Fig.
6. GS increase mitochondrial function against the hypoxia- and
OGD-induced injuries of the cardiomyocytes through the activation of
SIRT1. (A) H9c2 cells were pretreated with GS for 48 h and kept
in the medium with 800 μM CoCl2 (hypoxia) or serum and
glucose-free and 800 μM CoCl2 (OGD) for 9 h. Cell
viability was analyzed by the CCK8 assay kit and showed as the
percentages. (B-C) Basal OCR and ATP content were measured in
H9c2 cells, after GS pretreatment for 48 h and hypoxia/OGD incubation
for 9 h. (D) H9c2 cells treated with GS for 48 h and incubated
with hypoxia exposure for 9 h were collected and lysed to analyze the
levels of complex I-V by Western blot. (E) Relative levels of
CV-ATP5A, CIII-UQCRC2, CIV-MTCO1, CII-SDHB, and CI-NDUFB8 from (D) were
calculated by Image J. (F) After GS treatment for 48 h, the
expressions of SIRT1 and PGC-1α in H9c2 cells subjected to hypoxia and
OGD injury were examined by Western blot. (G) Bar graphs show
relative levels of SIRT1 and PGC-1α from (F). β-Actin is loading
control. Ctrl: control group, CoCl2: cobalt chloride.
*P < 0.05, **P < 0.01, and ***P< 0.001 versus Ctrl group; #P< 0.05 and ##P < 0.01versus hypoxia or OGD group.