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Updated: May 11, 2026
In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
Published on: October 27, 2020
Protective Role of Tumor Necrosis Factor-Stimulated Gene-6 Against Cobalt Chloride -Induced Hypoxic Injury in H9c2
Biao Zhang1, Longlong Li1, Hui Li1
1Department of Cardiothoracic Surgery, The Fifth Affiliated Hospital of Anhui Medical University, Fuyang, Anhui, China.
Introduction:
Myocardial hypoxia contributes to cardiomyocyte injury through oxidative stress, apoptosis, and impaired angiogenesis. The tumor necrosis factor-stimulated gene 6 (TSG-6) produces a glycoprotein involved in immune regulation and tissue repair. This work was designed to evaluate the protective bearing of TSG-6 in cobalt chloride-induced hypoxic injury in H9c2 cardiomyocytes and explore the underlying mechanisms.
Materials And Methods:
A hypoxia model was established using 200 μM cobalt chloride in H9c2 cells. Cells were assigned to normoxic, hypoxia, TSG-6 treatment, or TSG-6 neutralization groups. Cell Counting Kit-8 assay, quantitative real time-polymerase chain reaction, terminal deoxynucleotidyl transferase dUTP nick end labeling staining, Western blot, and oxidative stress assays were consumed to assess cell viability, apoptosis, angiogenic factor expression, and oxidative status.
Results:
TSG-6 significantly improved cell viability under hypoxia, with 200 ng/mL being the most effective concentration (P < 0.05). It reduced enhancing B-cell lymphoma-2 while attenuating Bcl-2-associated X and cleaved caspase-3 expression (P < 0.01). In addition, by inducing vascular endothelial growth factor and hypoxia-inducible factor-1 alpha, TSG-6 helped relieve oxidative stress, evidenced by lowered reactive oxygen species and malondialdehyde levels and heightened superoxide dismutase activity (P < 0.01). Neutralization of TSG-6 partially reversed these effects, confirming the specificity of its protective function.
Conclusions:
TSG-6 exerted protective effects on hypoxia-injured H9c2 cardiomyocytes by inhibiting apoptosis, promoting angiogenesis, and reducing oxidative stress. These observations suggest that TSG-6 may serve as an effective therapeutic candidate for conditions linked to myocardial hypoxia.
