目的:肺纤维化的确切病因尚不清楚,但它是一种慢性进行性疾病,可导致呼吸衰竭和肺组织破坏。高糖饮食被认为是促进肺纤维化的一个可能的危险因素,但高糖饮食影响肺纤维化的具体机制尚不清楚。在这项研究中,我们对高糖饮食对肺纤维化影响机制进行进一步探索。方法:C57BL/6小鼠给予博来霉素(BLM)建立了有效的肺纤维化动物模型。我们给予BLM引起肺纤维化的小鼠给予20%葡萄糖水或常规饮用水。通过苏木精–伊红染色法(HE),马松染色(Masson)评估肺纤维化的严重程度。采用16s rRNA检测小鼠肠道菌群的改变。结果:高糖喂养的小鼠的血糖明显高于正常喂养的小鼠血糖(P 0.05)。高糖喂养的小鼠的肺指数即肺脏体重/小鼠体重明显高于正常喂养的小鼠血糖(P α多样性和β多样性相比于正常喂养的小鼠具有显著差异(P Purpose: The exact etiology of pulmonary fibrosis is unknown, but it is a chronic, progressive illness that can cause respiratory failure and the destruction of lung tissues. High-glucose diets are considered a possible risk factor for promoting pulmonary fibrosis, but the specific mechanisms by which high-glucose diets affect pulmonary fibrosis are not clear. In this study, we investigated the mechanisms underlying lung fibrosis and the means by which a high-glucose diet affects them. Methods: BLM administration in mice establishes an effective animal model of pulmonary fibrosis. Mice with BLM-induced pulmonary fibrosis were given either 20% glucose water or regular drinking water. Hematoxylin-eosin staining (HE) and Masson staining were used to evaluate the severity of pulmonary fibrosis. The changes of intestinal flora in mice were detected by 16s rRNA. Results: The blood glucose levels in mice subjected to a high-glucose diet were significantly elevated compared to those in mice on a standard diet (P 0.05). The lung index, calculated as the ratio of lung weight to body weight, was significant
