Figure 6.

Ginsenoside Rb1 reversibly inhibits NADH dehydrogenase of mitochondrial complex I. A, mRNA expressions of Ndufv1, Ndufv2, Ndufs1, Ndufs4, Ndufs6, and Ndufa12 in H/R-treated cardiomyocytes. B-C, ROS level (B) and cell viability (C) of H9c2 cells transfected with Ndufv1, Ndufv2, Ndufs1, Ndufs4, Ndufs6, or Ndufa12 siRNA. D, NADH dehydrogenase activity in adult primary cardiomyocytes with ginsenoside Rb1 or rotenone treatment. E, NADH dehydrogenase activity in adult primary cardiomyocytes upon hypoxia (1 h) followed by 15 min of reperfusion. F, Adult primary cardiomyocytes were pretreated with ginsenoside Rb1 (10 µM) for 1 h. Then ginsenoside Rb1 was then either left on for the further assay, or washed out. The culture was continued for another 1 h. NADH dehydrogenase activity was measured. G, Ndi1 protein expression in H9c2 cells transfected with Ndi1 plasmid. Oxygen consumption rate (OCR, % baseline) in Ndi1-expressing cells in the presence of ginsenoside Rb1 (10 µM), FCCP (2.5 µM), pyruvate (Pyr, 10 mM) and antimycin A (AA, 1 µM). H, Ndi1 protein expression. ROS levels in Ndi1-expressing cells in response to H/R injury. I, Ndi1 protein expression. ROS production in Ndi1-expressing cells subjected to dimethyl succinate and oligomycin for 2 h. Data were expressed as mean ± SD. ^*p < 0.05: vs. the untreated control, H/R only treatment or suc plus oligo treatment; ^#p < 0.05: vs. indicated treatment; ns. no significance: vs. untreated control. H/R, hypoxia/reoxygenation; Oligo, oligomycin; Rb1, ginsenoside Rb1; Rot, rotenone; Suc, succinate.