Journal: Experimental and Therapeutic Medicine

Article Title: Apelin‑13 reduces high glucose‑induced mitochondrial dysfunction in cochlear hair cells by inhibiting endoplasmic reticulum stress

doi: 10.3892/etm.2024.12515

Figure Lengend Snippet: ER stress agonist reverses the effects of Apelin-13 on oxidative stress and apoptosis. HEI-OC1 cells were pretreated with TM to stimulate ER stress, and (A) the impacts of TM on oxidative stress were determined by measuring indicators. (B) Flow cytometry revealed the proportion of apoptotic cells. (C) Quantitative results of flow cytometry. (D) Caspase3 kit revealed intracellular caspase3 activity. *** P<0.001 vs. control; ### P<0.001 vs. HG; & P<0.05, && P<0.01 and &&& P<0.001 vs. HG + Apelin-13. ER, endoplasmic reticulum; TM, tunicamycin; HG, high glucose.

Article Snippet: For mechanistic studies, HEI-OC1 cells were pretreated with the endoplasmic reticulum (ER) stress agonist tunicamycin (TM; 5 μg/ml; Selleck Chemicals) for 6 h.

Techniques: Flow Cytometry, Activity Assay, Control

Journal: Experimental and Therapeutic Medicine

Article Title: Apelin‑13 reduces high glucose‑induced mitochondrial dysfunction in cochlear hair cells by inhibiting endoplasmic reticulum stress

doi: 10.3892/etm.2024.12515

Figure Lengend Snippet: ER stress agonist reverses the effects of Apelin-13 on mitochondrial dysfunction. (A) The impacts of TM on mitochondrial membrane potential as reflected by JC-1 probes (magnification, x200. (B) The impacts of TM on mtROS production as reflected by MitoSOX Red probes (magnification, x200). (C) The impacts of TM on ATP production. *** P<0.001 vs. control; ### P<0.001 vs. HG; &&& P<0.001 vs. HG + Apelin-13. ER, endoplasmic reticulum; TM, tunicamycin; mtROS, mitochondrial reactive oxygen species; HG, high glucose.

Article Snippet: For mechanistic studies, HEI-OC1 cells were pretreated with the endoplasmic reticulum (ER) stress agonist tunicamycin (TM; 5 μg/ml; Selleck Chemicals) for 6 h.

Techniques: Membrane, Control