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CQZC02对力竭性跑步小鼠结肠损伤的调控及运动能力的改善

Regulation of colon injury and improvement of exercise performance in exhausted running mice by CQZC02.

作者信息

Cai Limin, Wang Beibei

机构信息

Department of Physical Education, North China Electric Power University, Beijing, China.

Department of Physical Education, University of International Business and Economics, Beijing, China.

出版信息

Front Physiol. 2024 Sep 20;15:1475413. doi: 10.3389/fphys.2024.1475413. eCollection 2024.

Abstract

In this study, strenuous forced exercise caused intestinal damage and reduced the exercise capacity of mice. However, the antioxidant and anti-inflammatory properties of CQZC02 (LPCQZC02) were found to improve both the intestinal barrier and exercise function in mice. The effectiveness of LPCQZC02 was confirmed through various methods, including kit detection, pathological observation, quantitative reverse transcription polymerase chain reaction (qRT-PCR), and intestinal flora analysis. The findings demonstrated that LPCQZC02 could control colonic index, lessen colonic enlargement caused by intense exercise, and extend the running duration of mice. Serum levels of total superoxide dismutase (T-SOD), glutathione (GSH), and interleukin-10 (IL-10) were elevated, whereas those of malondialdehyde (MDA), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were reduced. The findings of the mRNA expression analysis revealed that in the colons of mice who remarkably exercised, LPCQZC02 could increase the expression levels of zonula occludens-1 (ZO-1), occludin-1, and claudin-1 genes. Additionally, in skeletal muscle tissue, it could downregulate TNF-α expression level and upregulate copper/zinc superoxide dismutase (Cu/Zn-SOD) and manganese superoxide dismutase (Mn-SOD) expression levels. Furthermore, LPCQZC02 could both reduce and promote beneficial bacteria in the intestines of mice undergoing intense exercise. In conclusion, LPCQZC02 emerged as a functional probiotic and demonstrated a notable advantage over sulfasalazine, a medication for intestinal conditions, in mitigating oxidative inflammation, repairing intestinal barrier damage, and enhancing motor function in mice subjected to strenuous exercise.

摘要

在本研究中,剧烈强迫运动导致小鼠肠道损伤并降低其运动能力。然而,发现CQZC02(LPCQZC02)的抗氧化和抗炎特性可改善小鼠的肠道屏障和运动功能。通过多种方法证实了LPCQZC02的有效性,包括试剂盒检测、病理观察、定量逆转录聚合酶链反应(qRT-PCR)和肠道菌群分析。研究结果表明,LPCQZC02可以控制结肠指数,减轻剧烈运动引起的结肠肿大,并延长小鼠的跑步持续时间。血清总超氧化物歧化酶(T-SOD)、谷胱甘肽(GSH)和白细胞介素-10(IL-10)水平升高,而丙二醛(MDA)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)水平降低。mRNA表达分析结果显示,在剧烈运动的小鼠结肠中,LPCQZC02可以增加紧密连接蛋白-1(ZO-1)、闭合蛋白-1和Claudin-1基因的表达水平。此外,在骨骼肌组织中,它可以下调TNF-α表达水平并上调铜/锌超氧化物歧化酶(Cu/Zn-SOD)和锰超氧化物歧化酶(Mn-SOD)表达水平。此外,LPCQZC02可以减少并促进剧烈运动小鼠肠道中的有益细菌。总之,LPCQZC02作为一种功能性益生菌出现,并在减轻氧化炎症、修复肠道屏障损伤和增强剧烈运动小鼠的运动功能方面显示出比用于肠道疾病的药物柳氮磺胺吡啶更显著的优势。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c14/11450257/71445e54722d/fphys-15-1475413-g001.jpg

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