Fig 1: Caspase-3 level in rat testes homogenate affected by CuO NPs and CuSO4 0.5 (H2O). Data represent the mean ± standard error (SE). *Significantly different (P = 0.05) from the control group.
Fig 2: PFT alleviated STZ-induced alterations in caspase-3 level in the hippocampus. Each bar with vertical line represents the mean ± SD of 6 mice per group; *significantly different from the sham control group at p < 0.05, ****significantly different from the sham control group at p < 0.0001, ####significantly different from STZ group at p < 0.0001 using one-way ANOVA followed by Tukey's multiple comparisons test.
Fig 3: Empagliflozin ameliorates mitochondrial structural disorder in cardiomyocytes during CRS-3. (A–C) Cardiomyocytes were freshly isolated from mouse hearts after CRS-3. Representative pictures of immunofluorescence staining of the mitochondrial morphology are shown. The average mitochondrial length and the number of cardiomyocytes with fragmented mitochondria were recorded. (D) Electron microscopy was used to observe the mitochondrial morphology in cardiomyocytes. (E–H) RNA was isolated from heart tissues, and qPCR was used to analyze the transcription of Mfn2, Opa1, Drp1 and Fis1. (I, J) The duration of mPTP opening in cardiomyocytes was recorded, and the mPTP opening rate was normalized to that of the control group. (K) An ELISA was applied to analyze caspase-3 activity in cardiomyocytes. *p < 0.05.
Fig 4: The effect of meleagrin on the protein expression levels of caspase-3 in the lung tissue of the experimental mice determined by immunohistochemistry. Data of the percentage of positive stained area are expressed as mean ± SD and analyzed using one-way ANOVA followed by Bonferroni’s post hoc test (n = 8). * significantly different vs. the normal control group; # significantly different vs. the meleagrin group; ^ significantly different vs. the bleomycin group; $ significantly different vs. the bleomycin + meleagrin group. Differences were considered significant at p < 0.05.
Fig 5: DNA-PKcs deletion reduces LPS-mediated mitochondrial oxidative stress and apoptosis in hepatocytes. (A-C) Immunofluorescence staining of mitochondrial ROS and cytoplasmic ROS was performed in control and DNA-PKcs-depleted L02 hepatocytes following LPS treatment. (D-F) ELISA was used to analyze changes in SOD, GPX, and GSH expression in cultured liver cells. (G-H) The expression of caspase-3 and caspase-9 was measured in LPS-exposed hepatocytes through ELISA. (I-J) ELISA analysis of Bax expression and mPTP opening. *p < 0.05.
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