LED Photobiomodulation at 630 nm Attenuates TNF-α-Induced Senescence-Associated Responses in Association with Mitochondrial Homeostasis
- 1Wu Lien-Teh Institute, Heilongjiang Key Laboratory of Immunity and Infection, Department of Microbiology, School of Basic Medical Sciences, Harbin Medical University, Harbin 150081, China
Abstract
Chronic inflammation can accelerate the aging of joint tissues, characterized by cellular senescence, inflammatory degeneration, and disrupted tissue homeostasis. The accumulation of senescent cells and the excessive release of senescence-associated secretory phenotype (SASP) factors are accompanied by mitochondrial dysfunction, including increased oxidative stress, reduced mitochondrial membrane potential, and impaired mitochondrial quality control. Since TNF-α is a key inflammatory mediator in arthritic tissues, we used TNF-α-stimulated human fibroblast-like synoviocytes (MH7A) and chondrocytes (C28/I2), along with hTNF-α transgenic mice, to investigate whether 630 nm LED photobiomodulation therapy (PBMT) attenuates inflammatory and senescence-associated responses and whether these effects are linked to the restoration of mitochondrial homeostasis. Transcriptomic analysis, cell-based assays, and tissue immunohistochemistry were used to assess inflammatory and senescence-associated gene expression, mitochondrial features, autophagy-related proteins, and SIRT1/PGC-1α levels. PBMT reduced the TNF-α-induced expression of IL-6, IL-1β, IL-8, MMP-3, MMP-13, p16, and p21 in both cell models. Further experiments in C28/I2 cells showed that TNF-α increased reactive oxygen species (ROS) production, reduced mitochondrial membrane potential, disrupted mitochondrial ultrastructure, altered autophagy-related protein expression, and decreased SIRT1 and PGC-1α expression. These alterations were partially reversed by PBMT, accompanied by the restoration of mitochondrial homeostasis-related markers. Extending the in vitro findings, in vivo experiments using hTNF-α transgenic mice showed that PBMT enhanced the immunostaining signals of SIRT1 and PGC-1α in joint tissues. Overall, these findings indicate that PBMT attenuates TNF-α-induced inflammatory and senescence-associated responses in joint cells, which are associated with mitochondrial homeostasis, supporting further mechanistic and functional evaluation of this intervention.
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BibTeX
@article{li2026photobiomodulation,
title = {{LED Photobiomodulation at 630 nm Attenuates TNF-α-Induced Senescence-Associated Responses in Association with Mitochondrial Homeostasis}},
author = {Xueqian Li and Lihong Zhang and Nan Wang and Xiao Yang and Wenting Xie and Qingtai Meng and Longfei Hu and Hailiang Liu and Wuqi Song},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = oct,
doi = {10.3390/ijms27219784},
url = {https://www.mdpi.com/1422-0067/27/21/9784},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - LED Photobiomodulation at 630 nm Attenuates TNF-α-Induced Senescence-Associated Responses in Association with Mitochondrial Homeostasis
AU - Xueqian Li
AU - Lihong Zhang
AU - Nan Wang
AU - Xiao Yang
AU - Wenting Xie
AU - Qingtai Meng
AU - Longfei Hu
AU - Hailiang Liu
AU - Wuqi Song
PY - 2026
DA - 2026/10/30
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27219784
UR - https://www.mdpi.com/1422-0067/27/21/9784
AB - Chronic inflammation can accelerate the aging of joint tissues, characterized by cellular senescence, inflammatory degeneration, and disrupted tissue homeostasis. The accumulation of senescent cells and the excessive release of senescence-associated secretory phenotype (SASP) factors are accompanied by mitochondrial dysfunction, including increased oxidative stress, reduced mitochondrial membrane potential, and impaired mitochondrial quality control. Since TNF-α is a key inflammatory mediator in arthritic tissues, we used TNF-α-stimulated human fibroblast-like synoviocytes (MH7A) and chondrocytes (C28/I2), along with hTNF-α transgenic mice, to investigate whether 630 nm LED photobiomodulation therapy (PBMT) attenuates inflammatory and senescence-associated responses and whether these effects are linked to the restoration of mitochondrial homeostasis. Transcriptomic analysis, cell-based assays, and tissue immunohistochemistry were used to assess inflammatory and senescence-associated gene expression, mitochondrial features, autophagy-related proteins, and SIRT1/PGC-1α levels. PBMT reduced the TNF-α-induced expression of IL-6, IL-1β, IL-8, MMP-3, MMP-13, p16, and p21 in both cell models. Further experiments in C28/I2 cells showed that TNF-α increased reactive oxygen species (ROS) production, reduced mitochondrial membrane potential, disrupted mitochondrial ultrastructure, altered autophagy-related protein expression, and decreased SIRT1 and PGC-1α expression. These alterations were partially reversed by PBMT, accompanied by the restoration of mitochondrial homeostasis-related markers. Extending the in vitro findings, in vivo experiments using hTNF-α transgenic mice showed that PBMT enhanced the immunostaining signals of SIRT1 and PGC-1α in joint tissues. Overall, these findings indicate that PBMT attenuates TNF-α-induced inflammatory and senescence-associated responses in joint cells, which are associated with mitochondrial homeostasis, supporting further mechanistic and functional evaluation of this intervention.
SN - 1422-0067
ER -