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. 2016 Feb 23;4(4):e12710. doi: 10.14814/phy2.12710

Figure 5.

Figure 5

(A) The mitochondrial profile of cultured H9c2 cells pretreated with nsPRP. The cells were exposed sequentially to oligomyosin, which inhibits ATP synthase (complex V), and the decrease in OCR correlates to the mitochondrial respiration associated with cellular ATP production. FCCP (carbonyl cyanide‐4) is an uncoupling agent that collapses the proton gradient leading to an uninhibited flow of electrons through the ETC. ETC and oxygen is maximally consumed by complex IV, and rotenone IV. Rotenone and antimycin A inhibits complexes I and III, respectively, and shuts down mitochondrial respiration. Spare respiratory capacity is a measure of the cell's ability to respond to increased energy demand and is calculated by subtracting the maximal OCR from the baseline OCR. nsPRP increases the spare respiratory capacity. *P < 0.001 for FCCP injection (B) and ATP production (C). Mito stress analysis was performed in the presence or absence of nsPRP pretreatment for 24 h, in H9c2 cells. Control cells were exposed to cell culture media (control) only. (D) Spare respiratory capacity in treated and control cells exposed to 8 mmol/L H2O2 and treated as previously described. Data were normalized to the number of cells/well. Data are representative of three independent experiments.