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Effects of triterpenoid-rich extracts of Ganoderma tsugae on airway hyperreactivity and Th2 responses in vivo
Authors:Chen Miaw-Ling  Lin Bi-Fong
Institution:Department of Biochemical Science and Technology, Institute of Microbiology and Biochemistry, College of Life Science, National Taiwan University, Taipei, Taiwan, ROC.
Abstract:BACKGROUND: Airway inflammation and Th2 responses play central roles in allergic asthma. We have previously reported that Ganoderma tsugae supplementation could attenuate airway inflammation in the murine model. Since it remains unclear which part of the G. tsugae exerts this effect on allergic asthma in vivo, this study was meant to investigate if triterpenoid extracts have anti-inflammatory effects on airway responses and regulatory effects on Th2 responses. METHODS: BALB/c mice sensitized intraperitoneally and challenged with ovalbumin (OVA) were treated with either triterpenoid-rich extracts (TRE) of G. tsugae or prednisolone for 2 weeks. The effects of TRE on bronchial airway hyperresponsiveness (AHR), airway inflammation, serum antigen-specific antibody levels, and cytokine secretions from splenocytes were evaluated. RESULTS: TRE supplementation significantly decreased AHR and reduced the total infiltrating leukocytes and eosinophils, as well as the levels of inflammatory mediators, such as interleukin (IL)-4, IL-5 and eotaxin in bronchoalveolar lavage fluid when compared with those of the control group. Lung histology also showed less cell recruitment and lung damage. TRE supplements suppressed IL-5 secretions from OVA-stimulated splenocytes, but did not affect the cell number of splenocytes, which was also reduced by prednisolone. Although OVA-specific immunoglobulin E levels were not significantly different among the groups, a lower level of OVA-specific immunoglobulin G1, another Th2-related antibody, was found in TRE and prednisolone treatment. CONCLUSIONS: TRE of G. tsugae exert anti-inflammatory effects on airway responses and attenuate Th2 responses without the overall immunosuppression effects in allergic murine models of asthma.
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