Fig 1: Expression levels of miR-133a and endothelial injury markers (vWF, H-FABP and cTnI) in a rat model of acute myocardial infarction. (A) Quantification of the expression levels of miR-133a in model rats, as determined by RT-qPCR. Expression levels of (B) vWF, (C) H-FABP and (D) cTnI in model rats, as determined by ELISA. Data are presented as the mean ± standard deviation. *P<0.05 vs. the Con group; #P<0.05 vs. the Model group; &P<0.05 vs. the Mimic group. Con: Control group, rats that underwent the sham operation were injected with a vector; Model: Model group, rats in the AMI model group were injected with NC; mimic, miR-133a mimic group, rats in the AMI model group were injected with a miR-133a mimic; inhibitor, miR-133a inhibitor group, rats in the AMI model group were injected with a miR-133a inhibitor; cTnI, cardiac troponin I; H-FABP, heart-type fatty acid-binding protein; miR-133a, microRNA-133a; vWF, Von Willebrand factor.
Fig 2: Expression levels of miR-133a and endothelial injury markers (vWF, H-FABP and cTnI) in patients with or without AMI. The expression levels of miR-133a, and vWF, H-FABP and cTnI, were detected in patients using reverse transcription-quantitative polymerase chain reaction and ELISA, respectively. AMI patients, patients with AMI following radical surgery for gastric cancer; Control patients, patients without AMI following radical surgery for gastric cancer. Data are presented as the mean ± standard deviation. *P<0.05 vs. the Control patients. AMI, acute myocardial infarction; cTnI, cardiac troponin I; H-FABP, heart-type fatty acid-binding protein; miR-133a, microRNA-133a; vWF, Von Willebrand factor.
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