Fig 1: The impact of oxygen-glucose deprivation and reoxygenation (OGD/R) injury on Hippo-YAP pathway and MCP-1 in vitro.A The effect of verteporfin (10 µM) on binding interaction between YAP and TEAD in vitro. B Cellular expressions of Hippo core proteins (LATS1, YAP, p-YAP[ser127], and TEAD) in HK-2 cells treated with oxygen-glucose deprivation and reoxygenation (OGD/R) injury. C Nuclear expression of YAP in HK2 cells after OGD/R treatment. D The effect of verteporfin on MCP-1 expression in HK-2 cells after OGD/R. Shown are representative blots from at least three separate experiments with similar results. E Representative images of immunofluorescent staining for YAP in verteporfin treated HK-2 cells after OGD/R. F Semi-quantification of nuclear YAP expression in immunofluorescent staining (n = 10 randomly captured images per group). Scale bar = 20 µm in all images of E. All values are means ± SEM. #p < 0.001 defined as significant.
Fig 2: Schematic diagram of YAP-MCP-1 mediating the crosstalk between tubular maladaptation and interstitial infiltration.Following ischemic AKI, YAP activation in tubular epithelial cells causes MCP-1 overexpression and promotes renal macrophage inflammation, which is a driven force for progressive fibrosis and AKI-CKD transition. In addition, hypoxia, oxidative stress, and cell cycle G2/M arrest might be the keys to activate YAP persistently in maladaptive-repaired tubular epithelial cells.
Fig 3: Gastrodin inhibits HG-induced inflammation and oxidative stress by activating the 5'AMP-activated protein kinase/nuclear factor erythroid 2-related factor 2 signaling pathway in MPC5 cells. (A) The secretion of inflammatory cytokines, TNF-α, IL-1β and IL-6 were analyzed by ELISA. (B) The expression levels of MCP-1, NLRP3, ASC and Caspase-1 were determined by western blotting and quantified. (C) MDA levels and the activities of LDH and SOD were quantified using their respective assay kits. Error bars represent the mean ± SEM from three independent experiments. **P<0.01 and ***P<0.001 vs. HG. #P<0.05, ##P<0.01 and ###P<0.001 vs. HG + 100 µM gastrodin. HG, high glucose; LDH, lactate dehydrogenase; SOD, superoxide dismutase; MDA, malondialdehyde; MCP-1, monocyte chemoattractant protein 1; ASC, apoptosis-associated speck-like protein; NLRP3, NOD-, LRR- and pyrin domain-containing protein 3.
Fig 4: Gastrodin alleviates HG-induced inflammation and oxidative stress in MPC5 cells. (A) The secretion of inflammatory cytokines TNF-α, IL-1β and IL-6 were analyzed by ELISA. (B) The expressions levels of MCP-1, NLRP3, ASC and Caspase-1 were determined by western blotting and quantified. (C) MDA levels and the activities of LDH and SOD were quantified using their respective assay kits. ***P<0.001 vs. NG. ###P<0.001 vs. HG. NG, normal glucose; HG, high glucose; MA, mannitol; LDH, lactate dehydrogenase; SOD, superoxide dismutase; MDA, malondialdehyde; MCP-1, monocyte chemoattractant protein 1; ASC, apoptosis-associated speck-like protein; NLRP3, NOD-, LRR- and pyrin domain-containing protein 3.
Fig 5: Effects of endurance exercise on aortic chemokine and proinflammatory cytokine expressions. VCAM-1, MCP-1, IL-1β, and TNF-α expression in the aorta was determined through Western blotting. Values are mean ± SEM (n = 6). Different superscript letters (a and b) indicate significant differences (P < 0.05) in one-way ANOVA.
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