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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Apoptosis, Cells, Cultured, Genetic Vectors, Hydrogen Peroxide, Lentivirus, Myocytes, Cardiac, Oxidative Stress, RNA Interference, RNA, Small Interfering, Rats, Scavenger Receptors, Class E.
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Does [ Lentivirus-mediated LOX-1-RNA interference attenuate oxidative stress-induced apoptosis in myocardial cells ]? Context: To construct a lectin-like oxidized low-density lipoprotein receptor (LOX-1) RNA interference (RNAi) lentivirus and explore the role of LOX-1 in H(2)O(2)-induced apoptosis of rat myocardial cells. LOX-1 shRNA sequence was synthesized and cloned into pLentiLox3.7 (pLL3.7) lentiviral vector to construct the lentiviral vector pLL3.7-LOX1. The lentiviral vectors (pLL3.7 and pLL3.7-LOX1) and the packaging vectors dR8.9 and VSVG were co-transfected into 293FT cells for packaging the lentivirus. H9C2 myocardial cells were infected by the lentiviruses to observe the inhibitory rate of LOX-1 on H(2)O(2)-induced apoptosis of H9C2 cells by RT-PCR, CCK-8, and Hochest33258 staining. Double restriction enzyme digestion and DNA sequencing confirmed correct insertion of the sequence. Suppression of LOX-1 by the lentivirus attenuated H(2)O(2)-induced cell viability reduction and apoptosis in the myocardial cells (P<0.01).
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LOX-1 activation may play an important role in H(2)O(2)-induced apoptosis of rat myocardial cells. Final Decision: yes