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Journal Article Research Support, Non-U.S. Gov't Ppublish 2 citations

PubMed: 38284902 DOI: 10.18632/aging.205386

Sesamin-mediated high expression of ameliorates cartilage endplate degeneration by reducing autophagy and inflammation.

Aging (Albany NY) 16(2):1145-1160

Authors: Baining Zhang, Zhiwei He, Jialin Guo, Feng Li, Zhi Huang, Wenkai Zheng, Wenhua Xing, Manglai Li, Yong Zhu, Xuejun Yang

Affiliations

  • Inner Mongolia Medical University, Hohhot, Inner Mongolia, China.
  • Department of Spine Surgery, Area A, The Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia, China.
  • Department of Bone and Soft Tissue Oncology, The Affiliated People’s Hospital of inner Mongolia Medical University, Peking University Cancer Hospital, Hohhot, Inner Mongolia, China.

Abstract

Lumbar disc degeneration (LDD) is a prevalent clinical spinal disease characterized by the calcification and degeneration of the cartilage endplate (CEP), which significantly reduces nutrient supply to the intervertebral disc. Traditional Chinese medicine offers a conservative and effective approach for treating LDD. We aimed to investigate the molecular mechanisms underlying the therapeutic effects of Sesamin in LDD treatment. Transcriptome sequencing was used to analyze the effect of Sesamin on LPS-induced ATDC5. We explored the role of BECN2, a target gene of Sesamin, in attenuating LPS-induced degeneration of ATDC5 cells. Our results revealed the identification of 117 differentially expressed genes (DEGs), with 54 up-regulated and 63 down-regulated genes. Notably, Sesamin significantly increased the expression of BECN2 in LPS-induced ATDC5 cell degeneration. Overexpressed BECN2 enhanced cell viability and inhibited cell apoptosis in LPS-induced ATDC5 cells, while BECN2 knockdown reduced cell viability and increased apoptosis. Furthermore, BECN2 played a crucial role in attenuating chondrocyte degeneration by modulating autophagy and inflammation. Specifically, BECN2 suppressed autophagy by reducing the expression of ATG14, VPS34, and GASP1, and alleviated the inflammatory response by decreasing the expression of inflammasome proteins NLRP3, NLRC4, NLRP1, and AIM2. experiments further supported the beneficial effects of Sesamin in mitigating LDD. This study provides novel insights into the potential molecular mechanism of Sesamin in treating LDD, highlighting its ability to mediate autophagy and inflammation inhibition via targeting the BECN2. This study provides a new therapeutic strategy for the treatment of LDD, as well as a potential molecular target for LDD.

MeSH

Cartilage, Apoptosis, Aging, Cells, Therapeutics, Cell Survival, Genes, Autophagy

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