Fig 1: Dose-response inhibition of mitochondrial protein synthesis of clinical oxazolidinones. MPS inhibition was quantified using the MitoBiogenesis in-cell ELISA kit (ab110217; Abcam) in HepG2 cells (see Fig. S1 in the supplemental material). The assay compared the production of two proteins: COX-1, synthesized by mitochondrial ribosomes, and SDHA, synthesized by cytoplasmic ribosomes. Cell viability was measured with the Janus green (JG) stain. Raw data were interpreted per the manufacturer’s instructions and plotted using GraphPad Prism to calculate the IC50 values of the relative inhibition of COX-1/SDH-A synthesis, and the percent cell viability. Chloramphenicol (CAM) and clarithromycin (CLR) were used as the positive and negative controls, respectively. The oxazolidinone abbreviations are as provided in Table 1. 95% CI, 95% confidence interval.
Fig 2: Rutin enhances mitochondrial biogenesis in prostate cancer cells. Cells were treated with rutin (0, 25, 50, and 100 μM) for 24 h, and mitochondrial biogenesis was assessed using the MitoBiogenesis™ In-Cell ELISA Kit. The assay measures mitochondrially encoded COX-I and nuclear-encoded SDHA as indicators of mitochondrial content. (A) PC3, (B) DU145, (C) LNCaP, and (D) LNCaP-Enz cells were analyzed. The mitochondrial biogenesis index was calculated as the ratio of COX-I to SDHA absorbance. Rutin increased mitochondrial biogenesis in a dose-dependent manner, with the most substantial effect observed in LNCaP-Enz cells. Data represent the mean±SD of three independent experiments. Statistical significance was determined by two-way repeated measures ANOVA followed by the Holm–Šidák post hoc test. *p<0.05 vs. vehicle at the same time point. SD: Standard deviation.
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