Albumin Antibody - #DF6396

Figure 1. Characterisation of EVs derived from the serum and plasma of NSCLC patients and controls. (a) The shape and structure of serum and plasma EVs isolated by EXOquick kit under TEM. The red arrow represents EVs with typical characteristics (scale bars are 200 nm). (b) The size of EVs derived from control groups and NSCLC groups was analysed by NTA. (c) Western blots of EVs membrane markers, including Alix, CD63, TSG101, CD9, and one negative marker ALB.

FIGURE 1 | Irradiation-induced liver damage in mice. C57BL/6J mice were exposed to 8.0 Gy of total body irradiation (TBI). Liver tissues were harvested at days 1, 3, and 7 post-exposure (n = 6). (A) Representative pictures by HE staining are shown. Scale bar = 50 μm. Arrows indicate edema hepatocytes. (B and C) ALB and AFP expression in liver tissues (n = 3). Expression of ALB (B) and AFP (C) was detected by western blotting.

Figure 1 AOPPs accumulate in IVDD, up-regulate the expression of NOX4, senescence markers, and their associated inflammatory proteins, and accelerate IVDD. (A) MRI of a persistent lumbar degeneration model showed significant disc degeneration. (B) Immunofluorescence of AOPPs showed massive accumulation of AOPPs in AF tissues at two months of degenerative discs. Scale bar: 25 µm. (C) The DMMB assay of the rat lumbar discs showed a gradual decrease in GAG content after surgery, suggesting IVDD. (D) Western blot analysis of lumbar discs showed that albumin and AOPPs accumulated in IVDD, up-regulating NOX4, senescence markers p53, p21, p16, and senescence-associated inflammatory proteins IL-1β and TNF-α expression. (E) Western blot analysis of the caudal discs showed that albumin and AOPPs accumulated in IVDD up-regulated the expression of NOX4, senescence markers, and senescence-associated inflammatory proteins. (F) X-rays of Co6/7 and Co8/9 showed lower DHI in the puncture + intra-discal AOPPs group. (G, H, I) Immunohistochemical staining of AF tissue for p16 and NOX4 was positive in the punctured discs and much higher after stimulation with exogenous AOPPs. Scale bars: 100 µm and 200 µm. (J) DMMB measurements of rat lumbar discs showed a decrease in GAG content in all puncture groups, indicating IVDD in all puncture groups, with the lowest content and most severe degeneration in the intra-discal injection AOPPs group. Sham, sham surgery. IP, intra-peritoneal injection. N = 6 per group. *P < 0.05 compared to Sham and IP for AOPPs. ** P < 0.01 compared to Sham and IP for AOPPs. #P < 0.05 compared to the other five groups. All experiments were repeated at least three times. Error bars represent standard errors.

Figure 2 Effects of BMAL1 overexpression on oxidative stress, BBB injury, brain edema, inflammation and neurobehaviors after ICH. (A) Western blot analysis of levels of the BMAL1 and Albumin proteins (index of BBB injury) in the sham, ICH, ICH + Vector and ICH + Over-BMAL1 groups at 24 h after ICH. (B) Quantification of the relative BMAL1 protein levels in the four groups. (C) ROS levels in the brain tissues from rats in the four groups. (D) Quantification of the relative Albumin protein levels in the four groups. (E) The effects of BMAL1 overexpression on the brain water content of rats in the four groups. (F) Concentrations of IL-1β in the serum of the sham ICH, ICH + Vector and ICH+Over-BMAL1 groups at 24 h after ICH. (G) Concentrations of TNF-α in the serum of the four groups listed above. (H) The scores on the modified Garcia test in the sham, ICH, ICH + Vector and ICH + Over-BMAL1 groups at 24 h after ICH. (I) Representative images illustrate swimming trajectories at 25 d (learning) and escape latency in the Morris water maze test at 21 to 25 d after ICH in the sham, ICH, ICH + Vector and ICH + Over BMAL1 rats. (J) Representative images illustrate swimming trajectories at 26 d (memory) and time spent in the platform quadrant in the Morris water maze test at 26 d after ICH in the groups listed above. **P