RESUMO
Long non-coding RNA plays an increasingly important role in transcriptional, post-transcriptional and epigenetic levels. In ischemic heart disease, most studies on long non-coding RNA focused on myocardial infarction, hypertrophy and fibrosis, and a few of reports directly focused on the pathological process of myocardial reperfusion injury. Thus, the purpose of this review is to introduce the processes of long non-coding RNA in myocardial reperfusion injury field, aiming to provide a novel research and theraputic method for exploring the mechanism and molecular regulation network involed with reperfusion injury.
RESUMO
Objective To study the protective effect of lipoic acid (LA) on H9c2 cardiomyocytes hypoxia/reoxygenation injury model, and explore its relevant mechanism. Methods Eight strains of H9c2 cardiomyocytes, passaged after cultured to a full view, were divided into 3 groups:normoxia group, hypoxia/reoxygenation group and LA group. The cell survival rate, lactate dehydrogenase (LDH) activity, malondialdehyde (MDA) and heme oxygenase-1 (HO-1) levels were detected and compared. Results The cell survival rates of H9c2 cardiomyocytes in hypoxia/reoxygenation group and LA group were significantly lower than those in normoxia group:(52.86 ± 6.39)％, (69.25 ± 7.63)％vs. (92.31 ± 7.82)％, while the cell survival rate of H9c2 cardiomyocytes in LA group was significantly higher than that in hypoxia/reoxygenation group, and there were statistical differences (P<0.01). The LDH activity and MDA in hypoxia/reoxygenation group and LA group were significantly higher than those in normoxia group:(286.37 ± 27.49), (209.72 ± 25.63) U/L vs. (126.32 ± 18.94) U/L, and (1.72 ± 0.06), (1.13 ± 0.07)μmol/L vs. (0.68 ± 0.06) μmol/L, while those data in LA group were significantly lower than those in hypoxia/reoxygenation group, and there were statistical differences (P<0.01). The HO-1 in hypoxia/reoxygenation group and LA group were significantly higher than that in normoxia group:(213.71 ± 18.94)％, (367.26 ± 23.07)％vs. (87.92 ± 19.23)％, and HO-1 in LA group was significantly higher than that in hypoxia/reoxygenation group, and there were statistical differences (P<0.01). Conclusions The LA plays a protective role on myocardial cell with hypoxia/reoxygenation injurythough increasing the level of HO-1 against oxidative stress.
RESUMO
AIM: Mutations in lipoprotein-associated phospholipase A2 (Lp-PLA2) are related to atherosclerosis. However, the molecular effects of Lp-PLA2 on atherosclerosis have not been fully investigated. Therefore, this study attempted to elucidate this issue. METHODS: Monocytes were isolated from randomly selected healthy male volunteers according to each Lp-PLA2 genotype (wild-type Lp-PLA2 [Lp-PLA2 (V/V)], the heterozygous V279F mutation [LpPLA2 (V/F)] and the homozygous V279F mutation [Lp-PLA2 (F/F)]) and differentiated into macrophages. The level of apoptosis in the macrophages following incubation without serum was measured using the annexin V/propidium iodide double staining method, and the underlying mechanisms were further examined using a culture cell line. RESULTS: The average plasma Lp-PLA2 concentration [Lp-PLA2 (V/V): 129.4 ng/mL, Lp-PLA2 (V/F): 70.7 ng/mL, Lp-PLA2 (F/F): 0.4 ng/mL] and activity [Lp-PLA2 (V/V): 164.3 nmol/min/mL, LpPLA2 (V/F): 100.9 nmol/min/mL, Lp-PLA2 (F/F): 11.6 nmol/min/mL] were significantly different between each genotype, although the basic clinical characteristics were similar. The percentage of apoptotic cells was significantly higher among the Lp-PLA2 (F/F) macrophages compared with that observed in the Lp-PLA2 (V/V) macrophages. This induction of apoptosis was independent of the actions of acetylated low-density lipoproteins. In addition, the transfection of the expression plasmid of V279F mutant Lp-PLA2 into Cos-7 cells or monocyte/macrophage-like U937 cells promoted apoptosis. The knockdown of Lp-PLA2 also increased the number of apoptotic cells. Among the cells expressing mutant Lp-PLA2, the caspase-7 activity was increased, while the activated Akt level was decreased. CONCLUSIONS: The V279F mutation of Lp-PLA2 positively regulates the induction of apoptosis in macrophages and Cos-7 cells. An increase in the caspase-7 activity and a reduction in the activated Akt level are likely to be involved in this phenomenon.
