Changes in PI3K/AKT and NRF2/HO-1 signaling expression and intestinal microbiota in bleomycin-induced pulmonary fibrosis

文献类型： 外文期刊

第一作者： Li, Chenchen

作者： Li, Chenchen;Cao, Yuxia;Peng, Yousheng;Ma, Ting;Hua, Yongli;Bai, Tong;Wei, Yanming;Ji, Peng;Wang, Xiuqin;Wu, Fanlin

作者机构：

关键词： Bleomycin; Pulmonary fibrosis; NRF2/HO-1; PI3K/AKT; Pathway; Intestinal flora

期刊名称：FOOD AND CHEMICAL TOXICOLOGY （ 影响因子：3.9； 五年影响因子：4.5 ）

ISSN： 0278-6915

年卷期： 2024 年 190 卷

页码：

收录情况： SCI

摘要： Pulmonary fibrosis is the outcome of the prolonged interstitial pneumonia, characterized by excessive accumulation of fibroblasts and collagen deposition, leading to its development. This study aimed to study the changes in PI3K/AKT and NRF2/HO-1 signaling expression and intestinal microbiota in a rat model of a novel bleomycin-induced pulmonary fibrosis. The findings of our study showed the model was successfully established. The results showed that the alveolar septum in the model was significantly widened and infiltrated by severe inflammatory cells. Alveolar atrophy occurred due to the formation of multiple inflammatory foci. During this period, fibrous tissue was distributed in strips and patches, primarily around the pulmonary interstitium and bronchus. Moreover, lung damage and fibrosis progressively worsened over time. The mRNA expression of HO-1 and NRF2 in the model decreased while the mRNA expression of HIF-1 alpha, VEGF, PI3K and AKT increased. Furthermore, it was observed to decrease the protein expression of E-cad, HO-1 and NRF2, and increase the protein expression of alpha-SMA and p-AKT. Additionally, this model leaded to an imbalance in the intestinal microbiota. This study demonstrate that the novel pulmonary fibrosis model activates the NRF2/HO-1 pathway and the PI3K/AKT pathway in rat lung tissues, and leading to intestinal barrier disorder.

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