LDHA Antibody - #DF6280

Fig. 4. | Bruceine A induces cell growth inhibition and apoptosis via PFKFB4-mediated glycolysis in MIA PaCa-2 cells. (C) MIA PaCa-2 cells were treated with various concentrations of bruceine A for 24 h. Protein levels of GLUT1, HK2, PFKFB4, PFKM, PKM2, LDHA, and β-actin were detected. β-actin was served was as control. Results were expressed as means ± SD of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 versus control cultured with 0.1% DMSO by one-way ANOVA and post hoc tests.

Fig. 3. Pimozide inhibits PKM2 protein and mRNA in both MCF-7 and MDA-MB-231 cells in vitro. (A-B) Cells were treated with the indicated concentrations of Pimozide for 24 h, and the protein expression of glycolytic enzymes in MCF-7(A) and MDA-MB-231(B) cells were determined by Western blot analysis (left panel). Densitometry analysis was performed to assess the glycolytic enzymes protein expression (normalized to β-actin expression), PKM2 decreased significantly compared with untreated cells (right panel). (C-D) The mRNA expression of PKM2 in MCF-7(C) and MDA-MB-231(D) cells untreated or treated with Pimozide was determined by qRT-PCR. GAPDH was used as a control. Data represent mean ± SD from three biological replicates (*p < 0.05, **p < 0.01).

Fig. 1. LDHA and AMPK were up-regulated synchronously in breast cancer. A. Expression levels of LDHA, AMPK and pAMPK were assessed by Western blot (above) and gray image scanning (below) in eight different breast cancer cell lines, including four NTNBC cell lines and four TNBC cell lines. GAPDH was used as a loading control. B. Expression levels of LDHA and AMPK were determined by qRT-PCR (above). The differences between TNBC and NTNBC cell lines were analyzed (below). GAPDH was used as an internal control. C. Expression levels of LDHA, AMPK and pAMPK were assessed by Western blot (above) and gray image scanning (below) in eight different breast cancer tissues, including four NTNBC tissues and four TNBC tissues. GAPDH was used as a loading control. D. Expression levels of LDHA and AMPK were determined by qRT-PCR (above). The diffe

Fig. 2. The expression of LDHA and AMPK showed a positive correlation in breast cancer. A. The expression of LDHA and AMPK were detected by IHC using breast cancer TMAs of 112 patients. Representative IHC images of four staining degrees (no-weak-medium-strong) of LDHA and AMPK expression under a microscope were showed (400). B. The correlation between LDHA and AMPK expression scores of 112 breast cancer patients was analyzed and a positive correlation between them was showed.

Figure 7 Oxamate reduced glycolysis and ER stress in silicotic mice. (A) HE. staining of lung tissue in mice exposed to silica (scale bar = 100 µm). (B) Sirius red staining of lung tissue in mice exposed to silica (scale bar = 50 µm). (C) Expression of LDHA in mice exposed to silica measured by IF staining (scale bar = 50 µm). (D) Expression of p-PERK in silicotic mice measured by IF staining (scale bar) = 50 µm. (E) Positive expression of p-IRE-1α in silicotic mice observed by IHC staining (scale bar = 50 µm). (F) Expression levels of collagen type I (Col I), LDHA, p-PERK, and p-IRE-1α in mice lungs measured by Western blotting. Data are presented as the mean ± SD, n = 6 per group.

Figure 1 JWH133 (2 mg/kg, 28 days) activated the CB2 receptor on microglia to inhibit AngII-induced hypertension by suppressing glycolytic enzymes and proinflammatory cytokines in the PVN. (a) The expression of the CB2 receptor in microglia was upregulated in the PVN of AngII-induced hypertension mice. Iba1 (blue) and CB2 receptor (red). Scale bar = 10 μm. JWH133 activation of the CB2 receptor inhibited MAP (b), plasma norepinephrine levels (c), proinflammatory factors TNF-α, IL-1β, and IL-6 production (d), glycolytic enzymes PFK and LDHa expression (e) in AngII-induced hypertension mice. The results are expressed as mean ±SEM (n = 5 mice in each group, * p < 0.05, ** p < 0.01, *** p < 0.001). Original blot images can be found in Supplementary File S1.