Protection of SAL B with H9C2 cells

Salvianolic acid B (Sal B) is regarded as a potent antidiabetic agent and has been reported to possess cardioprotective effect in vivo.

This study investigated the cardioprotective effects of Sal B on H9c2 cells injury caused by high glucose in vitro, and clarified the possible mechanisms.

Di ferent concentrations of Sal B were incubated with cells for 12 h prior being exposed to high glucose for 24 h. Cardioprotective effects of Sal B were evaluated using CCK-8 assay, ELISA, Hoechst 33258 nucleus staining, and western blot.

Following a 24 h exposure of H9c2 to high glucose, obvious reduction was found in cell viability (45%), GSH (54.8 ± 9.4 ng/mg protein), catalase (1.22 ± 0.12 U/mg protein), and GPX level (67.9 ± 9.4 U/mg protein), which were associated with the increases of GSSG (1.99 ± 0.28 ng/mg protein) and ROS (2.00 ± 0.19 RFU/mg protein) production. High glucose also elevated IL-6 (1.8-fold), IL-1β (1.9-fold), and TNF-α (1.6-fold) level, as well as induced cell apoptosis and NF-κB (6.1-fold) activation. However, Sal B (25 and 50 μM) elevated cell viability (28% and 44%), ameliorated oxidative stress (GSH, 1.3- and 1.6-fold; catalase, 1.9- and 2.0-fold; GPX, 1.1- and 1.4-fold; GSSG, 0.9- and 0.8-fold; ROS, 0.6- and 0.5-fold), and inflammatory response (IL-6, 0.9- and 0.7-fold; IL-1β, 0.8- and 0.6-fold; TNF-α, 0.9- and 0.8-fold), and inhibited cell apoptosis and NF-κB (0.5- and 0.2-fold) expression.

Sal B attenuated high glucose-induced injury and cytotoxicity through inhibiting inflammatory cytokine production in H9c2 cardiac cells.