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10.1016/j.phymed.2017.04.002 http://scihub22266oqcxt.onion/10.1016/j.phymed.2017.04.002 28545665!ä!28545665 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Phytomedicine 2017 ; 30 (ä): 10-17 Nephropedia Template TP {{tp|p=28545665|t=2017. Astragaloside? against cardiac fibrosis by inhibiting TRPM7 channel |pdf=|usr=}}{{28545665}} gab.com Text Astragaloside against cardiac fibrosis by inhibiting TRPM7 channel JO: Phytomedicine http://www.kidney.de/pget.php?&tw=1&pmid=28545665 #FOAvip BACKGROUND: Astragaloside ? (ASG-?, (Fig. 1) is the most active component of Chinese sp. Astragalus membranaceus Bunge (Fabaceae) that has showed antioxidant, antiapoptotic and antiviral activities among others. It is reported to play an important role in cardiac fibrosis (CF), but the mechanism remains unclear. PURPOSE: To investigate the mechanism of ASG-? on inhibiting myocardial fibrosis induced by hypoxia. STUDY DESIGN: We studied the relationship between anti-fibrotic effect of ASG-? and transient receptor potential cation channel, subfamily M, member 7 (TRPM7) by in vivo and in vitro experiments. METHODS: In vivo, CF was induced by subcutaneous isoproterenol (ISO) for 10 days. Rat hearts were resected for histological experiment and reverse transcription real-time quantitative poly merase chain reaction (RT-qPCR). In vitro, molecular and cellular biology technologies were used to confirm the anti-fibrosis effect underlying mechanism of ASG-?. RESULTS: Histological findings and the collagen volume fraction showed that ASG-? decreased fibrosis in heart tissues. Hypoxia could stimulate the proliferation and differentiation of cardiac fibroblast which indicated that the degree of fibrosis was increased significantly. Anoxic treatment could also obviously up-regulate the expression of TRPM7 protein and current. ASG-? groups showed the opposite results. Knock-down TRPM7 experiment further confirmed the role of TRPM7 channel in hypoxia-induced cardiac fibrosis. CONCLUSION: Our results suggest that the inhibition of hypoxia-induced CF in vivo and in vitro by ASG-IV is associated with reduction of the expression of TRPM7. The moderate inhibition of the TRPM7 channel may be a new strategy for treating cardiac fibrosis. Twit Text FOAVip Astragaloside against cardiac fibrosis by inhibiting TRPM7 channel ????Phytomedicine http://www.kidney.de/pget.php?&tw=1&pmid=28545665 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28545665 #FOAvip English Wikipedia <ref>{{Cite pmid|28545665}}</ref> Astragaloside? against cardiac fibrosis by inhibiting TRPM7 channel #MMPMID28545665 Lu J; Wang QY; Zhou Y; Lu XC; Liu YH; Wu Y; Guo Q; Ma YT; Tang YQ Phytomedicine 2017[Jul]; 30 (ä): 10-17 PMID28545665show ga BACKGROUND: Astragaloside ? (ASG-?, (Fig. 1) is the most active component of Chinese sp. Astragalus membranaceus Bunge (Fabaceae) that has showed antioxidant, antiapoptotic and antiviral activities among others. It is reported to play an important role in cardiac fibrosis (CF), but the mechanism remains unclear. PURPOSE: To investigate the mechanism of ASG-? on inhibiting myocardial fibrosis induced by hypoxia. STUDY DESIGN: We studied the relationship between anti-fibrotic effect of ASG-? and transient receptor potential cation channel, subfamily M, member 7 (TRPM7) by in vivo and in vitro experiments. METHODS: In vivo, CF was induced by subcutaneous isoproterenol (ISO) for 10 days. Rat hearts were resected for histological experiment and reverse transcription real-time quantitative poly merase chain reaction (RT-qPCR). In vitro, molecular and cellular biology technologies were used to confirm the anti-fibrosis effect underlying mechanism of ASG-?. RESULTS: Histological findings and the collagen volume fraction showed that ASG-? decreased fibrosis in heart tissues. Hypoxia could stimulate the proliferation and differentiation of cardiac fibroblast which indicated that the degree of fibrosis was increased significantly. Anoxic treatment could also obviously up-regulate the expression of TRPM7 protein and current. ASG-? groups showed the opposite results. Knock-down TRPM7 experiment further confirmed the role of TRPM7 channel in hypoxia-induced cardiac fibrosis. CONCLUSION: Our results suggest that the inhibition of hypoxia-induced CF in vivo and in vitro by ASG-IV is associated with reduction of the expression of TRPM7. The moderate inhibition of the TRPM7 channel may be a new strategy for treating cardiac fibrosis. |Animals[MESH] |Cell Differentiation/drug effects[MESH] |Cell Hypoxia/drug effects[MESH] |Cell Proliferation/drug effects[MESH] |Endomyocardial Fibrosis/chemically induced/*drug therapy/*metabolism[MESH] |Fibroblasts/drug effects/metabolism[MESH] |Heart/drug effects[MESH] |Isoproterenol/pharmacology/toxicity[MESH] |Male[MESH] |Mice[MESH] |NIH 3T3 Cells/drug effects[MESH] |Rats[MESH] |Rats, Sprague-Dawley[MESH] |Saponins/*pharmacology[MESH] |TRPM Cation Channels/genetics/*metabolism[MESH] |Triterpenes/*pharmacology[MESH]Astragaloside? against cardiac fibrosis by inhibiting TRPM7 channel (epmc).pdf DeepDyve Pubget Overpricing