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In this report, we have investigated the apoptosis and autophagy of chondrocytes induced by the T-2 and HT-2 toxins. The viability of chondrocytes was measured by the MTT assay. Malondialdehyde (MDA) and superoxide dismutase (SOD) kits were used to measure the oxidative stress of chondrocytes. The apoptosis of chondrocytes was measured using flow cytometry. Hoechst 33258 and MDC staining agents were introduced to analyze apoptosis and autophagy induction in chondrocytes, respectively. Protein expression of Bax, caspase-9, caspase-3, and Beclin1 was examined by western blotting analysis. The T-2 and HT-2 toxins significantly decreased the viability of chondrocytes in a time-dependent manner. The level of oxidative stress in chondrocytes induced by the T-2 toxin was significantly higher when compared with that of the HT-2 toxin. The apoptosis rate of chondrocytes induced by the T-2 toxin increased from 3.26 ± 1.03%, 18.38 ± 1.28%, 34.5 ± 1.40% to 49.67 ± 5.31%, whereas apoptosis rate of chondrocytes induced by the HT-2 toxin increased from 3.82 ± 1.03%, 11.61 ± 1.27%, 25.72 ± 2.95% to 36.28 ± 2.81% in 48 h incubation time. Hoechst 33258 staining confirmed that apoptosis of chondrocytes induced by the T-2 toxin was significantly higher than that observed when the chondrocytes were incubated with the HT-2 toxin. MDC staining revealed that the autophagy rate of chondrocytes induced by the T-2 toxin increased from 6.38% to 63.02%, whereas this rate induced by the HT-2 toxin changed from 6.08% to 53.33%. The expression levels of apoptosis and autophagy related proteins, Bax, caspase-9, caspase-3, and Beclin1 in chondrocytes induced by the T-2 toxin were significantly higher when compared with those levels induced by the HT-2 toxin.
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http://dx.doi.org/10.3390/toxins11050260 | DOI Listing |
J Extracell Vesicles
September 2025
Division of Sports Medicine and Adult Reconstructive Surgery, Department of Orthopedic Surgery, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, China.
Osteoarthritis (OA), the prevalent debilitating joint disorder, is accelerated by dysregulated intercellular crosstalk, yet the role of fibroblast-like synoviocyte (FLS)-derived extracellular vesicles and particles (EVPs) in disease progression remains to be elucidated. Here, integrative analysis of clinical specimens, animal models, and publicly available datasets revealed significant alterations in exosomal pathways within OA synovium. Proteomic profiling revealed distinct molecular signatures in EVPs derived from inflammatory and senescent FLSs, reflecting the pathophysiological status of their parent cells.
View Article and Find Full Text PDFJ Biochem Mol Toxicol
September 2025
Department of Rehabilitation Medicine, The Second Affiliated Hospital of Anhui Medical University, Hefei, China.
Heat shock protein family A member 4-like (HSPA4L) has been shown to be overexpressed in osteoarthritis (OA) patients, but its role in OA process still unknown. Chondrocytes were stimulated with interleukin-1β (IL-1β) to mimic OA cell model in vitro, and rat was injected with monosodium iodoacetate (MIA) to construct OA rat model in vivo. The expression of HSPA4L, methyltransferase-like 3 (METTL3) and extracellular matrix (ECM)-related markers was examined by qRT-PCR or western blot.
View Article and Find Full Text PDFZhong Nan Da Xue Xue Bao Yi Xue Ban
May 2025
Department of Rehabilitation Medicine, Second Xiangya Hospital, Central South University, Changsha 410011.
Objectives: Osteoarthritis (OA) is one of the most common chronic degenerative diseases, with chondrocyte apoptosis and extracellular matrix (ECM) degradation as the major pathological changes. The mechanical stimulation can attenuate chondrocyte apoptosis and promote ECM synthesis, but the underlying molecular mechanisms remain unclear. This study aims to investigate the role of primary cilia (PC) in mediating the effects of mechanical stimulation on OA progression.
View Article and Find Full Text PDFJ Adv Res
September 2025
State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi International Joint Research Center for Oral Diseases, Department of Oral Anatomy and Physiology and TMD, School of Stomatology, The Fourth Military Medical Univ
Introduction: Aberrant biomechanical force-induced chondrocyte adipogenesis is involved in the development of temporomandibular joint osteoarthritis (TMJ OA). Growth differentiation factor 11 (GDF11) has been implicated in this process. However, whether mechanosensitive histone deacetylase 3 (HDAC3) regulates GDF11 signaling in the context of TMJ OA remains to be elucidated.
View Article and Find Full Text PDFJ Med Food
September 2025
Department of Food Innovation and Health, Kyung Hee University, Yongin, Republic of Korea.
Osteoarthritis (OA) is a chronic degenerative joint disease characterized by progressive cartilage damage, inflammatory responses, and apoptosis of chondrocytes. In this study, we investigated the therapeutic potential properties of proteoglycans (PG) extracted from salmon nasal cartilage in both (HTB-94 human chondrocytic cells) and (monosodium iodoacetate-induced OA rat model) approaches. Rats were treated with PG, and key parameters related to cartilage integrity, inflammation, and apoptosis were evaluated.
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