biostudies-literatureUnknown9(26)Feng L<i>Background</i>: Metformin, an antidiabetic drug, has been reported to be involved in atherosclerosis (AS). In this study, the effects of metformin on oxidized low-density lipoprotein (Ox-LDL)-induced macrophage apoptosis were investigated, and the mechanisms involved in this process were examined. <i>Methods</i>: qRT-qPCR analysis was performed to detect the expression of miR-34a in macrophage cells. Cell proliferation was determined by MTT assays and colony formation assays. Cell apoptosis was assessed by the detection of apoptotic rate and caspase 3 activity. Western blot analysis was performed to evaluate the expression of Bcl2 protein. <i>Results</i>: Metformin treatment promoted proliferation and suppressed apoptosis in macrophages following the treatment of oxidized low-density lipoprotein (Ox-LDL). Metformin could inhibit miR-34a in macrophages. miR-34a overexpression could reverse the effect of metformin on proliferation and apoptosis in Ox-LDL-treated macrophages. Moreover, metformin could increase the expression of the miR-34a target gene Bcl2. Furthermore, metformin treatment exerted the pro-proliferation and anti-apoptosis effect through regulating Bcl2 expression in Ox-LDL-stimulated macrophages. <i>Conclusion</i>: Metformin facilitated proliferation and inhibited apoptosis of macrophages treated with Ox-LDL through the miR-34a/Bcl2 axis, indicating the potential value of metformin in AS therapy.RSC advances14670-14676https://www.ebi.ac.uk/biostudies/studies/S-EPMC9064147biostudies-literatureMetformin promotes proliferation and suppresses apoptosis in Ox-LDL stimulated macrophages by regulating the miR-34a/Bcl2 axis.PMC9064147Liu XFeng LYang YMei XHuang HXiao WTian SLiu TShi JBai YfalseMetformin promotes proliferation and suppresses apoptosis in Ox-LDL stimulated macrophages by regulating the miR-34a/Bcl2 axis.<i>Background</i>: Metformin, an antidiabetic drug, has been reported to be involved in atherosclerosis (AS). In this study, the effects of metformin on oxidized low-density lipoprotein (Ox-LDL)-induced macrophage apoptosis were investigated, and the mechanisms involved in this process were examined. <i>Methods</i>: qRT-qPCR analysis was performed to detect the expression of miR-34a in macrophage cells. Cell proliferation was determined by MTT assays and colony formation assays. Cell apoptosis was assessed by the detection of apoptotic rate and caspase 3 activity. Western blot analysis was performed to evaluate the expression of Bcl2 protein. <i>Results</i>: Metformin treatment promoted proliferation and suppressed apoptosis in macrophages following the treatment of oxidized low-density lipoprotein (Ox-LDL). Metformin could inhibit miR-34a in macrophages. miR-34a overexpression could reverse the effect of metformin on proliferation and apoptosis in Ox-LDL-treated macrophages. Moreover, metformin could increase the expression of the miR-34a target gene Bcl2. Furthermore, metformin treatment exerted the pro-proliferation and anti-apoptosis effect through regulating Bcl2 expression in Ox-LDL-stimulated macrophages. <i>Conclusion</i>: Metformin facilitated proliferation and inhibited apoptosis of macrophages treated with Ox-LDL through the miR-34a/Bcl2 axis, indicating the potential value of metformin in AS therapy.2019-01-01T00:00:00Z2019 May2025-04-04T12:43:21.965Z2025-04-04T12:43:21.965ZS-EPMC90641473551631910.1039/c9ra00705a