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991.
AIM: To observe the expression of microRNA-126-5p during myocardial injury and its role in myocardial cell injury induced by adriamycin (also called doxorubicin, DOX). METHODS: The BALB/c mouse model of DOX-induced acute and chronic myocardial injury was established via intraperitoneal injection of DOX. HE staining was applied to observe the morphological changes of myocardial tissues. Lactate dehydrogenase (LDH) in serum was detected and PowerLab system was used to detect the influence of DOX on the changes of ±dp/dtmax. The expression of microRNA-126-5p in injured myocardial tissues and the H9c2 cells exposed to DOX was detected by real-time PCR. Gain-and loss-of-function experiments were conducted to detect the role of microRNA-126-5p in H9c2 cells treated with DOX on LDH release and caspase-3 activation. RESULTS: In acute and chronic DOX myocardial damage models in mice, HE staining showed disarranged myocardial fibers, dissolved myofibril and inflammatory cell infiltration. Higher serum LDH level and lower ±dp/dtmax in DOX-treated mice than those in normal mice were found. Compared with the normal mice, the expression level of microRNA-126-5p was significant increased in the myocardium with DOX-induced injury. Similarly, the expression level of microRNA-126-5p was significant increased in the H9c2 cells treated with DOX. In addition, over-expression of microRNA-126-5p decreased cell viability and promoted apoptosis, while microRNA-126-5p ablation promoted the viability and inhibited the apoptosis of H9c2 cells. CONCLUSION: The microRNA-126-5p expression is up-regulated in myocardial injury induced by DOX, and microRNA-126-5p inhibits cell viability and promotes apoptosis induced by DOX.  相似文献   
992.
AIM:To investigate the protective effect of exogenous hydrogen sulfide (H2S) on obstructive renal injury in mice, and to explore the possible potential mechanisms involved in this animal model. METHODS:Male C57BL/6 mice (8 weeks old) were randomly divided into sham group, operation group and H2S group, with 5 rats in each group. The model of obstructive renal injury was induced by unilateral ureteral obstruction (UUO). The mice in H2S group were intraperitoneally injected with NaHS daily, while the mice in sham group and operation group were administered with the same volume of saline intraperitoneally. After 7 d, the mice were executed and the renal tissues were taken out for experiments. RNA was extracted to detect the mRNA expression of H2S catalytic enzymes in the mice of 3 groups. HE staining was performed to observe the structural changes of renal tissues in the mice. Renal fibrosis in the mice of 3 groups was evaluated by Masson staining. The content of cystatin C in the plasma was detected to reflect glomerular filtration ability. The protein expression of LC3, beclin-1 and fibronectin (FN) in the mice of 3 groups was determined by Western blot. RESULTS:Compared with sham group, the mRNA expression of cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3-MST) in operation group decreased significantly. The collagen fiber content in operation group was increased significantly, while collagen fiber content in H2S group was decreased significantly as compared with operation group. Compared with sham group, the protein expression of FN in operation group was increased significantly, while the protein expression of FN in H2S group was decreased significantly as compared with operation group. Compared with sham group, the protein expression of LC-Ⅱ and beclin-1 in operation group was increased significantly, while the protein expression of LC-Ⅱ and beclin-1 in H2S group was increased significantly as compared with the operation group. CONCLUSION:Exogenous H2S possibly mitigates renal fibrosis in UUO mice by up-regulating autophagy.  相似文献   
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AIM: To investigate the effect of Ca2+/calmodulin-dependent protein kinase Ⅱ (CaMKⅡ) on hypoxia/reoxygenation (H/R) injury in H9c2 cells. METHODS: H9c2 cells were randomized into 4 groups:control group, KN-93 (an inhibitor of CaMKⅡ; 1 μmol/L) treatment group, H/R group and H/R+KN-93 (1 μmol/L) treatment group. The cells in KN-93 group and KN-93+H/R group were pretreated with KN-93 for 2 h before the other treatment was performed. The viability of H9c2 cells in each group was measured by CCK-8 assay. Lactate dehydrogenase (LDH) activity in the culture medium was detected. The protein levels of phosphorylated CaMKⅡ (p-CaMKⅡ), phosphorylated phospholamban (p-PLN) and cleaved caspase-3 were determined by Western blot. The apoptosis was analyzed by TUNEL staining and the flow cytometry. RESULTS: No significant difference of all indexes tested between control group and KN-93 group was observed. H/R treatment significantly reduced the cell viability, and increased the activity of LDH (P<0.01), the protein levels of p-CaMKⅡ, p-PLN and cleaved caspase-3 (P<0.05), and the apoptotic rate (P<0.01). KN-93 (1 μmol/L) significantly increased the cell viability, and decreased the activity of LDH (P<0.01), the protein levels of p-CaMKⅡ, p-PLN and cleaved caspase-3 (P<0.05), and the apoptotic rate (P<0.01). CONCLUSION: CaMKⅡ aggravates hypoxia/reoxygenation injury in the H9c2 cells by activating apoptosis.  相似文献   
995.
为探明山葡萄叶片低温伤害的生理机制,以抗寒性差异明显的‘双丰’(山葡萄种内杂交种)和‘左优红’(种间杂交种)为试材,对低温处理过程中叶绿素荧光参数和活性氧代谢的相关指标进行测定。结果表明,随低温胁迫加剧,两个品种叶片的叶绿素含量、Chl.a/b、Fv/Fm值均呈显著下降趋势,1–qp值及MDA含量明显增加;整个胁迫过程中NPQ值较稳定的‘双丰’其叶片遭受低温伤害程度较轻,NPQ值一直下降的‘左优红’叶片伤害程度较重,‘双丰’的NPQ值始终显著高于‘左优红’。‘双丰’叶片的SOD和APX活性始终较‘左优红’高。说明低温使山葡萄叶片叶绿素分解,PSⅡ电子传递受阻,激发能增加,造成叶绿体膜脂过氧化损伤;热耗散及抗氧化酶共同作用减轻了活性氧对叶片PSⅡ的伤害程度。由此可见,热耗散NPQ值及活性氧清除酶SOD和APX活性的差异可能是造成两个山葡萄品种叶片低温伤害程度不同的重要原因。  相似文献   
996.
AIM: To explore the expression level of tristetraprolin (TTP) in rats after subarachnoid hemorrhage (SAH) as well as the potential role of TTP in the early brain injury (EBI) after SAH in rats.METHODS: In the first experiment setting, total 56 adult male SD rats were randomly divided into sham group and SAH group. The SAH model was performed by endovascular perforation. The brain tissues were taken out after SAH at 5 different time points (0, 12, 24, 48, 72 h and 1 week). The expression of TTP in the brain tissues was detected by Western blot. In the second experiment, a total of 60 SD rats were divided into 4 groups:sham group, SAH group, SAH+vector group and SAH+TPP group. Neurological score, brain water content and blood-brain barrier were evaluated at 48 h after SAH. TUNEL staining was performed to detect cell apoptosis in the rat brain tissue. ELISA method was used for quantitative detection of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). The protein levels of TTP, Bax, Bcl-2 and cleaved caspase-3 in the rat brain tissue were detected by Western blot.RESULTS: The protein expression of TTP in the brain was downregulated markedly from 12 h after SAH, reached the lowest level at 48 h, and then had an upward trend. After modeling for 48 h, Garcia neurological score was significantly reduced, and brain water content and Evans blue (EB) content of the brain tissue of the rats in SAH group were significantly higher than those in sham group (P<0.05). SAH induced significant increases in IL-6 and TNF-α levels in the brain tissue (P<0.05). The number of TUNEL-stained cells was increased in the subcortical brain region after SAH compared with sham group. In addition, a lower level of Bcl-2 and higher levels of Bax and cleaved caspase-3 in the rat brains were observed at 48 h after SAH. However, the neurological deficit score was significantly increased, and the brain water content and EB content in the rat brains were significantly reduced in SAH+TTP group in comparison with SAH+vector group (P<0.05). Over-expression of TTP dramatically suppressed the levels of IL-6 and TNF-α in the rat brains, and reduced the number of TUNEL positive cells. Furthermore, upregulation of TTP significantly decreased the levels of cleaved caspase-3 and Bax, and evidently enhanced the expression of Bcl-2 (P<0.01).CONCLUSION: The expression of TTP is significantly decreased in early period after SAH, and enhancing the level of TTP effectively inhibits EBI following SAH in rats.  相似文献   
997.
AIM: To determine the expression of matrix metalloproteinase-9 (MMP-9), tissue inhibitor of me-talloproteinase-1 (TIMP-1) and collagen type IV (IV-C) in the lung of rats with multiple organ dysfunction syndrome (MODS) and to investigate the mechanism of lung injury in MODS. METHODS: Adult male Sprague-Dawley (SD) rats (n=40) were randomly divided into sham control group and cecal ligation and puncture (CLP) model group. The rats in CLP group were divided into 4 subgroups as different intervals (6 h, 12 h, 24 h and 48 h), and there were 8 rats in each group. The rat model of MODS was established by CLP. All rats were sacrificed at various intervals. The functions of the liver, kidney and lung were determined by blood biochemical and blood gas analysis. The morphological changes of the lung tissues were observed with HE staining. The serum levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, MMP-9 and TIMP-1 were measured by ELISA. The expression of MMP-9 and TIMP-1 in the lung tissues was detected by RT-PCR and immunohistochemistry, and the expression of IV-C in the lung tissues was detected by immunofluorescence and Western blot. RESULTS: Compared with sham control group, the functions of the liver, kidney and lung were damaged at different degrees in model groups. No histopathological change in the lung tissues of sham control group was found, and the lung injury was serious in model groups. Compared with sham control group, the serum levels of TNF-α, IL-1β, MMP-9 and TIMP-1 in model groups increased significantly (P<0.05) and peaked at the interval of 12~24 h after modeling (P<0.01). The expression of MMP-9 and TIMP-1 in the lung tissues of model groups increased, and peaked at 12 and 24 h, respectively (P<0.01). The protein level of IV-C in MODS 6 h group was not changed as compared with control group, while that at the interval of 12~48 h after modeling was significantly decreased and dropped to the lowest at 24 h (P<0.01). CONCLUSION: MMP-9 and TIMP-1 play important roles in lung injury of MODS rats by regulating the synthesis and decomposition of IV-C which is the main component of extracellular matrix.  相似文献   
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