Safranal Treatment Induces Sirt1 Expression and Inhibits Endoplasmic Reticulum Stress in Mouse Chondrocytes and Alleviates Osteoarthritis Progression in a Mouse Model

• DOI: 10.1021/acs.jafc.2c01773
• Publication Date: 2022-07-28T11:41:47Z
• Authors: Zhao Zhang; Jingtao Wu; Cheng Teng; Jinquan Wang; Libo Wang; Long Wu; Wenhao Chen; Zhen Lin; Zhongke Lin
• Keywords: Safranal; Tetramethylpyrazine; Tunicamycin

Osteoarthritis (OA) is an age-related degenerative disease. Oxidative stress (OS) modulates OA pathogenesis by enhancing chondrocyte apoptosis and extracellular matrix (ECM) degeneration via activation of the endoplasmic reticulum (ER) stress. Prior studies revealed that safranal plays a critical role in multiple diseases treatments, but there are no reports on its effect OA. Therefore, investigating needed. As compound can lead excessive reactive oxygen species (ROS) accumulation, tert-butyl hydroperoxide (TBHP) was used to induce OS OS-mediated for imitating vitro. Besides, bilateral medial meniscus removed joint instability friction surface establish destabilization initiation progression vivo. We, next, conducted Western blot RT-PCR analyses identify biomarkers underlying signaling pathway. Our results demonstrated 30 μM strongly upregulated Sirt1 expression, suppressed TBHP-mediated ER stress, and, turn, prevented ECM degeneration. Furthermore, compared with other two classic pathways inhibit PERK-eIF2α-CHOP axis at lower concentration (5 15 μM). In vivo, using Safranin O staining, X-ray, immunofluorescence (IF), immunohistochemical (IHC) we be postponed intraperitoneal injection 90 180 mg/kg mouse model. Taken together, our potentially prevent development.