ABSTRACT
ObjectiveTo investigate the regulatory effects of Xuanfu Daizhetang on a mouse model of allergic asthma induced by ovalbumin （OVA）. MethodSixty female BALB/c mice （6-8 weeks old， SPF） were randomly divided into groups. Ten mice were assigned to the normal group and given 0.2 mL of saline， while the remaining groups received intraperitoneal injections of Al（OH）3 at 5 g·L-1 and OVA at 1 g·L-1. The mice were divided into normal group （10 mL·kg-1 saline）， OVA model group （10 mL·kg-1 saline）， dexamethasone group （OVA+DEX， 1 mg·kg-1）， OVA+ low-dose Xuanfu Daizhetang group （OVA+XL， 7.065 g·kg-1）， OVA+ medium-dose Xuanfu Daizhetang group （OVA+XM， 14.13 g·kg-1）， and OVA+ high-dose Xuanfu Daizhetang group （OVA+XH， 28.26 g·kg-1）. An OVA-induced asthma model was established in mice. Hematoxylin-eosin （HE） and periodic acid-Schiff （PAS） staining methods were used to observe bronchial tissue pathological changes. Enzyme-linked immunosorbent assay （ELISA） was performed to measure the levels of immunoglobulin E （IgE）， interleukin-4 （IL-4）， IL-5， IL-13， IL-17A， and γ interferon （IFN-γ） in bronchoalveolar lavage fluid. Western blot was used to detect the phosphorylation of extracellular signal-regulated kinase （ERK）， p38 mitogen-activated protein kinase （MAPK）， and c-Jun N-terminal kinase （JNK） proteins in lung tissue. ResultCompared with the normal group， the OVA model group showed increased inflammatory cell infiltration in mouse alveoli， elevated levels of IL-4， IL-5， IL-13， IL-17A， IFN-γ in bronchoalveolar lavage fluid， and IgE in serum （P<0.05， P<0.01）， and promoted phosphorylation of MAPK signaling pathway-related proteins. Compared with the model group， the OVA+XL， OVA+XM， and OVA+XH groups showed reduced inflammatory cell infiltration in mouse alveoli， decreased levels of IL-4， IL-5， IL-13， IL-17A， IFN-γ in bronchoalveolar lavage fluid， and IgE in serum （P<0.05， P<0.01）， and inhibited phosphorylation of MAPK signaling pathway-related proteins. ConclusionThe results of this study suggest that Xuanfu Daizhetang has potential anti-allergic asthma activity， providing a theoretical basis for its future clinical application.
ABSTRACT
BACKGROUND: Micro-nano-sized modification of the material surface provides an effective way to enhance the endothelialization of cardiovascular implants. Shear stress plays an important role in the endothelialization of cardiovascular implants.OBJECTIVE: To review the effects of flow shear stress on endothelial cell cytoskeleton alignment, migration, adhesion and apoptosis on the micropatterned substrates.METHODS: The author performed a retrieval of PubMed and CNKI databases from 2002 to 2017 to search literatures about the effects of shear stress on endothelial cells on the micropatterned substrates. The keywords were micrometer topology, micropattern, flow shear stress, endothelial cells in English and Chinese, respectively.RESULTS AND CONCLUSION: The shear stress parallel to the long axis of the micropattern which is applied to the endothelial cells on micropatterned substrates promotes endothelial cell microfilaments alignment along the long axis direction of micropattern, strengthens endothelial cell migration along the flow direction, increases the level of FAK phosphorylation, enhances endothelial cell adhesion, and improves endothelial cell activity. However, there are some controversies on the effects of parallel shear stress on the microtubule arrangement of endothelial cells on micropatterned substrates. Some studies have reported that parallel shear stress promotes endothelial cell microtubules alignment along the long axis of micropatterns. But others have found that parallel shear stress has no effect on endothelial cell microtubule arrangement. There are different conclusions about the effects of shear stress perpendicular to the long axis of the micropattern on endothelial cells on the micropatterned substrates. Some literatures have found vertical shear stress destroys the structure of endothelial cell microfilaments and microtubules,weakens the degree of microfilaments and microtubules arranged along the long axis of micropatterns, and attenuates endothelial cell adhesion and cell activity. But some have found vertical shear stress does not destroy the structure and alignment of endothelial cell microfilaments and microtubules, and still can promote endothelial cell migration along the flow direction. The magnitude of shear force affects endothelial cell migration, and the number of endothelial cells on the micropatterned substrates migrating along the flow direction increases with the increasing intensity of shear stress.