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10.2147/DDDT.S377624 http://scihub22266oqcxt.onion/10.2147/DDDT.S377624 36033133!9416535!36033133     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=36033133&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Drug+Des+Devel+Ther 2022 ; 16 (?): 2767-2782 Nephropedia Template TP {{tp|p=36033133|t=2022. Ginsenoside Rd Promotes Cardiac Repair After Myocardial Infarction by Modulating Monocytes/Macrophages Subsets Conversion |pdf=|usr=}}{{36033133}} gab.com Text Ginsenoside Rd Promotes Cardiac Repair After Myocardial Infarction by Modulating Monocytes/Macrophages Subsets Conversion JO: Drug Des Devel Ther http://www.kidney.de/pget.php?&tw=1&pmid=36033133 #FOAvip PURPOSE: This study aimed to elucidate the potential molecular mechanisms by which GSRd improves cardiac inflammation and immune environment after MI. MATERIALS AND METHODS: The potential target genes of GSRd were predicted using the STITCH database. In vivo, MI mice models were established by left anterior descending ligation and were divided into the sham group, MI + Vehicle group, and MI + GSRd group. DMSO, DMSO, and GSRd 50 muL/day were intraperitoneally injected, respectively. After 28 days, echocardiography, Masson staining, immunofluorescence staining, flow cytometry, RT-PCR, and Western blot were performed. Mice peritoneal macrophages were extracted in vitro, and Western blot was performed after GSRd and/or Akt inhibitor MK2206 intervention. RESULTS: GSRd significantly improved mouse myocardial function, attenuated cardiac fibrosis, and inhibited inflammation and apoptosis in myocardial tissues after myocardial infarction. Meanwhile, GSRd increased non-classical Ly6C(low) Mos/Mps while reduced of classical Ly6C(high) Mos/Mps at the same time in myocardial tissues. In addition, GSRd significantly reversed the activity of p-Akt and p-mTOR in the heart Mos/Mps after MI. In vitro studies showed that the activity of p-Akt and p-mTOR in peritoneal macrophages were significantly increased in a dose-dependent manner after GSRd treatment. Furthermore, the AKT inhibitor MK2206 was found to block the enhanced activity of p-Akt and p-mTOR induced by GSRd in peritoneal macrophages. CONCLUSION: GSRd can enhance the transformation of Ly6C(high) Mos/Mps to Ly6C(low) Mos/Mps in mice after MI by activating the Akt/mTOR signaling pathway, inhibiting cardiac dysfunction and promoting cardiac repair. Twit Text FOAVip Ginsenoside Rd Promotes Cardiac Repair After Myocardial Infarction by Modulating Monocytes/Macrophages Subsets Conversion ????Drug Des Devel Ther http://www.kidney.de/pget.php?&tw=1&pmid=36033133 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=36033133 #FOAvip English Wikipedia <ref>{{Cite pmid|36033133}}</ref> Ginsenoside Rd Promotes Cardiac Repair After Myocardial Infarction by Modulating Monocytes/Macrophages Subsets Conversion #MMPMID36033133 Zhao T; Wang X; Liu Q; Yang T; Qu H; Zhou H Drug Des Devel Ther 2022[]; 16 (?): 2767-2782 PMID36033133show ga PURPOSE: This study aimed to elucidate the potential molecular mechanisms by which GSRd improves cardiac inflammation and immune environment after MI. MATERIALS AND METHODS: The potential target genes of GSRd were predicted using the STITCH database. In vivo, MI mice models were established by left anterior descending ligation and were divided into the sham group, MI + Vehicle group, and MI + GSRd group. DMSO, DMSO, and GSRd 50 muL/day were intraperitoneally injected, respectively. After 28 days, echocardiography, Masson staining, immunofluorescence staining, flow cytometry, RT-PCR, and Western blot were performed. Mice peritoneal macrophages were extracted in vitro, and Western blot was performed after GSRd and/or Akt inhibitor MK2206 intervention. RESULTS: GSRd significantly improved mouse myocardial function, attenuated cardiac fibrosis, and inhibited inflammation and apoptosis in myocardial tissues after myocardial infarction. Meanwhile, GSRd increased non-classical Ly6C(low) Mos/Mps while reduced of classical Ly6C(high) Mos/Mps at the same time in myocardial tissues. In addition, GSRd significantly reversed the activity of p-Akt and p-mTOR in the heart Mos/Mps after MI. In vitro studies showed that the activity of p-Akt and p-mTOR in peritoneal macrophages were significantly increased in a dose-dependent manner after GSRd treatment. Furthermore, the AKT inhibitor MK2206 was found to block the enhanced activity of p-Akt and p-mTOR induced by GSRd in peritoneal macrophages. CONCLUSION: GSRd can enhance the transformation of Ly6C(high) Mos/Mps to Ly6C(low) Mos/Mps in mice after MI by activating the Akt/mTOR signaling pathway, inhibiting cardiac dysfunction and promoting cardiac repair. |*Myocardial Infarction[MESH] |*Proto-Oncogene Proteins c-akt[MESH] |Animals[MESH] |Dimethyl Sulfoxide[MESH] |Ginsenosides[MESH] |Inflammation[MESH] |Macrophages, Peritoneal[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Monocytes[MESH] |Myocardium[MESH]Ginsenoside Rd Promotes Cardiac Repair After Myocardial Infarction by (epmc).pdf DeepDyve Pubget Overpricing