Abstract

Curcumin is a natural phenolic component of yellow curry spice, exhibits antioxidant and anti-inflammatory properties. In this study we investigated whether curcumin suppresses heat-induced apoptosis in chicken embryonic fibroblast cells (CEF) and the underlying mechanism.CEF cells line was divided into 6 groups (4 repetitions per group) including normal temperature group (NC), high temperature control group (H) and 4 experimental groups (H1(5 μmol/L), H2(10 μmol/L), H3(20 μmol/L) and H4(40 μmol/L)). Control groups were cultured in basic medium without Curcumin, while, the experimental groups were supplemented with 5, 10, 20 and 40 μmol/L, respectively. The experimental groups and H control group were cultured at 43 ℃ (95% air/5% CO2), whereas NC group cells were cultured at 37 °C. After 6, 12 and 24 h of culture, cells were collected for viability, proliferation, apoptosis, antioxidant status and gene expression analysis.Results showed that heat stress trigged the ROS production and induced the apoptosis, leading to decrease the cell viability and proliferation. The enzymatic activities of antioxidants (SOD, CAT, and GPX) were down-regulated. The expression of antioxidant enzyme (CAT, SOD1, SOD2, GSTO1, GSTT1 and GSTA3) and MAPK-Nrf2 pathway genes (Nrf2, Jnk, Erk and P38) were down-regulated under heats stress condition. While, the Curcumin treated groups had decreased ROS and MDA content. Down-regulation of the activity and expression of antioxidant enzyme induced by heat were also reversed by curcumin. Furthermore the up-regulation in expression of Nrf2, Jnk, Erk and P38 in supplemented groups revealed the involvement of MAPK-Nrf2 signaling pathway to alleviate oxidative stress induced by heat stress. This study demonstrates that curcumin has the ability to ease the oxidative damage through activating the MAPK-Nrf2 signaling pathway in CEF cells.

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