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- W2285786668 abstract "Abstract Airway smooth muscle cell (ASMC) was known to involve in the pathophysiology of asthma. Schisandrin B was reported to have anti‐asthmatic effects in a murine asthma model. However, the molecular mechanism involving in the effect of Schisandrin B on ASMCs remains poorly understood. Sprague–Dawley rats were divided into three groups: rats as the control (Group 1), sensitized rats (Group 2), sensitized rats and intragastric‐administrated Schisandrin B (Group 3). The expression of miR‐135a and TRPC1 was detected in the rats from three groups. Platelet‐derived growth factor (PDGF)‐BB was used to induce the proliferation of isolated ASMCs, and the expression of miR‐135a and TRPC1 was detected in PDGF‐BB‐treated ASMCs. Cell viability was examined in ASMCs transfected with miR‐135a inhibitor or si‐TRPC1. The expression of TRPC1 was examined in A10 cells pretreated with miR‐135a inhibitor or miR‐135a mimic. In this study, we found that Schisandrin B attenuated the inspiratory and expiratory resistances in sensitized rats. Schisandrin B upregulated the mRNA level of miR‐135a and decreased the expression of TRPC1 in sensitized rats. In addition, Schisandrin B reversed the expression of miR‐135a and TRPC1 in PDGF‐BB‐induced ASMCs. Si‐TRPC1 abrogated the increasing proliferation of ASMCs induced by miR‐135a inhibitor. We also found that miR‐135a regulated the expression of TRPC1 in the A10 cells. These results demonstrate that Schisandrin B inhibits the proliferation of ASMCs via miR‐135a suppressing the expression of TRPC1." @default.
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- W2285786668 date "2016-05-04" @default.
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- W2285786668 title "Schisandrin B inhibits the proliferation of airway smooth muscle cells via microRNA-135a suppressing the expression of transient receptor potential channel 1" @default.
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- W2285786668 doi "https://doi.org/10.1002/cbin.10597" @default.
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