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在儿童中,慢性炎症和人体蛋白调节之间存在一种新的联系

Yunhan Zhao¹, Outi Mäkitie^2,3, Saila Laakso²

¹Department of Women's and Children's Health, Karolinska Institutet and Pediatric Endocrinology Unit, Karolinska University Hospital, Solna, Sweden.

Frontiers in endocrinology

|February 7, 2024

概括

患有炎症性肠病 (IBD) 的儿童的人类蛋白水平较低,影响骨健康. 人类类类比治疗显示出对炎症诱导的骨生长障碍的潜在治疗效果.

科学领域:

儿科内分泌学儿科内分泌学
炎症性肠道疾病研究研究
骨生物学和新陈代谢

背景情况:

患有炎症性肠病 (IBD) 的儿童经常经历骨生长和健康受损.
假设在慢性炎症期间,骨中发现的保护因子人被抑制.

研究的目的:

为了研究IBD儿童的humanin水平.
检查IBD血清和TNF对生长板软骨中人体蛋白表达的作用.
评估人氨酸在缓解炎症引起的骨生长障碍方面的治疗潜力.

主要方法:

在儿科IBD患者和健康对照中,使用ELISA量化血清胰岛素水平.
人体生长板扩展物被活体培养成IBD血清或TNF,随后对人体素和相关标记物进行免疫组织化学.
人类类相应物 (HNG) 的治疗疗效被评估为体外培养的胎儿大腿骨.

主要成果:

与对照组相比,患有IBD的儿童的血清人氨酸水平显著降低.
IBD血清和TNF暴露抑制了人类生长板软骨中的人体表达.
TNF降低了人氨酸,PCNA,SOX9和TRAF2的表达;人氨酸模拟HNG改善了TNF诱导的骨生长缺陷.

结论:

儿童IBD血清胰岛素降低表明慢性炎症和胰岛素失调之间存在联系.
IBD血清抑制了生长板软骨中人体的表达,突出了骨健康受损的潜在机制.
人类素可以作为治疗目标,治疗与炎症性肠病相关的骨并发症.

关键词:

IBD IBD IBD IBD IBD IBD IBD IBD IBD IBD IBD IBD IBD IBD IBD 这就是TNF TNF.冠状腺细胞冠状腺细胞增长板的增长板是什么人类在人类在人类.

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