College of Traditional Chinese Medicine, Changchun University of Chinese Medical, Changchun, China.
Department of Pediatrics, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, Jilin, China.
J Asthma. 2024 Jul;61(7):725-735. doi: 10.1080/02770903.2024.2303755. Epub 2024 Apr 22.
This study aims to explore the effect of YiQi GuBen capsule on improving mitochondrial dysfunction in an animal model of asthma. The mice ( = 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). 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. This study suggests YiQi GuBen capsule can effectively improve mitochondrial dysfunction in the OVA-induced mouse model.
本研究旨在探讨益气固本胶囊对改善哮喘动物模型中线粒体功能障碍的作用。将小鼠(n=8)分为四组:对照组(NC)、卵清蛋白(OVA)组、地塞米松(OVA+DEX)组和益气固本(OVA+YQGB)组。首先,除 NC 组外,我们建立了 OVA 诱导的小鼠哮喘模型,然后用地塞米松和益气固本胶囊进行治疗。随后,采用 HE 染色和 Masson 染色进行小鼠肺组织的病理分析。接下来,我们使用透射电子显微镜(TEM)观察益气固本胶囊对线粒体超微结构的影响。流式细胞术用于分析肺组织中 ROS 水平、膜电位和线粒体数量。此外,我们分析了线粒体 DNA(mtDNA)的拷贝数以及激活过氧化物酶体增殖物激活受体γ共激活因子 1α(PGC-1α)和线粒体转录因子 A(TFAM)的表达水平。病理分析结果表明,经益气固本胶囊治疗后,肺组织损伤明显减轻。此外,我们观察到线粒体的超微结构损伤得到改善。流式细胞术证实,经益气固本胶囊治疗后,线粒体中 ROS 水平有效降低,而线粒体膜电位降低,数量显著增加。此外,我们发现 mtDNA 的拷贝数显著增加,PGC-1α 和 TFAM 的表达水平显著上调。本研究表明,益气固本胶囊可有效改善 OVA 诱导的小鼠模型中线粒体功能障碍。