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Angelicin, a furocoumarin found in Psoralea corylifolia L. fruit, has been reported to have anti-inflammatory activity. The purpose of this study was to determine the protective effects of angelicin on allergic asthma induced by ovalbumin (OVA) in mice. Mice were sensitized to OVA (on days 0 and 14) and challenged with OVA three times (on days 21 to 23). Angelicin (2.5, 5, 10 mg/kg) was given intraperitoneally 1 h before OVA treatment after the initial OVA sensitization. The production of IL-4, IL-5, and IL-13 in BALF and IgE in the serum were measured by ELISA. Lung histological changes were detected by using hematoxylin and eosin (H&E) stain. The results showed that angelicin significantly inhibited inflammatory cells infiltration into the lungs. Histological studies showed that angelicin significantly attenuated OVA-induced lung injury. Meanwhile, treatment of angelicin dose-dependently inhibited OVA-induced the production of IL-4, IL-5, and IL-13 in BALF and IgE in the serum. Furthermore, angelicin was found to inhibit airway hyperresponsiveness and NF-kB activation. In conclusion, our results suggested that angelicin inhibited allergic airway inflammation and hyperresponsiveness by inhibiting NF-kB activation.

TIM-1, a member of T-cell immunoglobulin domain and mucin domain (TIM) gene family, was implicated as an asthma susceptibility gene in previous studies. TIM-1 was expressed on CD4(+) T cells after activation and its expression was sustained preferentially in T-helper type 2 (T(H)2) but not in T(H)1 cells, therefore TIM-1 became a good candidate gene for atopic diseases. Recent studies indicated that two insertion/deletion (ins/del) coding genetic polymorphisms in exon 4 of TIM-1 were associated with asthma susceptibility in some but not in all populations. In order to investigate the relationship between TIM-1 genetic polymorphisms and asthma in Chinese Han population, we performed a case-control study for two insertion/deletion polymorphisms in TIM-1 exon 4 (5383_5397ins/del and 5509_5511delCAA) and a single nucleotide polymorphism (SNP) in intron 8 (IVS 8+9 G/A) between a healthy control group of 309 people and an asthma patient group of 352 people recruited from Chinese Han population. The polymorphisms were genotyped and the allele and genotype frequencies were analysed, but none of the three polymorphisms showed association with asthma susceptibility in single-locus association analyses. Linkage disequilibrium (LD) analyses demonstrated that the two insertion/deletion polymorphisms were in strong LD but the haplotypes constructed from these two polymorphisms showed no significant association with asthma. In conclusion, our findings suggest that 5383_5397ins/del, 5509_5511delCAA and SNP IVS 8+9 G/A polymorphisms are not associated with asthma susceptibility in Chinese Han population.

Asthma is a complex polygenic disease with gene-environment interactions being important. It has been previously suggested that ADAM33, which is a member of a gene family that encodes membrane-anchored proteins with a disintegrin and a metalloprotease domain, is primarily expressed in lung fibroblasts and bronchial smooth muscle cells and has been associated with airway remodelling and bronchial hyperresponsiveness. A significant association has previously been demonstrated between single nucleotide polymorphisms (SNPs) and haplotypes of the ADAM33 and asthma in ethnically diverse populations. To assess whether SNPs or haplotypes of ADAM33 are related to asthma in a Chinese Han population, we genotyped three SNPs of ADAM33 (7575G/A in intron 6, 11188A/T in intron 19, and 12433T/C in exon 20) in a case-control study involving 296 patients with asthma and 270 healthy controls. No significant association was detected between these three SNPs and asthma susceptibility in the Chinese population.