Astaxanthin Attenuates Hypertensive Vascular Remodeling by Protecting Vascular Smooth Muscle Cells from Oxidative Stress-Induced Mitochondrial Dysfunction

Figure 1

ATX improves Ang II-induced mitochondrial dysfunction in VSMCs. (a) The fluorescence intensity of Ca²⁺ concentration in VSMCs. The relative values were shown as the comparison between the peak and the baseline fluorescence intensity. The fluorescence intensities of Ca²⁺ concentration in experimental groups were calculated to draw the time-course curves. . (b) MMP of VSMCs was imaged by confocal microscopy. The orange fluorescence represents the superposition of green fluorescence (JC-1 monomer) and red fluorescence (JC-1 aggregate). The mitochondrial MMP in each group was quantified. . (c) Evaluation of VSMCs mitochondrial bioenergy metabolism function. (A) Schematic general view of mitochondrial oxygen consumption rate (OCR), including basal OCR, ATP-related OCR, maximal respiration, proton leak, spare respiratory capacity, and nonmitochondrial OCR. (B) Analyses of mitochondrial OCRs data in real-time. (C) Quantitative analyses of the impact of ATX on mitochondrial OCRs. (d) Impacts of ATX on the decline of cellular ATP generation. (e) Cell apoptosis was assessed by TUNEL staining, and the percentage of TUNEL-positive VSMCs was quantified. . The protein expressions of cytoplasm and mitochondria cytochrome C (f), Bax, Bcl-2 (g) as well as cleaved caspase 3 (h) were analyzed by Western blot analysis. Data are represented as of 6 independent experiments. vs. untreated controls; ^# vs. VSMCs induced by Ang II (1 μM).

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