YiQi GuBen capsule alleviates OVA-induced asthma through improving mitochondrial dysfunction

<b>Objective:</b> This study aims to explore the effect of YiQi GuBen capsule on improving mitochondrial dysfunction in an animal model of asthma.<b>Methods: </b>The mice (<i>n</i> = 8) were divided into four groups including control (NC), ovalbumin (OVA), dexamethasone (OVA + DEX), and YiQi GuBen (OVA + YQGB) groups. Firstly, we established an OVA-induced mouse asthma model except for the NC group, which then were treated with dexamethasone and YiQi GuBen capsule. Subsequently, HE staining and Masson staining were used for pathological analysis of mice lung tissues. Next, we used transmission electron microscopy (TEM) to observe the effect of the Yiqi Guben capsule on the ultrastructure of mitochondria. Flow cytometry was used to analyze the ROS level, membrane potential, and the number of mitochondria in lung tissue. Moreover, we analyzed the copy number of mitochondrial DNA (mtDNA) and the expression levels of activator peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and mitochondrial transcription factor A (TFAM).<b>Results:</b> The results of the pathological analysis showed that after treatment with the YiQi GuBen capsule, the lung tissue damage was significantly reduced. In addition, we observed that the ultrastructural damage of mitochondria was improved. Flow cytometry proved that after treatment with the YiQi GuBen capsule, the level of ROS in the mitochondria was effectively reduced, while the mitochondrial membrane potential decreased and the number increased significantly. Moreover, we found that the copy number of mtDNA was significantly increased and the expression levels of PGC-1α and TFAM were significantly upgraded.<b>Conclusion:</b> This study suggests YiQi GuBen capsule can effectively improve mitochondrial dysfunction in the OVA-induced mouse model.

<b>研究目的：</b>本研究旨在探讨益气固本胶囊（YiQi GuBen capsule）对哮喘动物模型中线粒体功能障碍的改善作用。
<b>方法：</b>将8只小鼠分为4组，分别为对照组（NC）、卵清蛋白（ovalbumin, OVA）组、地塞米松（dexamethasone, DEX）干预组（OVA+DEX）及益气固本胶囊干预组（OVA+YQGB）。除对照组外，其余各组均构建OVA诱导的小鼠哮喘模型，随后分别给予地塞米松与益气固本胶囊干预。采用HE染色与Masson染色对小鼠肺组织开展病理分析；通过透射电子显微镜（transmission electron microscopy, TEM）观察益气固本胶囊对线粒体超微结构的影响；采用流式细胞术分析肺组织中活性氧（ROS）水平、线粒体膜电位及线粒体数量；此外，检测线粒体DNA（mitochondrial DNA, mtDNA）拷贝数，以及过氧化物酶体增殖物激活受体γ辅激活因子1α（peroxisome proliferator-activated receptor γ coactivator-1α, PGC-1α）与线粒体转录因子A（mitochondrial transcription factor A, TFAM）的表达水平。
<b>结果：</b>病理分析结果显示，经益气固本胶囊干预后，小鼠肺组织损伤显著减轻。同时，线粒体超微结构损伤得到改善。流式细胞术检测证实，益气固本胶囊干预可有效降低线粒体ROS水平，同时线粒体膜电位降低、线粒体数量显著增加。此外，mtDNA拷贝数显著升高，PGC-1α与TFAM的表达水平显著上调。
<b>结论：</b>本研究表明，益气固本胶囊可有效改善OVA诱导的小鼠哮喘模型中的线粒体功能障碍。