Sesamin-mediated high expression of BECN2 ameliorates cartilage endplate degeneration by reducing autophagy and inflammation.

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. In vivo 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.

Enhancement and Repair of Degenerative Intervertebral Disc in Rats Using Platelet-Rich Plasma/Ferulic Acid Hydrogel.

BACKGROUND: Intervertebral degenerative disc (IDD) disease is one of the most common clinical conditions causing low back pain. The main objective of this study was to investigate the repair effect of platelet-rich plasma (PRP) and ferulic acid (FA) hydrogel compound on degenerative discs in rats in combination with bioengineering technology, which may provide a strong theoretical basis for the future treatment of IDD. METHODS: Forty-five male Sprague-Dawley rats were randomly divided into groups A-F; MRI was performed in each group at 0, 4, and 8 weeks after injection; and disc tissues were obtained after executing the animals. The histomorphology, apoptosis, and protein synthesis of intervertebral discs in each group were observed by hematoxylin-eosin, Masson, terminal deoxynucleotidyl transferase dUTP nick end labeling staining, and Western blot. RESULTS: The release concentration of all groups reached the peak at 12 hours, and the highest concentration was found in the hydrogel/PRP/FA group at the same time. The MTT assay showed that hydrogel/PRP/FA is well-cytocompatible. The results of animal experiments show that hydrogel/PRP/FA has a good effect on degenerative intervertebral disc in rats. CONCLUSION: PRP/FA-rich hydrogel compound plays an active role in promoting extracellular matrix synthesis, strengthening and repairing degenerated intervertebral discs in rats.