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The aim of this study was to detect early changes (within 1-4 h) in the brain natriuretic peptide (BNP) levels of rats with acute myocardial infarction (AMI). A total of 35 Wistar rats were established as models of AMI and 30 sham-operated rats were used as the control group. The myocardia of the two groups were observed using a transmission electron microscope (TEM) prior to and following surgery. A double-antibody sandwich enzyme-linked immunosorbent assay (ELISA) was used to detect the serum BNP and cardiac troponin I (cTnI) concentrations before and 1-4 h after surgery. Following the successful establishment of the AMI models, serum BNP concentrations were significantly increased within 1-4 h compared with the values prior to surgery and with those of the control group (all P<0.01). The serum BNP concentration reached its highest level 2 h after AMI (532.25±15.16 ng/l). No significant changes were observed in the cTnI serum levels of the AMI group within 1-4 h compared with the values before AMI and those in the control group (all P>0.05). In the 1-4 h following the establishment of the AMI model, significant positive correlations were identified between the serum BNP concentrations and the size of the AMI and the most marked correlation occurred 2 h after AMI (r=0.72, P<0.05). No significant differences were noted in the serum concentrations of BNP and cTnI in the control group prior to and following the sham surgery (all P>0.05). BNP may be used as a blood marker for the early diagnosis of AMI, particularly 1-4 h after the onset of AMI, and to predict the size of the infarct area.

The teleost fish has been widely used in creating neurodegenerative models. Here we describe the teleost medaka fish Parkinson's disease (PD) models we developed using toxin treatment and genetic engineering. 1-Methyl-4-phenyl-1,2,3,4-tetrahydropyridine (MPTP), 6-hydroxydopamine (6-OHDA), proteasome inhibitors, lysosome inhibitors and tunicamycin treatment in our model fish replicated some salient features of PD: selective dopamine cell loss and reduced spontaneous movement with the last three toxins producing inclusion bodies ubiquitously in the brain. Despite the ubiquitous distribution of the inclusion bodies, the middle diencephalic dopaminergic neurons were particularly vulnerable to these toxins, supporting the idea that this dopamine cluster is similar to the human substantia nigra. PTEN-induced putative kinase 1 (PINK1) homozygous mutants also showed reduced spontaneous swimming movements. These data indicate that medaka fish can serve as a new model animal of PD. In this review we summarize our previous data and discuss future prospects.