UCP2 Antibody - #DF8626

Fig. 6. Hsp22 regulates PGC1α via AMPK signaling pathway in rats after SAH Beam balance scores, Modified Garcia scores and Brainwater content in various groups. n = 6 per group. (B) Representative photomicrographs of TUNEL staining and quantitative analyses in the indicated groups. n = 4 per group. Scale bar = 100 μm. (C) Typical photomicrographs showing double immunofluorescence staining of PGC1α (green) and NeuN (red) in diverse experimental groups. n = 4 per group. Scale bar = 50 μm. (D) Western blot images and quantitative analyses of p-AMPK/AMPK, PGC1α, Drp1, Nrf1, TFAM, UCP2, Cleaved caspase-3/Caspase-3, Bcl2, Bax, Cytosolic and mitochondrial cytochrome c. n = 6 per group. Bars represent mean ± SD. **P < 0.01, *P < 0.05 vs. Sham group. ##P < 0.01, #P < 0.05 vs. SAH + Vehicle group. &&P < 0.01, &P < 0.05 vs. SAH + hsp22+scramble siRNA. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

Fig. 4 The mitochondrial function was improved by CX3CL1 deficiency in mice with cisplatin-induced AKI. A TEM images of renal tissues were captured. Scale bar = 500 nm. B The relative expression profiles of the mitochondrial proteins UCP2, Mfn2, and PGC1α in kidney tissues were determined by Western blotting. C DHE staining was conducted to determine the ROS level in renal tissues. Scale bar = 20 μm. D TEM was employed to capture images of podocytes. Scale bar = 500 nm. E Western blot analysis illustrating the relative expression patterns of the mitochondrial proteins UCP2, Mfn2, and PGC1α in podocytes. F The ROS level was detected through DCFH-DA labeling. Scale bar = 10 μm. G JC-1 staining was conducted to detect MMP in podocytes. Scale bar = 10 μm. (AKI, acute kidney injury; TEM, transmission electron microscopy; UCP2, uncoupling protein 2; Mfn2, Mitofusin 2; PGC1α, peroxisome proliferators-activated receptor γ coactivator l-alpha; DHE, dihydroethidium; ROS, reactive oxygen species; DCFH-DA, 2,7-dichlorodihydrofluorescein diacetate; MMP, matrix metalloproteinase; P value was calculated by one-way analysis of variance and Tukey’s test. *p 

FIGURE 9 Reduction of ADAMTS1 expression inhibits mitochondria-mediated renal apoptosis in I/R mice. (A–F) Detection of Bax, Bcl-2, PGC1-α, UCP2, and Cyt-c levels using Western blotting. (G and H) TUNEL staining of mouse kidney tissues, scale bar = 50 μm. (I and J) Electron microscopy of mouse kidney tissues, scale bar = 0.5 μm. (K) Immunofluorescence detection of ADAMTS1, AQP1, TNF-α, and Bax protein levels in mouse kidney tissues. Scale bar = 50 μm.

FIGURE 4 UCP2 promoted NSCLC progression through the mTOR/HIF-1α pathway. (A) Western blotting assay underwent conduct after PC9, H1975, and A549 cell lines were transfected. (B) ImageJ software was used to quantify the protein expression. **p 

Figure 4 Melatonin improves mitochondrial function and inhibits ferroptosis in the IR-induced acute kidney injury. (a) Renal tissues were imaged using transmission electron microscopy (TEM). Red arrows indicate mitochondrial cristae disappearance and outer membrane rupture. Scale bar = 200 nm. (b) Western blot analysis of mitochondrial proteins and their relative protein levels of UCP2 (c) and MFN2 (d). (e) Renal relative PGC-1a and TFAM levels were evaluated by RT-PCR. (f) Quantification of mRNA levels of Acsl4, Cox-2, and GPX4 kidney tissue by real-time PCR. (g) Western blots of NRF2, Slc7a11, and GPX4 proteins and their relative protein levels of NRF2 (h), Slc7a11 (i), and GPX4 (j). Data represent the mean ± SEM of six mice in each group. ∗p < 0.05,  ∗∗p < 0.01, and∗∗∗p < 0.001 compared to the Sham and Sham+MT (20 mg/kg) groups. #p < 0.05,  ##p < 0.01, and###p < 0.001 compared to the IR-treated group.