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• W4283387837 abstract "Background: Depression is a common complication of cardiovascular disease, which deteriorates cardiac function. Shuangxinfang (psycho-cardiology formula, PCF) was reported to alleviate myocardial ischemia injury and improve depression-like behavior. Interestingly, our previous proteomics study predicted that the protein S100A9 appeared as an important target, and macrophage/microglial inflammation might be involved in the process of PCF improving depression induced by acute myocardial infarction (AMI). This study aims to validate the proteomics results. Methods: AMI rat models were established in vivo, followed by the administration of PCF or ABR-215757 (also named paquinimod, inhibiting S100A9 binding to TLR4) for 5 days. Forced swimming test (FST) and open field test (OFT) were applied to record depression-like behavior, and echocardiography was employed to evaluate cardiac function. Morphological changes of cardiomyocytes were assessed by HE staining and TUNEL staining on day 7 after cardiac surgery, as well as Masson trichrome staining on day 21. Hippocampal neurogenesis was determined by Nissl staining, while 5-hydroxytryptamine (5-HT), tryptophan/kynurenine ratio, and brain-derived neurotrophic factor (BDNF) in the hippocampus were analyzed as biochemical indicators of depression. We employed RT-qPCR, western blotting, and immunofluorescence to detect the expression of pathway-related genes and proteins. Myocardial and hippocampal expression of inflammatory factors were performed by ELISA. The activation of macrophage and microglia was assessed via immunoreaction using CD68 and Iba1, respectively. For in vitro confirmation, BV2 cells were primed with recombinant protein S100A9 and then treated with PCF serum or ferulic acid to determine alterations in microglial inflammation. Results: Rats in the AMI group showed heart function deterioration and depression-like behavior. Coronary ligation not only brought about myocardial inflammation, cell apoptosis, and fibrosis but also reduced the neurogenesis, elevated the tryptophan/kynurenine ratio, and decreased the content of 5-HT. PCF could ameliorate the pathological and phenotypic changes in the heart and brain and inhibit the expression of the S100A9 protein, the activation of the microglial cell, and the secretion of IL-1β and TNF-α raised by AMI. ABR-215757 showed therapeutic effect and molecular biological mechanisms similar to PCF. Treatment with PCF serum or ferulic acid in vitro was proved to efficiently block the hyperactivation of BV2 cells and increment of cytokine contents induced by recombinant protein S100A9. Conclusion: We identify S100A9 as a novel and potent regulator of inflammation in both the heart and brain. Macrophage/microglia inflammation mediated by S100A9 is considered a pivotal pathogenic in depression after AMI and a major pathway for the treatment of PCF, suggesting that PCF is a promising therapeutic candidate for psycho-cardiology disease." @default.
• W4283387837 created "2022-06-25" @default.
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• W4283387837 date "2022-06-24" @default.
• W4283387837 modified "2023-10-16" @default.
• W4283387837 title "Shuangxinfang Prevents S100A9-Induced Macrophage/Microglial Inflammation to Improve Cardiac Function and Depression-Like Behavior in Rats After Acute Myocardial Infarction" @default.
• W4283387837 cites W1829893638 @default.
• W4283387837 cites W1902881336 @default.
• W4283387837 cites W1931569217 @default.
• W4283387837 cites W1964349393 @default.
• W4283387837 cites W1968594434 @default.
• W4283387837 cites W1986876625 @default.
• W4283387837 cites W1997152175 @default.
• W4283387837 cites W1999871144 @default.
• W4283387837 cites W2003263043 @default.
• W4283387837 cites W2005779732 @default.
• W4283387837 cites W2057457444 @default.
• W4283387837 cites W2069657883 @default.
• W4283387837 cites W2070058327 @default.
• W4283387837 cites W2072013779 @default.
• W4283387837 cites W2072121441 @default.
• W4283387837 cites W2092744841 @default.
• W4283387837 cites W2133610914 @default.
• W4283387837 cites W2142832537 @default.
• W4283387837 cites W2152049933 @default.
• W4283387837 cites W2152958471 @default.
• W4283387837 cites W2178549252 @default.
• W4283387837 cites W2231750274 @default.
• W4283387837 cites W2237598232 @default.
• W4283387837 cites W2288655475 @default.
• W4283387837 cites W2291959673 @default.
• W4283387837 cites W2306321045 @default.
• W4283387837 cites W2309165118 @default.
• W4283387837 cites W2340791623 @default.
• W4283387837 cites W2507945432 @default.
• W4283387837 cites W2601063088 @default.
• W4283387837 cites W2611774751 @default.
• W4283387837 cites W2613572458 @default.
• W4283387837 cites W2613996502 @default.
• W4283387837 cites W2724120353 @default.
• W4283387837 cites W2765326305 @default.
• W4283387837 cites W2789964320 @default.
• W4283387837 cites W2790209689 @default.
• W4283387837 cites W2800417059 @default.
• W4283387837 cites W2883826253 @default.
• W4283387837 cites W2884872821 @default.
• W4283387837 cites W2886601508 @default.
• W4283387837 cites W2890629796 @default.
• W4283387837 cites W2896656403 @default.
• W4283387837 cites W2897334371 @default.
• W4283387837 cites W2902694081 @default.
• W4283387837 cites W2903371348 @default.
• W4283387837 cites W2904077359 @default.
• W4283387837 cites W2913496702 @default.
• W4283387837 cites W2918213194 @default.
• W4283387837 cites W2924576838 @default.
• W4283387837 cites W2939948226 @default.
• W4283387837 cites W2942783247 @default.
• W4283387837 cites W2951406926 @default.
• W4283387837 cites W2953193043 @default.
• W4283387837 cites W2954998565 @default.
• W4283387837 cites W2957191422 @default.
• W4283387837 cites W2961010215 @default.
• W4283387837 cites W2988380919 @default.
• W4283387837 cites W2999775511 @default.
• W4283387837 cites W3010535096 @default.
• W4283387837 cites W3015503258 @default.
• W4283387837 cites W3027743527 @default.
• W4283387837 cites W3033716639 @default.
• W4283387837 cites W3081467215 @default.
• W4283387837 cites W3083267621 @default.
• W4283387837 cites W3095047659 @default.
• W4283387837 cites W3110508632 @default.
• W4283387837 cites W3121179527 @default.
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• W4283387837 doi "https://doi.org/10.3389/fphar.2022.832590" @default.
• W4283387837 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35814253" @default.
• W4283387837 hasPublicationYear "2022" @default.
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