ABSTRACT
Aim: To compare the differential expression of proteins in testicular tissues of ionized irradiated mice and normal mice, in order to explain the mechanism of ionizing irradiation on testicular tissue damage from proteomics perspective. Methods: The mouse ionizing radiation damage model was established by cobalt 60-ray irradiation. Comparative proteomics method, iTRAQ combined with LC-MS/MS detection technology were used to extract differentially expressed proteins of testis tissues from mouse irradiated group and normal group, then David6. 8, StringlO. 5 and Cytoscape 3. 6. 1 database were employed for KEGG enrichment analysis and interaction analysis on differential proteins. Results: Twenty-one biological signaling pathways (P <0. 05) were identified by KEGG enrichment analysis, with 13 differentially expressed proteins enriched in phosphoric oxide signaling pathways, and both were downgrades of expression. The pathway involved several subgroups of ATP synthase, cytochrome and NADH dehydrogenase, which were mainly involved in mitochondrial electron transfer, mitochondrial respiratory chain complex I assembly, ATP biosynthesis and so on. Conclusions: Ionizing radiation is responsible for the expression of oxidative phosphorylation signaling pathway in mouse testis tissues. The low expression of 13 differential proteins leads to the synthesis of cell ATP. It is an important mechanism of radiation damage.
ABSTRACT
<p><b>OBJECTIVE</b>To explore the effects of trimetazidine therapy on left ventricular (LV) function after percutaneous coronary intervention (PCI).</p><p><b>METHODS</b>A total of 106 patients with unstable angina pectoris underwent successful elective PCI were randomly assigned to standard therapy group (control, n = 55) or trimetazidine group (n = 51, 60 mg trimetazidine loading dose prior to PCI followed by 20 mg Tid after PCI on top of standard therapy). cTnI level was measured before and at 16-18 hours after PCI. LV function was evaluated by echocardiography and major adverse cardiac events (MACE, including death, re-infarction and target vessel revascularization) at 12 months after PCI was compared between the two groups.</p><p><b>RESULTS</b>Post procedural cTnI level increased from [0.02 (0.01, 0.03)] µg/L at baseline to [0.11 (0.07, 0.13)] µg/L (P < 0.05) at 16-18 hours in the trimetazidine group, while [0.02(0.01, 0.03)] µg/L to [1.31(0.44, 2.31)] µg/L in the control group (P < 0.05). Post procedural cTnI level was significantly reduced in the trimetazidine group compared to the control group (P < 0.05). At 12 months follow-up, left ventricular ejection fraction in the trimetazidine group was significantly higher than in control group [(65.65 ± 3.94)% vs. (62.29 ± 3.06)%, P < 0.01] while incidence of MACE was similar between the two groups.</p><p><b>CONCLUSION</b>Trimetazidine can reduce the post-PCI cTnI release and improve left ventricular function after PCI in patients with unstable angina pectoris.</p>