PKC epsilon Antibody - #AF7845

Figure 5 PKC was activated during contraction of CAS coronary arteries in vivo (n = 5 per group). Pit-induced PKC translocation in coronary arteries. (A) Representative WB shows PKCα in cytosolic and membrane particulate fractions. Results are expressed as the grayscale ratio of cytoplasmic PKCα to cell membrane PKCα. (B) Representative WB shows PKCδ in cytosolic and membrane particulate fractions. Results are expressed as the grayscale ratio of cytoplasmic PKCδ to cell membrane PKCδ. (C) Representative WB shows PKCε in cytosolic and membrane particulate fractions. Results are expressed as the grayscale ratio of cytoplasmic PKCε to cell membrane PKCε. Data presented as mean ± SEM. ns, no significance; *** p < 0.001 vs. control group. PKC: protein kinase C.

Figure 3 Western blot analysis of the proteins related to activated neurocytes during inflammatory pain. Examples (a) and mean values (b–g) of c-Fos, GFAP, Iba-1, PKCε, STAT3, and IL-6 proteins in the spinal cord. Intrathecally injected T-5224 (c-Fos/AP-1 inhibitor, 500 μg/50 μL), minocycline (Mino, 100 μg/50 μL), and L-2-aminoadipic acid (LAA, 1 mg/50 μL) reduced c-Fos, GFAP, Iba-1, PKCε, and IL-6 protein levels in FCA-treated rats, whereas STAT3 expression did not change between groups (P > 0.05). Data were normalized against GAPDH and are expressed as ratios (%) of control. Data are shown as means ± SD (n = 4–5). ∗P < 0.05, ∗∗P < 0.01; ∗∗∗P < 0.001, one-way ANOVA with Bonferroni tests.

Figure 6 Detection of PKCε and STAT3 coexpression in vivo and their immune complexes in vitro. (a–f) Immunofluorescence staining for PKCε (red) and STAT3 (green) coexpression (yellow) and DAPI (blue in merged image) in spinal cord sections (a–e). Ratios of cells with immunoreactive PKCε-/STAT3 among total cells. (f) Inhibitors of PKCε and STAT3 significantly decreased the coexpression of PKCε/STAT3 after APTSTAT3-9R administration. Bar = 40 μm. Data are shown as means ± SD (n = 6). ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001; one-way ANOVA followed by Bonferroni tests.

Figure 5 Hsa-miR-218-5p promotes HL-7702 cells apoptosis by regulating PRKCE. (A) HL-7702 cells were transfected with hsa-miR-218-5p mimic or NC control for 24 hours. Cell apoptosis was detected by flow cytometry. (B) The apoptotic rate (Q3 + Q2) of HL-7702 cells based on the result of flow cytometry. Expression levels of PRKCE were detected after transfection of hsa-miR-218-5p mimic (C), OE-SNHG12 (E) and sh-SNHG12 (G) by qRT-PCR. GAPDH served as an endogenous control. Expression levels of PRKCE protein in HL-7702 cells were detected after transfection of hsa-miR-218-5p mimic (D), OE-SNHG12 (F) and sh-SNHG12(H) by western blot analysis. Data were shown as mean ± SD. *P < .05 and **P < .01, compared with the control group. DMF, N, N-dimethylformamide; NC (A, B, C, D), mimic negative control; NC (G, H), negative control of sh-SNHG12