Lactiplantibacillus plantarum P101 Ameliorates TiO2 NP-Induced Bone Injury in Young Rats by Remodeling the Gut Microbiota and Inhibiting the Production of Pro-Inflammatory Cytokines.

IF 6.6 2区 医学 Q1 NANOSCIENCE & NANOTECHNOLOGY
International Journal of Nanomedicine Pub Date : 2024-11-09 eCollection Date: 2024-01-01 DOI:10.2147/IJN.S473270
Lixin Xie, Lihua Feng, Xiaomin Tang, Yunping Xu, Hengyi Xu, Yang Liu
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引用次数: 0

Abstract

Purpose: To evaluate the therapeutic effect of oral administration of Lactiplantibacillus plantarum P101 (P101) on skeletal injury in young rats exposed to titanium dioxide nanoparticles (TiO2 NPs), and explore the potential mechanism.

Methods: Four-week-old male rats were orally administration to TiO2 NPs and supplemented with P101 2 hours later for 4 weeks. The growth and development, food intake, bone metabolism and serum inflammatory markers of the rats were evaluated. Their tibias were observed and evaluated using microcomputed tomography (micro-CT), tartrate-resistant acid phosphatase (TRAP) staining, immunohistochemistry (IHC) and real-time quantitative PCR (RT-qPCR). We observed the tibia growth plate using safranin and fast green staining. 16S rDNA sequence analysis of fecal samples was performed to observe changes in the gut microbiota.

Results: Our results showed that TiO2 NPs can lead to bone growth inhibition and osteoporosis, induce intestinal flora imbalance, and induce inflammation in young rats. Further mechanistic studies suggested that TiO2 NPs disrupts intestinal flora and increases serum IL-1β levels, which increased the expression of RANKL in bone, thereby enhancing osteoclast differentiation and function, leading to bone loss. Through a P101 supplementation experiment, we found that P101 ameliorated the inflammation and osteoporosis on bone caused by TiO2 NPs.

Conclusion: This study showed that the mechanism by which P101 alleviates bone damage caused by TiO2 NPs may be through restoring intestinal microbial homeostasis and inhibiting inflammatory response.

植物乳杆菌 P101 通过重塑肠道微生物群和抑制促炎细胞因子的产生来改善二氧化钛氮氧化物诱发的幼鼠骨损伤
目的:评估口服植物乳杆菌 P101(P101)对暴露于二氧化钛纳米粒子(TiO2 NPs)的幼年大鼠骨骼损伤的治疗效果,并探讨其潜在机制:方法:给4周大的雄性大鼠口服TiO2 NPs,2小时后补充P101,连续4周。对大鼠的生长发育、食物摄入量、骨代谢和血清炎症指标进行评估。使用微型计算机断层扫描(micro-CT)、耐酒石酸磷酸酶(TRAP)染色、免疫组织化学(IHC)和实时定量 PCR(RT-qPCR)对大鼠的胫骨进行了观察和评估。我们使用黄绿素和快速绿染色法观察了胫骨生长板。对粪便样本进行了 16S rDNA 序列分析,以观察肠道微生物群的变化:结果:我们的研究结果表明,TiO2 NPs可导致幼鼠骨生长受抑制和骨质疏松症,诱发肠道菌群失调和炎症。进一步的机理研究表明,TiO2 NPs会破坏肠道菌群,增加血清中IL-1β的水平,而IL-1β会增加骨中RANKL的表达,从而增强破骨细胞的分化和功能,导致骨质流失。通过补充 P101 的实验,我们发现 P101 可改善 TiO2 NPs 引起的炎症和骨质疏松:本研究表明,P101减轻TiO2 NPs引起的骨损伤的机制可能是通过恢复肠道微生物平衡和抑制炎症反应。
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来源期刊
International Journal of Nanomedicine
International Journal of Nanomedicine NANOSCIENCE & NANOTECHNOLOGY-PHARMACOLOGY & PHARMACY
CiteScore
14.40
自引率
3.80%
发文量
511
审稿时长
1.4 months
期刊介绍: The International Journal of Nanomedicine is a globally recognized journal that focuses on the applications of nanotechnology in the biomedical field. It is a peer-reviewed and open-access publication that covers diverse aspects of this rapidly evolving research area. With its strong emphasis on the clinical potential of nanoparticles in disease diagnostics, prevention, and treatment, the journal aims to showcase cutting-edge research and development in the field. Starting from now, the International Journal of Nanomedicine will not accept meta-analyses for publication.
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