LAMP2 Antibody - #DF6719

Figure 5. Exercise enhances the degradation of hepatic LDs in lysosomes of HFD mice. (A–F) Representative of autophagy-associated proteins immunoblotting and quantified data, including ATGL, Beclin1, LC3B, ATG5, and p62, (G) representative of lipophagy-related immunofluorescence by the colocalization of PLIN2 and LAMP1 in the liver (scar bar: 50 um, n = 3), (H–L) representative of lipophagy-associated lysosomal proteins immunoblotting and quantified data, including LAMP1, LAMP2, LAL, and CTSD. Unless otherwise specified, six mice per group were used in each experiment. The data are expressed as mean ± SEM. * p < 0.05, ** p < 0.01 versus NS mice; # p < 0.05, ## p < 0.01 versus HS mice.

Fig. 3. Effect of FSCR on the NLRP3 inflammasome-related autophagy signaling pathway in uterine tissue of CPID rats. Detection of mRNA expression in NLRP3 inflammatory bodies by RT-PCR: NLRP3, CASP1, ASC, IL-1β, and IL-18 (A). Western blot detection of proteins in the NLRP3 inflammatory body: NLRP3, cleaved-CASP1, and cleaved-IL-1β (B). Western blot detection of proteins in the autophagy pathway: Beclin1, p-VPS34, and p62 (C). The expression of NLRP3 inflammatory bodies and autophagic vesicles in uterine tissues was observed by IF: NLRP3 was labeled with red fluorescence, VPS34 was labeled with green fluorescence, and nuclei were labeled with DAPI with blue fluorescence (D). Western blot detection of proteins in the lysosomal pathway: LAMP2, Ubiquitin and LC3 Ⅱ. (E). Results are presented as the mean ± S.E.M.

Figure 2. MiR-22-3p suppresses atherosclerotic lesion development in ApoE–/– mice fed a high fat diet: (a) oil red O staining and quantitative analysis of aortic sections from MiR-22-3p agomir or negative control (NC) mice; (b) Masson’s staining and quantitative analysis of aortic sections from MiR-22-3p agomir or NC mice (original magnification, × 40; bar = 500 μm); (c) sirius red staining and quantitative analysis of aortic sections from MiR-22-3p agomir or NC mice (original magnification, × 40; bar = 500 μm); (d) macrophage antigen-3 (Mac-3) immunostaining and quantitative analysis of aortic sections from MiR-22-3p agomir or NC mice (original magnification, × 40; bar = 200 μm); and (e) quantitative analysis of smooth muscle cells by α-smooth muscle actin immunostaining of aortic sections from MiR-22-3p agomir or NC mice (original magnification, × 40; bar = 500 μm). (*P