Foeniculum vulgare Mill. Protects against Lipopolysaccharide-induced Acute Lung Injury in Mice through ERK-dependent NF-kB Activation

Foeniculum vulgare Mill. (fennel) is used to flavor food, in cosmetics, as an antioxidant, and to treat microbial, diabetic and common inflammation. No study to date, however, has assessed the anti-inflammatory effects of fennel in experimental models of inflammation. The aims of this study were to investigate the anti-inflammatory effects of fennel in model of lipopolysaccharide (LPS)-induced acute lung injury. Mice were randomly assigned to seven groups (n=7~10). In five groups, the mice were intraperitoneally injected with 1% Tween 80-saline (vehicle), fennel (125, 250, 500micro l/kg), or dexamethasone (1 mg/kg), followed 1 h later by intratracheal instillation of LPS (1.5 mg/kg). In two groups, the mice were intraperitoneally injected with vehicle or fennel (250microl/kg), followed 1 h later by intratracheal instillation of sterile saline. Mice were sacrificed 4 h later, and bronchoalveolar lavage fluid (BALF) and lung tissues were obtained. Fennel significantly and dose-dependently reduced LDH activity and immune cell numbers in LPS treated mice. In addition fennel effectively suppressed the LPS-induced increases in the production of the inflammatory cytokines interleukin-6 and tumor necrosis factor-alpha, with 500microl/kg fennel showing maximal reduction. Fennel also significantly and dose-dependently reduced the activity of the proinflammatory mediator matrix metalloproteinase 9 and the immune modulator nitric oxide (NO). Assessments of the involvement of the MAPK signaling pathway showed that fennel significantly decreased the LPS-induced phosphorylation of ERK. Fennel effectively blocked the inflammatory processes induced by LPS, by regulating pro-inflammatory cytokine production, transcription factors, and NO.

Comparison of Serum Interleukin-8 and Regulated on Activation in Normal T-Cell Expressed and Secreted Levels in Atopic and Non-Atopic Children with Lower Respiratory Tract Infections / 소아알레르기및호흡기학회지

PURPOSE: Several studies have shown that viral respiratory infections induce more severe respiratory symptoms in atopic patients than in normal subjects. We attempted to investigate if there is any difference in the viral etiology, clinical manifestations, production of interleukin (IL)-8, and regulated on activation in normal T-cell expressed and secreted (RANTES) between atopic and non-atopic subjects with lower respiratory infections. METHODS: Sera and nasopharyngeal aspirates (NPA) were collected from 97 children with lower respiratory infections who were admitted to the pediatric ward. Seventy-one children were classified as atopic subjects. We detected respiratory viruses with multiplex reverse transcriptase-polymerase chain reaction in NPA and measured total immunoglobulin E (IgE) and specific IgE in sera. IL-8 and RANTES levels measured in sera by enzyme-linked immunosorbent assay, etiology, and clinical manifestations were compared between atopic and non-atopic subjects. Atopic patients were defined as having elevated specific IgE to more than one allergen or age-matched, high serum total IgE levels. RESULTS: Both serum IL-8 and RANTES levels were significantly higher in atopic than in non-atopic patients. There was no significant difference in viral etiology and clinical diagnosis between the two groups. The frequency of wheezing was higher in atopic than in non-atopic patients. CONCLUSION: Our study showed that both serum IL-8 and RANTES levels and the frequency of wheezing were significantly higher in atopic than in non-atopic patients. That suggests that chemokine responses to viral respiratory infection may be different between atopic and non-atopic patients and may be associated with a difference in clinical manifestation, such as wheezing, between the two groups. However, further prospective large-scaled studies are required to clarify our conclusion.

Vitamin D Receptor Gene 3' End Polymorphisms in Patients with Graves' Disease in Koreans / 대한내분비학회지

BACKGROUND: The aim of this study was to evaluate the association of vitamin D receptor (VDR) gene polymorphisms with Graves' disease in Koreans. We also investigated the association of VDR gene polymorphisms with the clinical characteristics and titers of TSH receptor antibodies in patients with Graves' disease. SUBJECTS AND METHODS: The VDR gene polymorphisms were evaluated in 117 patients with Graves' disease and 156 normal controls. The polymorphisms were represented according to restriction fragment length polymorphism; Aa(ApaI), Bb(BsmI) and Tt(TaqI), with the capital letters signifying the absence, and small letters the presence of restriction sites. RESULTS: The distribution of the ApaI polymorphism genotype was: AA(17.1%), Aa(50.4%) and aa(32.5%). The BsmI polymorphism genotype distribution was: BB(7.1%), Bb(35.4%) and bb(57.5%); and the TaqI polymorphism genotype distribution was: TT(92.6%), Tt(6.2) and tt(1.2%). No significant differences in either genotypic or allelic distributions were observed, between the patients with Graves' disease and the normal controls, associated with the VDR gene polymorphisms. No significant differences were observed with age, sex, size of goiter or the presence of ophthalmopathy, in patients with Graves' disease associated with the VDR gene polymorphisms. However, the titers of the TBII were significantly higher in the aa than the Aa genotype, and were also higher in the group without the A allele than in groups with(aa 55.9+/-18.3 vs. Aa 43.2+/-23.4, p<0.05; aa 55.9+/-18.3 vs. AA and Aa 42.9+/-23.5, p<0.05). Thyroid stimulating antibodies measured with a CHO cell transfected with a wild type of human TSH receptor, were also higher in patients without the A allele than in those with(aa 620+/-829 vs. AA and Aa 353+/-306, p<0.05). The titers of the anti-thyroglobulin antibodies were significantly higher in the groups not containing the B allele than in the group that did(bb 50.9+/-42.8 vs. BB and Bb 31.9+/-38.9, p<0.05). The serum alkaline phosphatase activities were higher in the group having the b allele than in the group that did not(Bb and bb 139+/-68 vs. BB 82.2+/-15.5, p<0.05). CONCLUSIONS: The VDR gene 3' end polymorphism was not associated with susceptibility to Graves' disease in Koreans. The studies of other polymorphism sites of the VDR gene might be required to elucidate the association of VDR gene polymorphisms with Graves' disease in Koreans.