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Heat-Killed subsp. 557 Extracts Protect Chondrocytes from Osteoarthritis Damage by Reducing Inflammation: An In Vitro Study.
Nutrients
December 2024
Department of Biochemistry, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807378, Taiwan.
Background: Osteoarthritis (OA) is a chronic condition characterized by joint pain and disability, driven by excessive oxidative stress and inflammatory cytokine production in chondrocytes, resulting in cell death and cartilage matrix breakdown. Our previous study showed that in monosodium iodoacetate (MIA)-induced OA rats, oral administration of heat-killed subsp. 557 (LDL557) could significantly decrease OA progression.
View Article and Find Full Text PDFRoot Extract Attenuates Osteoarthritis Progression by Inhibiting Inflammation and Cartilage Degradation in Interleukin-1β and Monosodium Iodoacetate-Induced Osteoarthritis Models.
Nutrients
November 2024
Department of Pathology, College of Korean Medicine, Wonkwang University, 460, Iksan 54538, Jeonbuk, Republic of Korea.
Background: Osteoarthritis (OA) is a common degenerative joint condition caused by an imbalance between cartilage synthesis and degradation, which disrupts joint homeostasis. This study investigated the anti-inflammatory and joint-improving effects of root extract powder (PDREP) in both in vitro and in vivo OA models.
Methods/results: In an in vitro OA model, in which SW1353 human chondrosarcoma cells were treated with interleukin (IL)-1β, PDREP treatment significantly reduced the mRNA levels of matrix metalloproteinase (MMP)-1, MMP-3, and MMP-13 while enhancing collagen type II alpha 1 (Col2a1) mRNA level, and decreased IL-6 and prostaglandin E2 (PGE2) levels.
Artemisinin emulgel ameliorates cartilage degradation in knee osteoarthritis: and studies.
Ther Deliv
November 2024
Department of Pharmaceutics, National Institute of Pharmaceutical Education & Research, Hyderabad, Telangana, India.
Laboratory scale-up of artemisinin-loaded emulgel (ART-emulgel) was carried out and characterized for therapeutic performance in osteoarthritis (OA). The solubility of ART in various oils, surfactants and co-surfactants were screened for construction of pseudo ternary phase diagram (TPD), followed by scale-up of artemisinin loaded nanoemulsion (ART-NE). ART-NE was amalgamated with Carbopol Ultrez 10-NF to prepare ART-emulgel that was later characterized and to analyze therapeutic efficacy in monosodium-iodoacetate (MIA) induced knee OA.
View Article and Find Full Text PDFInhibitory Effects of Houtt. on Pain and Cartilage Breakdown in Osteoarthritis Based on Its Multifaceted Anti-Inflammatory Activity: An In Vivo and In Vitro Approach.
Int J Mol Sci
October 2024
Department of Herbal Pharmacology, College of Korean Medicine, Gachon University, 1342 Seongnamdae-ro, Sujeong-gu, Seongnam-si 13120, Republic of Korea.
In the past 30 years, the number of years lived with disability due to osteoarthritis (OA) has doubled, making it an increasing global health burden. To address this issue, interventions that inhibit the progressive pathology driven by age-related low-grade inflammation, the primary mechanism of OA, are being actively pursued. Recent investigations have focused on modulating the age-related low-grade inflammatory pathology of this disease as a therapeutic target.
View Article and Find Full Text PDFBDNF sensitizes bone and joint afferent neurons at different stages of MIA-induced osteoarthritis.
Bone
December 2024
Department of Anatomy and Physiology, University of Melbourne, Victoria, Australia. Electronic address:
There is emerging evidence that Brain Derived Neurotrophic Factor (BDNF), and one of its receptors TrkB, play important roles in the pathogenesis of osteoarthritis (OA) pain. Whilst these studies clearly highlight the potential for targeting BDNF/TrkB signaling to treat OA pain, the mechanism for how BDNF/TrkB signaling contributes to OA pain remains unclear. In this study, we used an animal model of mono-iodoacetate (MIA)-induced OA, in combination with electrophysiology, behavioral testing, Western blot analysis, and retrograde tracing and immunohistochemistry, to identify roles for BDNF/TrkB signaling in the pathogenesis of OA pain.
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