fig1

Figure 1. YH inhibits HK-2 cell injury induced by HG. (A) Chemical structure of YH; (B and C) MTT assay results showing cell viability under various treatments; (D-F) Relative expression of inflammatory markers (TNF-α, IL-1β, MCP-1) across different experimental groups; (G-I) Oxidative stress parameters including MDA, ROS, and SOD activities; (J-M) Cellular proliferation assessed by EdU incorporation (Scale bar = 20 μm) and migration capacity (Scale bar = 100 μm) determined by transwell assay. ^*P < 0.05; ^**P < 0.01; ^***P < 0.001. HK-2: Human kidney-2; MTT: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; TNF-α: tumor necrosis factor alpha; IL-1β: interleukin-1 beta; MCP-1: monocyte chemoattractant protein-1; MDA: malondialdehyde; ROS: reactive oxygen species; SOD: superoxide dismutase; EdU: 5-ethynyl-2’-deoxyuridine; NG: normal glucose; HG: high glucose; YH: yohimbine.