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10.3892/ijmm.2021.4935 http://scihub22266oqcxt.onion/10.3892/ijmm.2021.4935 33907819!ä!33907819 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 284.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 284.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Int+J+Mol+Med 2021 ; 47 (6): ä Nephropedia Template TP {{tp|p=33907819|t=2021. Naringin protects H9C2 cardiomyocytes from chemical hypoxia?induced injury by promoting the autophagic flux via the activation of the HIF?1alpha/BNIP3 signaling pathway |pdf=|usr=}}{{33907819}} gab.com Text Naringin protects H9C2 cardiomyocytes from chemical hypoxia induced injury by promoting the autophagic flux via the activation of the HIF 1alpha/BNIP3 signaling pathway JO: Int J Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=33907819 #FOAvip Naringin, a natural bioflavonoid, has been shown to exert protective effects in multiple cardiovascular diseases; however, the protective effects of naringin against hypoxic/ischemia?induced myocardial are not yet fully understood. Autophagy is a vital factor involved in the pathogenesis of myocardial injury. The aim of the present study was to investigate the protective effects of naringin on H9c2 cells against chemical hypoxia [cobalt chloride (CoCl(2))]?induced injury. The role of autophagy and the hypoxia?inducible factor?1alpha (HIF?1alpha)/Bcl?2/BCL2 interacting protein 3 (BNIP3) signaling pathway in the protective effects of naringin were also assessed. The results revealed that naringin pre?treatment significantly attenuated the CoCl(2)?induced cytotoxicity and apoptosis, and also decreased caspase?3 activity, which had been increased by CoCl(2). In addition, CoCl(2) increased Beclin?1 expression, enhanced the IL3B?II/IL3B?I ratio and increased p62 expression in the H9C2 cells. Treatment with 3?methyladenine (3?MA), a selective inhibitor of autophagy, also blocked CoCl(2)?induced cytotoxicity and apoptosis. Notably, treatment with bafilomycin A1 (Baf A1), an inhibitor of the vacuolar H+ ATPase of lysosomes, resulted in an increase in the upregulation of the LC3B?II/LC3B?I ratio, but did not further increase the LC3B?II/LC3B?I ratio compared with CoCl(2) treatment. These results suggested that CoCl(2) inhibited the autophagic flux, which resulted in myocardial cell damage. Furthermore, naringin pre?treatment exacerbated Beclin 1 expression and the increased IL3B?II/IL3B?I ratio, and reduced p62 expression in CoCl(2)?treated H9C2 cells. 3?MA and Baf A1 both reversed the protective effects of naringin against CoCl(2)?induced injury, indicating that naringin attenuated CoCl(2)?induced myocardial cell injury by the increasing autophagic flux. Moreover, naringin treatment resulted in upregulated expression levels of HIF?1alpha and BNIP3 in the CoCl(2)?treated H9C2 cells. The inhibition of the HIF?1alpha/BNIP3 signaling pathway using 3?(5'?hydroxymethyl?2'?furyl)?1?benzylindazole (an inhibitor of HIF?1alpha) prevented the effects of naringin on the autophagic flux and reversed its protective effects against CoCl(2)?induced injury. Taken together, these results suggest that naringin protects the H9C2 cells against CoCl(2)?induced injury by enhancing the autophagic flux via the activation of the HIF?1alpha/BNIP3 signaling pathway. Twit Text FOAVip Naringin protects H9C2 cardiomyocytes from chemical hypoxia induced injury by promoting the autophagic flux via the activation of the HIF 1alpha/BNIP3 signaling pathway ????Int J Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=33907819 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33907819 #FOAvip English Wikipedia <ref>{{Cite pmid|33907819}}</ref> Naringin protects H9C2 cardiomyocytes from chemical hypoxia?induced injury by promoting the autophagic flux via the activation of the HIF?1alpha/BNIP3 signaling pathway #MMPMID33907819 Li S; Jiang J; Fang J; Li X; Huang C; Liang W; Wu K Int J Mol Med 2021[Jun]; 47 (6): ä PMID33907819show ga Naringin, a natural bioflavonoid, has been shown to exert protective effects in multiple cardiovascular diseases; however, the protective effects of naringin against hypoxic/ischemia?induced myocardial are not yet fully understood. Autophagy is a vital factor involved in the pathogenesis of myocardial injury. The aim of the present study was to investigate the protective effects of naringin on H9c2 cells against chemical hypoxia [cobalt chloride (CoCl(2))]?induced injury. The role of autophagy and the hypoxia?inducible factor?1alpha (HIF?1alpha)/Bcl?2/BCL2 interacting protein 3 (BNIP3) signaling pathway in the protective effects of naringin were also assessed. The results revealed that naringin pre?treatment significantly attenuated the CoCl(2)?induced cytotoxicity and apoptosis, and also decreased caspase?3 activity, which had been increased by CoCl(2). In addition, CoCl(2) increased Beclin?1 expression, enhanced the IL3B?II/IL3B?I ratio and increased p62 expression in the H9C2 cells. Treatment with 3?methyladenine (3?MA), a selective inhibitor of autophagy, also blocked CoCl(2)?induced cytotoxicity and apoptosis. Notably, treatment with bafilomycin A1 (Baf A1), an inhibitor of the vacuolar H+ ATPase of lysosomes, resulted in an increase in the upregulation of the LC3B?II/LC3B?I ratio, but did not further increase the LC3B?II/LC3B?I ratio compared with CoCl(2) treatment. These results suggested that CoCl(2) inhibited the autophagic flux, which resulted in myocardial cell damage. Furthermore, naringin pre?treatment exacerbated Beclin 1 expression and the increased IL3B?II/IL3B?I ratio, and reduced p62 expression in CoCl(2)?treated H9C2 cells. 3?MA and Baf A1 both reversed the protective effects of naringin against CoCl(2)?induced injury, indicating that naringin attenuated CoCl(2)?induced myocardial cell injury by the increasing autophagic flux. Moreover, naringin treatment resulted in upregulated expression levels of HIF?1alpha and BNIP3 in the CoCl(2)?treated H9C2 cells. The inhibition of the HIF?1alpha/BNIP3 signaling pathway using 3?(5'?hydroxymethyl?2'?furyl)?1?benzylindazole (an inhibitor of HIF?1alpha) prevented the effects of naringin on the autophagic flux and reversed its protective effects against CoCl(2)?induced injury. Taken together, these results suggest that naringin protects the H9C2 cells against CoCl(2)?induced injury by enhancing the autophagic flux via the activation of the HIF?1alpha/BNIP3 signaling pathway. |*Autophagy/drug effects[MESH] |*Cytoprotection/drug effects[MESH] |*Signal Transduction[MESH] |Animals[MESH] |Apoptosis/drug effects[MESH] |Cardiotonic Agents/pharmacology[MESH] |Cell Hypoxia/drug effects[MESH] |Cell Line[MESH] |Cobalt/toxicity[MESH] |Flavanones/*pharmacology[MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/*metabolism[MESH] |Membrane Proteins/*metabolism[MESH] |Mitochondrial Proteins/*metabolism[MESH] |Myocytes, Cardiac/drug effects/*metabolism/*pathology[MESH]Naringin protects H9C2 cardiomyocytes from chemical hypoxia?induced in(epmc).pdf DeepDyve Pubget Overpricing