Journal: Journal of Cellular and Molecular Medicine

Article Title: Paeonol Improves Cardiac Remodelling in MI Mice by Suppressing NOX2 mRNA Expression to Mitigate Oxidative Stress and Mitochondrial Dysfunction

doi: 10.1111/jcmm.70563

Figure Lengend Snippet: Schematic of the mechanism by which PAE improves myocardial remodelling in mice with MI. After complete ligation of LAD for a long time to induce cardiac remodelling in mice, mRNA and protein expressions of NOX2 in cardiomyocytes significantly increased, and the generation of O 2 − and ROS caused by it significantly increased, leading to oxidative stress. On the one hand, it could increase cardiomyocyte apoptosis and hypertrophy, while on the other hand, it could damage the structure and function of mitochondria, leading to a decrease in ATP level and MMP, and promote the generation of more O 2 − , which could exacerbate oxidative stress. Eventually, it could further lead to cardiomyocyte apoptosis and hypertrophy and form a vicious cycle. The application of PAE in the treatment of these MI mice could inhibit the protein expression of NOX2 by transcriptional negative regulation of its mRNA formation, thereby inhibiting the above pathways, alleviating oxidative stress, and maintaining mitochondrial function, achieving the effect of reducing cardiomyocyte apoptosis and hypertrophy.

Article Snippet: NOX2, phospho‐signal transducer and activator of transcription 3 (STAT3)‐Y705, and STAT3 were generated by ABclonal Technology.

Techniques: Ligation, Expressing

Journal: Journal of Cellular and Molecular Medicine

Article Title: Paeonol Improves Cardiac Remodelling in MI Mice by Suppressing NOX2 mRNA Expression to Mitigate Oxidative Stress and Mitochondrial Dysfunction

doi: 10.1111/jcmm.70563

Figure Lengend Snippet: PAE reduced NOX2 activity and oxidative stress, maintained mitochondrial function, and improved cardiomyocyte apoptosis and collagen deposition in the hearts of MI mice. (A) T‐SOD activity ( n = 8). (B) GSH‐Px activity ( n = 8). (C) MDA level ( n = 8). (D‐H) Activities of mitochondrial complex I, II, III, IV, and V ( n = 8). (I) ATP level ( n = 8). (J) Western blot analysis. (K, L) Quantitative analysis ( n = 3). (M) NOX2 mRNA expression ( n = 5). (N) NOX activity ( n = 8). ATP, adenosine triphosphate; GAPDH, glyceraldehyde‐3‐phosphate dehydrogenase; GSH‐P X , glutathione peroxidase; MDA, malonaldehyde; NOX, nicotinamide adenine dinucleotide phosphate oxidase; STAT3, signal transducer and activator of transcription 3; T‐SOD, total‐superoxide dismutase. Data are given as means ± SEM. ## p < 0.01, # p < 0.05 vs. SHAM group; ** p < 0.01, * p < 0.05 vs. MI group.

Article Snippet: NOX2, phospho‐signal transducer and activator of transcription 3 (STAT3)‐Y705, and STAT3 were generated by ABclonal Technology.

Techniques: Activity Assay, Western Blot, Expressing

Journal: Journal of Cellular and Molecular Medicine

Article Title: Paeonol Improves Cardiac Remodelling in MI Mice by Suppressing NOX2 mRNA Expression to Mitigate Oxidative Stress and Mitochondrial Dysfunction

doi: 10.1111/jcmm.70563

Figure Lengend Snippet: The mechanism of PAE regulating NOX2 mRNA expression in H9C2 cells. (A) Relative NOX2 mRNA expression ( n = 6). (B) Dual luciferase assay ( n = 5). (C) Western blot analysis. (D) Quantitative analysis ( n = 3). (E) Dual luciferase assay ( n = 5). DMSO: Dimethyl sulfoxide; NOX2p: NOX2 promoter. Data are given as means ± SEM. ** p < 0.01 or * p < 0.05 vs. DMSO group or vs. DMSO + pGL3 (NOX2p) group or DMSO + pGL3 (NOX2p)‐delta1 group or DMSO + pGL3 (NOX2p)‐delta2 group or DMSO + pGL3 (NOX2p)‐delta3 group; ## p < 0.01 vs. PAE + pGL3 (NOX2p)‐delta1 group or PAE + pGL3 (NOX2p)‐delta3 group.

Article Snippet: NOX2, phospho‐signal transducer and activator of transcription 3 (STAT3)‐Y705, and STAT3 were generated by ABclonal Technology.

Techniques: Expressing, Luciferase, Western Blot