Baicalin Ameliorates Cartilage Injury in Rats With Osteoarthritis via Modulating miR-766-3p/AIFM1 Axis
Language English Country Czech Republic Media print
Document type Journal Article
PubMed
39264083
PubMed Central
PMC11414588
DOI
10.33549/physiolres.935284
PII: 935284
Knihovny.cz E-resources
- MeSH
- Apoptosis drug effects MeSH
- Apoptosis Inducing Factor metabolism MeSH
- Flavonoids * pharmacology therapeutic use MeSH
- Cartilage, Articular drug effects metabolism pathology MeSH
- Rats MeSH
- MicroRNAs * metabolism genetics biosynthesis MeSH
- Osteoarthritis drug therapy metabolism pathology MeSH
- Oxidative Stress drug effects MeSH
- Rats, Sprague-Dawley * MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- baicalin MeSH Browser
- Apoptosis Inducing Factor MeSH
- Flavonoids * MeSH
- MicroRNAs * MeSH
The study aims to elucidate the therapeutic mechanism of Baicalin (BAI) in alleviating cartilage injury in osteoarthritic (OA) rat models, concentrating on its regulation of the miR-766-3p/AIFM1 axis. An OA rat model was developed with unilateral anterior cruciate ligament transection (ACLT). Interventions comprised of BAI treatment and intra-articular administration of miR-766-3p inhibitor. For evaluation, histopathological staining was conducted to investigate the pathological severity of knee cartilage injury. The levels of oxidative stress (OS) indicators including MDA, SOD, and GSH-Px, were quantified using colorimetric assays. Inflammatory factors (IFs; TNF-?, IL-1?, and IL-6) in knee joint lavage fluids were assessed using ELISA, while RT-PCR was employed to quantify miR-766-3p expression. TUNEL apoptosis staining was utilized to detect chondrocyte apoptosis, and western blotting examined autophagy-related markers (LC3, Beclin, p62), extracellular matrix (ECM) synthesis-associated indices (COL2A, ACAN, MMP13), and apoptosis-inducing factor mitochondrion-associated 1 (AIFM1). Histological examination revealed a marked amelioration of cartilage injury in the BAI-treated OA rat models compared to controls. BAI treatment significantly reduced inflammation and OS of knee joint fluid, activated autophagy, and decreased chondrocyte apoptosis and ECM degradation. Interestingly, the inhibitory effects of BAI on these pathological markers were significantly decreased by the miR-766-3p inhibitor. Further assessment revealed that BAI efficiently promoted miR-766-3p expression while inhibiting AIFM1 protein expression. BAI potentially mitigates articular cartilage injury in OA rats, likely through modulation of miR-766-3p/AIFM1 axis. Keywords: Baicalin, microRNA, AIFM1, Osteoarthritisv, Rat.
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