RESUMEN
Mining data in depth of genome-wide sequencing data generated from pathological target tissues under disease conditions is necessary for seeking novel functional genes, and developing more biological study directions for the field. Based on our previous published RNA-seq data generated from acute myocardial ischemia and ischemia-reperfusion in rat heart, we re-analysed these two data sets using bioinformatics tools. All these raw fastq files were extracted from Illumina BCL using the Illumina CASAVA program. Four groups were obtained: UD (genes up-regulated in MI but down-regulated in I/R injury), DU (genes down-regulated in MI but up-regulated in I/R injury), UU (genes both up-regulated in MI and I/R injury), and DD (genes both down-regulated in MI and I/R injury) groups. The results showed that 304 common genes in the UD group, 236 common genes in the DU group, 318 common genes in the UU group, and 159 common genes in the DD group detected by comparing data sets of the MI and the I/R injury. We then listed the top 30 DEGs for each group, and carried out GO and KEGG analyses for enrichment and pathway studies for those top expressed genes. Further analysis of INTERPRO Protein Domains and Features enriched by DEGs showed that 20% of the Domains enriched were related to c-type lectin, and 17% of these domains are related to neurotransmitter-gated ion-channel. 15% of PFAM Protein Domains were about Neurotransmitter-gated ion-channel. There were only 8 SMART Protein Domains DEGs enriched and 37.5% of which were concerned about leucine-rich. Collagen involvement in Reactome Pathways accounted for 22.7%. We found that only a few DEGs in these two disease conditions have been reported in the literatures, suggesting that there are many new genes would be considered in the future studies. These analyses would provide some information for seeking more novel targets of these two clinic diseases, acute myocardial ischemia and myocardial ischemia/reperfusion.
RESUMEN
OBJECTIVE: To study the effect of compound macrostem onion capsule (CMOC) on products of arachidonic acid metabolism in monocrotaline (MCT)-induced pulmonary artery hypertension rats. METHODS: Sixty SD rats were divided into a control group, a model group, and three experimental groups in which the rats were fed with captopril, small dose single dosage, and large dose (double dosage) of CMOC, respectively. The rat model was made by MCT peritoneal injection. The mean pulmonary arterial pressure (mPAP) and the mean right ventricular pressure (mRVP) were measured. Thromboxane B(2) (TXB(2)) and 6-keto-prostaglandin Fia (6-K-PGFia) were determined by RIA method. RESULTS: The mPAP in rats of the model group [(36.9 +/- 4.8) mm Hg, 1 mm Hg = 0.133 kPa] was significantly higher than that of the control group [(16.4 +/- 2.1) mm Hg, all P < 0.01]. The mPAP in rats of the double dosage and single dosage of CMOC groups were (26.2 +/- 2.8) mm Hg and (27.9 +/- 2.8) mm Hg, respectively; both were significantly lower than those of the model group (all P < 0.01). TXB(2) in rats of the model group was significantly higher than that of the control group (P < 0.05), while 6-K-PGFia in the model group was significantly lower than that of the control group (P < 0.01). TXB(2) in rats of the double dosage CMOC group was significantly lower than that of the model group, but 6-K-PGFia in rats of the CMOC groups was significantly higher than that of the model group (P < 0.05, < 0.01). CONCLUSION: CMOC is effective in reducing pulmonary artery hypertension. Inhibition of TXB(2) and augmentation of 6-K-PGFia might be the underlying mechanisms.
