Fig 1: Proteomic techniques revealed differential proteins influenced by KN93. (A) Principal component analysis of the identified proteins in the KN93 treatment group and control group. Red and blue dots represent the KN93 treatment group and control group, respectively. (B) Volcano plot indicated the differential proteins between KN93 treatment group and control group. Red dots indicated significantly upregulated proteins with adjusted P-values <0.01, blue dots indicated significantly down-regulated proteins with adjusted P-values <0.01 and gray dots indicated non-significantly expressed proteins. (C) Differential proteins were verified by western blotting, which was then (D) quantified. GAPDH was used as a loading control. The data are presented as the mean ± SD (n=3). **P<0.01,***P<0.001. NS, no significant difference; CYP51A1, cytochrome P450 family 51 family A member 1; FADD, fas-associated death domain; NCAM1, neural cell adhesion molecule 1; Cyct, cytochrome c, testis; IGFBP3, insulin-like growth factor binding protein 3; PLS1, plastin-1; PDZK1, PDZ domain-containing 1; ZP2, zona pellicida sperm-binding protein; YBX2, Y-box binding protein 2; BNIP3L, Bcl-2-interacting protein 3-like.
Fig 2: C5aRA protects H9c2 and AC16 cardiomyocytes against DOX-induced senescence. (A and B) Representative images of the co-staining for SA-ß-gal-positive cells. Magnification, x200. Scale bar, 50 µm. Arrows indicate positive cells. (C and D) Analysis of p53, p16, p21 and IGFBP3 protein expression levels. The results are representative of at least three independent experiments. ***P<0.001 vs. control group; ##P<0.01 and ###P<0.001 vs. DOX group. C5aRA, complement component 5a receptor antagonist; DOX, doxorubicin; SA-ß-gal, senescence-associated ß-galactosidase; IGFBP3, insulin-like growth factor binding protein 3.
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