Journal: Antioxidants

Article Title: Hydralazine Attenuates Lipopolysaccharide-Induced Murine Myocardial Dysfunction by Inhibition of Semicarbazide-Sensitive Amine Oxidase

doi: 10.3390/antiox14121502

Figure Lengend Snippet: Changes of 15 blood plasma cytokines in septic mice ( n = 5 for each group). Mice were randomly divided into three groups (LPS, LPS + HYD 10 mg/kg and Control). LPS + HYD and LPS groups were administered LPS at a dose of 25 mg/kg via i.p. injection, after 30 min received hydralazine (10 mg/kg) or equal saline via i.p. injection, respectively. Control group was administered equal saline. Blood plasma was collected at 24 h post-LPS injection (the acute phase of septic shock) to detect chemokines levels with Luminex assay. * p < 0.05 and ** p < 0.01 vs. the control group, # p < 0.05 and ## p < 0.01 vs. the LPS group. CCL, C-C motif chemokine ligand; CXCL, C-X-C motif chemokine ligand.

Article Snippet: The Bio-Plex Pro Mouse Chemokine Panel (Lot No. 12009159) was from Bio-Rad Laboratories (Hercules, CA, USA).

Techniques: Clinical Proteomics, Control, Injection, Saline, Luminex

Journal: Antioxidants

Article Title: Hydralazine Attenuates Lipopolysaccharide-Induced Murine Myocardial Dysfunction by Inhibition of Semicarbazide-Sensitive Amine Oxidase

doi: 10.3390/antiox14121502

Figure Lengend Snippet: The schematic illustrates the key pathophysiological processes in SIMD and the proposed mechanism of hydralazine. LPS challenge triggers a systemic inflammatory response. This study identifies a novel key event within the heart: the upregulation of SSAO activity. The elevated SSAO activity drives two major pathological pathways: (1) Oxidative Stress: SSAO contributes to oxidative stress by generating reactive oxygen species, leading to lipid peroxidation (increased MDA), depletion of antioxidants (reduced GSH, SOD, GSH-Px), and subsequent mitochondrial damage and cardiomyocyte injury. (2) Inflammation: SSAO/VAP-1 facilitates leukocyte adhesion and transmigration. Concurrently, a systemic chemokine storm promotes inflammatory cell infiltration into the myocardial tissue. These pathological processes collectively lead to myocardial dysfunction, hypotension, and increased mortality. Hydralazine, administered after sepsis onset, acts as a potent inhibitor of SSAO activity. By blocking SSAO, hydralazine attenuates both oxidative stress and inflammatory infiltration, which ultimately preserves cardiac function and improves survival. The “T-bars” indicate the inhibitory action of hydralazine. Arrow directions indicate changes in level: up (↑) for increase and down (↓) for decrease.

Article Snippet: The Bio-Plex Pro Mouse Chemokine Panel (Lot No. 12009159) was from Bio-Rad Laboratories (Hercules, CA, USA).

Techniques: Activity Assay, Transmigration Assay, Blocking Assay