Fermentation by Rhizopus spp. has been used as a traditional medicine for treating various inflammatory diseases. Allergic asthma is a chronic respiratory disease that is caused by an exaggerated immune response. This study was conducted to ascertain the anti-inflammatory effects of Rhizopus spp. fermentation extract (RU) on a mouse model of ovalbumin (OVA)-induced asthma. The animals were intraperitoneally injected OVA on day 1 and 7, followed by OVA intranasal inhalation on days 14 to 18. The animals were treated daily with RU (100 and 200 mg/kg) by oral gavage from day 18 to day 23. RU significantly decreased eosinophilia and the production of inflammatory cytokines and OVA specific immunoglobulin E in animals with asthma, along with reducing airway inflammation and mucus secretion in lung tissue. Histological changes in the lungs and levels of inflammatory mediators of allergic airway inflammation were evaluated. The regulatory effects of RU on type 2 helper T (Th2) cell activation were investigated. RU administration attenuated asthmatic changes such as inflammatory cell infiltration and mucus production, decreased the levels of Th2-related cytokines, and reduced Th2 cell activation. Administration of RU effectively reduced allergic responses in asthmatic mice, which is associated with regulating Th2 cell activation and differentiation. These results indicate that RU can attenuate the respiratory symptoms of asthma.

Celecoxib, a cyclooxygenase (COX)-2 selective inhibitor, was approved as a non-steroidal anti-inflammatory drug (NSAID), and this therapeutic application has been expanded to several other diseases, including colon cancer. Notably, a treatment strategy combining the use of celecoxib and radiation therapy has been employed for improving the control of local cancers. In this study, we examined the effect of celecoxib on irradiation-induced intestinal damage. The twenty four mice (BALB/c) were divided into four groups; 1) sham-irradiated control group, 2) celecoxib-treated group, 3) irradiated group, and 4) celecoxib-treated irradiation group. Mice were orally administered celecoxib at a dose of 25 mg/kg in a 0.1 mL volume, daily for 4 days after irradiation exposure (10 Gy). Then, histological examinations of the jejunal villous height, crypt survival, and crypt size were performed. The expression of COX-2 after administration of celecoxib in irradiated mice was examined by employing immunohistochemistry, Western blotting, and qPCR analysis. The jejunal villi height and the crypt survival were reduced in the irradiation group compared with the sham-irradiated group. Celecoxib treatment in irradiation mice even more decreased those indicators. Crypt size was increased in the radiation group compared to the sham-irradiated control group, whereas the size was decreased in the celecoxibtreated irradiation group compared with the group exposed to the radiation injury. COX-2 expression was detected in the crypt of the small intestine, and COX-2 expression was increased in the crypt lesion following radiation exposure. However, COX-2 expression was reduced in the celecoxib-treated irradiation group. Therefore, in the present study, we confirmed that celecoxib treatment after irradiation aggravated the irradiation-induced intestinal damage. These results suggest that a caution need to be administered when celecoxib treatment is performed in combination with radiation therapy for cancer treatment.