国际妇产科学杂志 ›› 2024, Vol. 51 ›› Issue (2): 161-166.doi: 10.12280/gjfckx.20231050

• 产科生理及产科疾病:综述 • 上一篇    下一篇

TNF-α和IL-6对胎儿生长受限胎儿骨骼肌的影响

王艳, 王雅慧, 王艳(), 裴飞   

  1. 150040 哈尔滨,黑龙江中医药大学(王艳,王雅慧);黑龙江中医药大学附属第二医院(王艳,裴飞)
  • 收稿日期:2023-12-14 出版日期:2024-04-15 发布日期:2024-04-19
  • 通讯作者: 王艳,E-mail:swallow-1113@163.com
  • 作者简介:审校者

The Effects of TNF-α and IL-6 on Skeletal Muscle of Fetuses with Fetal Growth Restriction

WANG Yan, WANG Ya-hui, WANG Yan(), PEI Fei   

  1. Heilongjiang University of Traditional Chinese Medicine, Harbin 150040, China (WANG Yan, WANG Ya-hui); The Second Affiliated Hospital of Heilongjiang University of Traditional Chinese Medicine, Harbin 150001, China (WANG Yan, PEI Fei)
  • Received:2023-12-14 Published:2024-04-15 Online:2024-04-19
  • Contact: WANG Yan, E-mail: swallow-1113@163.com

摘要:

胎儿生长受限(fetal growth restriction,FGR)是一种常见的产科疾病,其可导致新生儿低出生体质量和出生后肌肉量减少。这可能与肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)和白细胞介素-6(interleukin-6,IL-6)的调控密切相关。研究发现,这两种炎症因子在FGR胎儿中表达水平异常,可通过影响成肌细胞的增殖和分化,干扰正常骨骼肌的发育。此外,TNF-α与IL-6还可以激活特定的信号通路,如核因子κB(nuclear factor-κB,NF-κB)、Janus激酶/信号转导及转录活化因子(Janus kinase/signal transducer and activator of transcription,JAK/STAT)、丝裂原激活的蛋白激酶(mitogen-activated protein kinase,MAPK)等信号通路,调节肌细胞的代谢和功能。如使用特定的抗炎药物或生物制剂来降低TNF-α和IL-6的活性,可能有助于改善FGR胎儿的骨骼肌发育。总的来说,TNF-α和IL-6在FGR胎儿骨骼肌发育中的作用是一个多层面、复杂的过程,需要进一步的深入研究来阐明其具体机制,帮助理解FGR的病理生理学,并为治疗FGR胎儿提供新的思路。

关键词: 白细胞介素6, 肿瘤坏死因子α, 胎儿生长迟缓, 信号传导, 肌, 骨骼

Abstract:

Fetal growth restriction (FGR) is a common obstetric condition and resulting in low birth weight and reduced muscle mass in newborns after birth. This may be closely related to the regulatory mechanisms of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Studies have found that these two inflammatory factors are expressed at abnormal levels in FGR fetuses, affecting the proliferation and differentiation of myoblasts, interfering with the normal development of skeletal muscle. Moreover, TNF-α and IL-6 can activate specific signaling pathways, such as nuclear factor-κB (NF-κB), Janus kinase/signal transducer and activator of transcription (JAK/STAT), mitogen-activated protein kinase (MAPK), and other signaling pathways that regulate myocyte metabolism and function. Using specific anti-inflammatory drugs or biological agents to reduce the activity of TNF-α and IL-6 may help improve the skeletal muscle development in FGR fetuses. Overall, the role of TNF-α and IL-6 in the skeletal muscle development of FGR fetuses is a multifaceted and complex process, requiring further in-depth research to clarify their specific mechanisms, aiding to the understanding of the pathophysiology of FGR, and providing new ideas for the treatment of FGR fetuses.

Key words: Interleukin-6, Tumor necrosis factor-alpha, Fetal growth retardation, Signal transduction, Muscle, skeletal