Molecular basis of IL‐10 attenuation of TNF‐α induced NFκB pathway activation and cardiomyocyte apoptosis

Trolox
DOI: 10.1096/fasebj.23.1_supplement.1007.1 Publication Date: 2021-06-21T21:52:47Z
ABSTRACT
We have reported that tumor necrosis factor‐α (TNF‐α) increases oxidative stress and apoptosis in cardiomyocytes by upregulating p38 mitogen activated protein (MAP) kinase phosphorylation. Interleukin‐10 (IL‐10) blocked these effects of TNF‐α ERK 1/2 MAP However, the precise site this IL‐10 action is still unknown was investigated present study. Cardiomyocytes isolated from adult Sprague Dawley rats were exposed to (10ng/ml), (10ng/ml) IL‐10α (ratio 1) for 4hrs. Hydrogen peroxide (H2O2) antioxidant trolox used as positive controls. Exposure resulted an increase production reactive oxygen species, number apoptotic cells, caspase‐3 activation PARP cleavage. Increased using H2O2 also caused apoptosis. These changes due associated with IKK NFκB itself had no effect, but it prevented induced changes. Trolox mitigated Pre‐exposure cells inhibitor, inhibition attenuated protective role IL‐10. The study shows prevents TNF‐α‐induced proapoptotic inhibiting phosphorylation through MAPkinase. (Supported CIHR).
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