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| 酒精性骨质疏松模型大鼠肠道菌群及短链脂肪酸代谢特征分析 |
| Alterations in gut microbiota and short-chain fatty acid metabolism in a rat model of alcohol-induced osteoporosis |
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| DOI：10.3969/j.issn.1006-7108.2026.08.007 |
| 中文关键词: 酒精性骨质疏松 肠道菌群 短链脂肪酸 |
| 英文关键词:alcohol-induced osteoporosis gut microbiota short-chain fatty acids |
| 基金项目:国家自然科学基金项目（82374496）；黑龙江省中医药科研项目（ZHY18-066） |
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| 中文摘要: |
| 目的 分析酒精性骨质疏松大鼠肠道菌群结构与功能变化及短链脂肪酸代谢特征，探讨其在疾病发生中的作用机制。方法 采用随机数字表法将20只SD雄性大鼠分为正常对照组（normal control group 组，10只）和酒精组[Alcohol(AOP)组，10只]。取骨组织进行HE、Masson及Oil Red O染色，并采用micro-CT进行三维重建与定量分析（BV/TV、Tb.N、Tb.Th、Tb.Sp）；取结肠组织进行HE与Masson染色；同时检测血清钙（Ca）、磷（P）、IL-6和LPS水平。采集粪便进行16S rDNA测序与短链脂肪酸（SCFAs）靶向定量。结果 AOP组骨小梁变细、断裂、排列紊乱、间隙增大，胶原纤维减少、矿化减弱、脂滴增多；形态计量学显示BV/TV与Tb.N显著降低（P＜0.001）、Tb.Th降低（P＜0.05）、Tb.Sp升高（P＜0.01）。结肠上皮受损，黏膜下水肿及纤维化增强。血清Ca、P降低（P＜0.01、P＜0.001），IL-6与LPS升高（P＜0.01、P＜0.001）。肠道菌群α多样性下降（P＜0.05），β多样性显著分离；功能预测富集脂多糖生物合成、细菌分泌系统、趋化性及氨基糖代谢等通路。SCFAs总量降低（P＜0.01），其中丙酸、丁酸、异丁酸、戊酸显著下降（P＜0.01或P＜0.05）；乙酸、异戊酸、己酸虽无统计学差异，但均呈下降趋势。结论 长期酒精摄入下，肠道微生态失衡及SCFAs水平降低并存，伴随促炎相关功能通路上调与骨代谢异常，可能导致骨量丢失。 |
| 英文摘要: |
| Objective To analyze alterations in gut microbial composition and function and the metabolic profile of short-chain fatty acids (SCFAs) in rats with alcohol-induced osteoporosis (AOP), and to explore their potential roles in disease development. Methods Twenty male Sprague–Dawley rats were randomly assigned (random number table) to a normal control group (n=10) and an alcohol group (n=10). Bone tissues underwent hematoxylin–eosin (H&E), Masson’s trichrome, and Oil red O staining, and were assessed with micro-CT (μCT) for three-dimensional reconstruction and quantitative morphometry (BV/TV, Tb.N, Tb.Th, Tb.Sp). Colon tissues were examined with H&E and Masson’s staining. Serum calcium (Ca), phosphorus (P), interleukin-6 (IL-6), and lipopolysaccharide (LPS) were measured. Fecal samples were subjected to 16S rDNA sequencing and targeted quantification of SCFAs. Results Compared with the control group, the AOP group exhibited thinner and fractured trabeculae with disordered arrangement and enlarged inter-trabecular spaces. Collagen fibers were reduced, mineralization was attenuated, and lipid droplets increased. μCT morphometry showed decreases in BV/TV and Tb.N (both P<0.001), a decrease in Tb.Th (P<0.05), and an increase in Tb.Sp (P<0.01). Colon epithelium was damaged with submucosal edema and enhanced fibrosis. Serum Ca and P were reduced (P<0.01 and P<0.001, respectively), whereas IL-6 and LPS were elevated (both P<0.01 or P<0.001). Gut microbial α-diversity decreased (P<0.05) and β-diversity differed markedly among the groups. The functional prediction indicated enrichment of pathways related to lipopolysaccharide biosynthesis, bacterial secretion systems, chemotaxis, and amino sugar metabolism. Total fecal SCFAs were lower in the AOP group (P<0.01), with significant reductions in propionate, butyrate, isobutyrate, and valerate (P<0.01 or P<0.05). Acetate, isovalerate, and caproate showed downward trends without statistical significance. Conclusion Under chronic alcohol exposure, dysbiosis of the gut microbiota and reduced SCFA levels co-occur, accompanied by upregulation of pro-inflammatory functional pathways and abnormalities in bone metabolism, which may lead to bone loss. |
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