results indicate that SRG protects cisplatin-induced HEI-OC1 cell damage through inhibition of lipid peroxidation and scavenging activities of free radials.

Asarum sieboldii extracts attenuate growth, acid production, adhesion, and water-insoluble glucan synthesis of Streptococcus mutans.

Asarum sieboldii has been used in traditional folk medicine to treat dental caries and periodontal disease. In the present study, we investigated the inhibitory effect of the ethanol and aqueous extracts of A. sieboldii on the growth, acid production, adhesion, and water-insoluble glucan synthesis of Streptococcus mutans. The ethanol and aqueous extracts of A. sieboldii inhibited the growth and acid production of S. mutans. In the bacterial adherence assay, the ethanol and aqueous extracts of A. sieboldii significantly lowered the adherence of S. mutans. We also found that the ethanol and aqueous extracts of A. sieboldii significantly inhibited the synthesis of water-insoluble glucan by crude glucosyltransferase. These results suggest that A. sieboldii extracts may inhibit the caries-inducing properties of S. mutans. Further studies are necessary to clarify the active constituents of A. sieboldii extracts responsible for such biomolecular activities.