Anti-asthmatic effect of Sanguisorba officinalis L. and potential role of heme oxygenase-1 in an ovalbumin-induced murine asthma model

Abstract

Abstract. Sanguisorba officinalis L. is known to have antiinflammatory properties. However, the potential effects of S. officinalis against asthma have not been reported. In the present study, we investigated the protective effects and underlying mechanisms of S. officinalis in a murine ovalbumin (OVA)-induced asthma model. Mice were sensitized and challenged by OVA inhalation to induce airway inflammation and remodeling. S. officinalis ethanolic extract (SOEE) markedly decreased the number of infiltrated inflammatory cells, together with a reduction in the levels of T-helper type 2 cytokines and immunoglobulin E levels. Histopathological studies showed that inflammatory cell infiltration and mucus hypersecretion were inhibited by SOEE. In addition, OVAinduced increases in reactive oxygen species were attenuated by SOEE. All these effects were correlated with heme oxygenase-1 (HO-1) induction by SOEE. These results indicate that SOEE has therapeutic potential against bronchial asthma associated with allergic diseases that is due, at least in part, to HO-1 upregulation.

Ellagic acid, extracted from Sanguisorba officinalis, induces G1 arrest by modulating PTEN activity in B16F10 melanoma cells

“…***p < .001 in Student's t test TAN eT Al. melanoma cells. Sanguisorba officinalis has been used as a traditional Chinese medicine for treating inflammatory and metabolic diseases for decades (Lee et al, 2010;Zhang et al, 2012). Recently, its extract was reported to elicit cell cycle arrest and cell death in gastric carcinoma and breast cancer cell lines .…”

Anti-Inflammatory Effects of Jakyakgamcho-Tang in IL-4- and TNF-α-Stimulated Lung Epithelial Cells and Lipopolysaccharide-Stimulated Macrophages

“…Asthma is a chronic respiratory disease known to be caused by excessive airway inflammation and hyper-responsiveness that leads to obstruction of airway [1]. Airway inflammation in asthma is induced by complex regulatory mechanisms involving the release of T helper 2 (Th2) cytokines (interleukin (IL)-4, IL-5, and IL-13), chemokines (eotaxins and regulated on activation, normal T-cell expressed and secreted (RANTES)), and other signaling molecules such as nitric oxide (NO) [2,3].…”