recombinant mouse serum amyloid a2 protein saa2 (R&D Systems)
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Recombinant Mouse Serum Amyloid A2 Protein Saa2, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/recombinant+mouse+serum+amyloid+a2+protein+saa2/Recombinant+Mouse+Serum+Amyloid+A2+Protein%2C+CF/pm40215820-58-0-20
Average 93 stars, based on 2 article reviews
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1) Product Images from "Vaccarin ameliorates osteoarthritis by suppressing the c-Jun N-terminal kinase (JNK)-serum amyloid A2 (SAA2) pathway mediating chondrocyte senescence."
Article Title: Vaccarin ameliorates osteoarthritis by suppressing the c-Jun N-terminal kinase (JNK)-serum amyloid A2 (SAA2) pathway mediating chondrocyte senescence.
Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology
doi: 10.1016/j.phymed.2025.156697
Figure Legend Snippet: Fig. 4. Vaccarin regulates SAA2 expression through JNK inhibition, reversing IL-1β-induced chondrocyte senescence and inflammation. (A-D) Western blot analysis showing that SP600125 treatment reversed IL-1β-induced inflammation and senescence in chondrocytes, while exogenous SAA2 protein exacerbates these effects and reduced SP600125’s inhibitory effects. (E, F) Western blot confirmed that Vaccarin reduced IL-1β-induced inflammatory and senescence markers, an effect that was counteracted by exogenous SAA2 protein. (G) β-galactosidase and ROS staining demonstrated Vaccarin’s reduction of IL-1β-induced senescence and ROS production in chondrocytes, with SAA2 reversing this effect and enhancing senescence and ROS levels. (H) Relative β-galactosidase positive cells and ROS levels were both quantified. Significance: *p < 0.05; **p < 0.01; NS, non-significance; scale bars: 200 μm (G), 400 μm (H).
Techniques Used: Expressing, Inhibition, Western Blot, Staining
Figure Legend Snippet: Fig. 8. Mechanism by which Vaccarin restores mitochondrial function in IL-1β-inhibited chondrocytes by suppressing the JNK-SAA2 signaling pathway, thereby reversing IL-1β-induced inflammation and senescence in chondrocytes.
Techniques Used:
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