%0 Journal Article %T 高糖饮食重塑肠道菌群加重博来霉素诱导的肺纤维化
A High-Glucose Diet Aggravates Bleomycin-Induced Pulmonary Fibrosis by Reshaping the Gut Microbiota %A 朱梦婷 %A 李永怀 %J Advances in Clinical Medicine %P 923-931 %@ 2161-8720 %D 2025 %I Hans Publishing %R 10.12677/acm.2025.152427 %X 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)。但是高糖喂养的小鼠的体重只是略微比正常喂养的小鼠体重升高(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 < 0.01)。高糖喂养的小鼠的肺脏的肺纤维化评分(Score of Aschcroft)明显高于正常喂养的小鼠血糖(P < 0.01)。16s rRNA显示糖喂养的小鼠的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 < 0.05)。结论：高糖饮食可能通过重塑肠道菌群从而加重肺组织纤维化。我们的研究可能为临床肺纤维化的管理和预防提供新的视角和可能的治疗途径。
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). Conversely, the body weight of mice on the high-sugar diet was only marginally higher than that of the control group (P > 0.05). The lung index, calculated as the ratio of lung weight to body weight, was significantly increased in the high-sugar diet group compared to the control group (P < 0.01). Additionally, the pulmonary fibrosis score, as assessed by the Ashcroft scale, was significantly higher in the high-glucose fed mice than in the normally fed mice (P < 0.01). Analysis of 16S rRNA revealed that both α diversity and β diversity in the gut microbiota of sugar-fed mice differed significantly from those in the control group (P < 0.05). Conclusion: High-glucose diet may aggravate pulmonary fibrosis by remodeling gut microbiota. Our study may provide new perspectives and possible therapeutic pathways for the management and prevention of clinical %K 肺纤维化， %K 高糖饮食， %K 肠道菌群， %K 博来霉素
Pulmonary Fibrosis %K High-Glucose Diet %K Gut Microbiota %K Bleomycin %U http://www.hanspub.org/journal/PaperInformation.aspx?PaperID=107968