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Objective:To explore the factors influencing the clinical outcome of complex high-risk indicated patients percutaneous coronary intervention (CHIP-PCI) assisted by extracorporeal membrane oxygenation (ECMO).Methods:The clinical data of patients with CHIP-PCI assisted by ECMO in the First Affiliated Hospital of Zhengzhou University from April 2018 to April 2022 were retrospectively collected and analyzed. Patients were divided into the survival and death groups according to the in-hospital survival status. The baseline characteristic, the results of coronary angiography, and the use of ECMO, blood products and drug were compared between the two groups. The 24-h rate of change of biochemical test indicators after the use of ECMO were calculated and the univariate analysis was analyzed using rank sum test. According to the univariate analysis, the variables ( P<0.05) were included in multivariate logistic regression to analyze the factors affecting the clinical outcomes of patients. Results:A total of 67 CHIP patients who completed PCI with ECMO were included. In the survival group ( n=36), the duration of ECMO treatment was 59 (41, 87) h, 9 cases received continuous renal replacement therapy, and 11 cases received IABP. In the death group ( n=31), the duration of ECMO treatment was 31 (19, 80) h, 12 cases received continuous renal replacement therapy and10 cases received IABP. The proportion of patients with chronic total occlusion lesions (CTOs) in the survival group was lower than that in the death group, the duration of ECMO of the survival group was longer than that of the death group ( P<0.05). Multivariate logistic regression analysis showed that 24-h lactate change rate ( OR=2.864, 95% CI: 1.185-6.918, P=0.019), 24-h eGFR change rate ( OR=0.050, 95% CI: 0.003-0.871, P=0.040), 24-h D-dimer change rate ( OR=1.497, 95% CI: 1.044-2.146, P=0.028) and 24-h direct bilirubin change rate ( OR=2.617, 95% CI: 1.121-6.111, P=0.026) were associated with in-hospital mortality. Conclusions:Within 24 h after CHIP-PCI assisted by ECMO, the rapid decline in lactic acid, D-dimer and direct bilirubin, and the rapid recovery of eGFR, are associated with the decreased risk of hospital mortality from CHIP.
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OBJECTIVE@#To study the effect of down-regulating miR-488 targeting Jag1 on the injury of hypoxia-reoxygenation myocardial H9c2 cells.@*METHODS@#A hypoxic-reoxygenated myocardial H9c2 cell injury model was constructed. miR-488 inhibitor was used to transfect the cells. CCK-8 method and flow cytometry were used to detect cell proliferation and apoptosis in each group. Lactate dehydrogenase (LDH), superoxide dismutase (SOD), malonaldehyde (MDA), catalase (CAT) levels were detected. Western blotting was used to detect the expression of Bcl-2 associated X Protein (Bax) and B cell lymphoma/lewkmia-2 (Bcl-2). Target genes of miR-488 were predicted, and a luciferase reporter system was used to verify the targeting relationship between the two. Myocardial H9c2 cells were co-transfected with miR-488 inhibitor and Jag1 siRNA, and treated with hypoxia and reoxygenation, cell proliferation, apoptosis, LDH, SOD, MDA, CAT levels, and Bax, Bcl-2 protein expression were detected.@*RESULTS@#The expression of miR-488 in the hypoxia-reoxygenated myocardial H9c2 cells was increased, along with reduced cell proliferation, increased apoptosis, increased Bax protein expression, decreased Bcl-2 protein expression, increased MDA, decreased CAT and SOD, and increased LDH level in the supernatant of cell culture. When myocardial H9c2 cells were transfected with miR-488 inhibitor and treated with hypoxia and reoxygenation, the expression of miR-488 was decreased, along with increased cell proliferation, decreased apoptosis, decreased Bax protein expression, increased Bcl-2 protein expression, decreased MDA, increased CAT and SOD, and decreased LDH level in the supernatant of cell culture. Down-regulation of miR-488 could target and down-regulate Jag1 expression. And Jag1 siRNA could reverse the effect of miR-488 inhibitor on the proliferation, apoptosis, LDH, SOD, MDA, CAT levels and the expression of Bax and Bcl-2 of hypoxic-reoxygenated myocardial H9c2 cells.@*CONCLUSION@#Down-regulating miR-488 targeted Jag1 can attenuate hypoxia-reoxygenation induced myocardial H9c2 cell injury.
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Humans , Apoptosis/genetics , Down-Regulation , Hypoxia/genetics , Jagged-1 Protein/genetics , MicroRNAs/genetics , Myocardial Reperfusion Injury , Myocytes, CardiacABSTRACT
OBJECTIVE@#To explore the effect and mechanism of miR-125a-5p targeted regulation of scavenger receptor B1 (Scarb1) gene on anoxia/reoxygenation injury of rat cardiomyocytes.@*METHODS@#H9c2 rat cardiomyocytes were randomly divided into blank control group, hypoxia/reoxygenation group, transfection control group and mir-125a-5p transfection group. The expression of miR-125a-5p, cardiomyocyte viability, apoptosis rate, ATP content and the expression of Scarb1, Cyt C, Bax, Bcl-2 and NF-κB signaling pathway related proteins were determined. Target gene of miR-125a-5p was predicted with Targetscan software, and the targeting of miR-125a-5p on Scarb1 was verified by double luciferase reporter gene experiment.@*RESULTS@#Compared with the blank control group, the expression of miR-125a-5p, Bax, Cyt C and the apoptotic rate of cardiomyocytes in the hypoxia/reoxygenation group were significantly increased (P<0.05), while the expression of Scarb1, Bcl-2 and the content of ATP were significantly decreased (P<0.05). Compared with the control group, the situation of mir-125a-5p transfection group was just the opposite. Double luciferase reporter gene experiment has confirmed Scarb1 to be the target of miR-125a-5p. Hypoxia/reoxygenation can promote the expression of NF-κB p65, C-myc and Cyclin D1 in cardiomyocytes, while down-regulating the expression of miR-125a-5p can inhibit the expression of such proteins.@*CONCLUSION@#Hypoxia/reoxygenation can induce the expression of miR-125a-5p in rat cardiomyocytes. Inhibition of miR-125a-5p can protect cardiomyocytes from hypoxia/reoxygenation by up-regulating the expression of Scarb1. The mechanism may be related to the inhibition of activation of NF-κB signaling pathway.
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OBJECTIVE: To study the effects and mechanism of couplet medicines of Scutellaria baicalensis-Paeonia lactiflora on improving ulcerative colitis (UC) in mice. METHODS: A total of 70 mice were randomly divided into blank group, model group, S. baicalensis group (1. 5 g/kg), P. lactiflora group (1. 5 g/kg), S. baicalensis-P. lactiflora (2:1, 1:1, 1:2, m/m) groups (total amount of 1. 5 g/kg), with 10 mice in each group. Except for blank group, UC model of mice was induced in each group. The next day after modeling, treatment groups were given relevant medicine liquid 0. 2 mL/10 g (75 mg/mL, calculated by crude drug mass concentration), while blank group and model group were given constant volume of normal saline intragastrically, once a day, for consecutive 7 d. After administration, disease activity indexes (DAI) of rats were scored, and the serum levels of TNF-α, IL-1β, IL-6, D-LA and myeloperoxidase (DAO) were determined. The length of the colon was measured and the intestinal mass index was calculated in mice. The activities of medullary peroxide (MPO) and SOD, the levels of NO and MDA were determined in colon tissue. RESULTS: Compared with blank group, DAI score, serum levels of TNF-α, IL-1β, IL-6, D-LA and DAO, the levels of MPO, NO and MDA in colon were increased significantly in model group, while the length of colon, intestinal mass index and SOD level of colon tissue were decreased significantly, with statistical significance (P<0. 05 or P<0. 01). Compared with model group, DAI score, serum levels of TNF-α, IL-1β and DAO, the level of MDA in colon were decreased significantly in S. baicalensis group (P<0. 05 or P<0. 01). The serum levels of TNF-α and IL-1β, the level of MDA in colon were decreased significantly in P. lactiflora group (P<0. 05 or P<0. 01). Above indexes of S. baicalensis-P. lactiflora (2:1) group were improved significantly except for the length of colon (P<0. 05 or P<0. 01). Above indexes of S. baicalensis-P. lactiflora (1:1) group were improved significantly except for serum level of IL-6 and the level of SOD in colon (P<0. 05 or P<0. 01). Above indexes of S. baicalensis-P. lactiflora (1:2) group were improved significantly except for serum level of NO (P<0. 05 or P<0. 01). CONCLUSIONS: The couplet medicines of S. baicalensis-P. lactiflora can reduce the expression of proinflammatory factors, enhancing antioxidant activity of the body and decrease intestinal mucosal permeability so as to improve UC symptom of mice; and the effect of S. baicalensis-P. lactiflora (2:1) group is the best.
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Thirty-two male Sprague-Dawley rats were divided into control group (n =16) and fructose group (n =16) fed with 10％ fructose solution.After 4 weeks,the rats of two groups were treated with saline and 50 nmol/kg ghrelin for 6 weeks,respectively (each group n =8).Fasting plasma glucose,insulin,and blood lipid profile were measured.Insulin receptor (Ins-R) mRNA expression in muscle was detected by RT-PCR.The phosphorylation of insulin receptor substrate-1 (IRS-1) was measured by Western blot.The results showed that insulin level and homeostasis model assessment for insulin resistance index (HOMA-IR) in fructose group were higher than those in control group [(13.1±3.6 vs 9.0 ± 1.5) μU/ml,P＜0.05 ;2.78 ± 0.14 vs 1.81± 0.13,P ＜0.01)].After ghrelin treatment,plasma insulin concentration [(9.6 ± 2.5) μU/mL,P＜0.05] and HOMA-IR (1.96 ± 0.12,P＜0.01)significantly decreased,along with increased Ins-R mRNA and IRS-1 phosphorylation in skeletal muscle (P ＜0.01).These results suggest that ghrelin can ameliorate insulin resistance in fructose-fed rats by restoring Ins-R function.
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The association between fasting plasma ghrelin levels and insulin resistance and blood pressure (BP) in octogenarians was investigated in this study. A total of 487 unrelated octogenarians (including 203 men and 284 women) were enrolled in this cross-sectional study at the Healthy Care Center of Shanghai East Hospital, Tongji University, China, from October 2008 to April 2009. Plasma ghrelin was determined by using the enzyme linked immunosorbent assay (ELISA). Insulin sensitivity was assessed using the homeostasis model of assessment-insulin resistance (HOMA-IR). The age of the participants ranged from 80 to 89 years (mean=83.9+/-4.8 years) with a body mass index (BMI) of 25.3+/-4.9 kg/m(2). Plasma ghrelin levels were 20.94+/-5.34 mug/L, being 20.89+/-5.53 mug/L in men and 21.38+/-3.73 mug/L in women respectively. Plasma ghrelin was not associated with systolic (P=0.981) or diastolic (P=0.724) BP, waist circumference (P=0.278), fasting insulin (P=0.246), fasting blood glucose (FBG) (P=0.693) and HOMA-IR (P=0.232). In the control cohort, no significant differences in plasma ghrelin were found between genders (P=0.489), and among subjects with hypertension (BP>140/90 mmHg) (P=0.284) and type 2 diabetes (P=0.776). In conclusion, fasting plasma ghrelin levels are not directly correlated with insulin resistance and BP among octogenarians.
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A total of 167 coronary heart disease (CHD) patients were divided into metabolic syndrome (MS) group (68 cases) and non-MS group (99 cases). There were significant differences in the disease-related metabolic indicators and coronary angiography (multivessel lesions, diffuse stenosis, occlusive lesions, Ginsini score) between MS group and non-MS group ( all P<0.05 ). When the patients with MS were divided into 3 groups according to the number of componernts of MS, three lesions, diffuse stenosis, and occlusive lesions were more frequent in five components group compared with three components group. Ginsini points rised with the increased risk factors. There existed differences in Ginsini score between three components group and four, five components group (P<0. 05 or P<0.01 ). Multivariable logistic regression analysis showed that obesity, hypertension,diabetes, high low-density lipoprotein-cholesterol, and low high-density lipoprotein-cholesterol were the predictors of CHD in patients with MS (P<0.05 or P<0.01 ).
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OBJECTIVE: To determine whether Schwann cells (SCs) and fibronectin (FN) support the growth of damaged axons and their conductive function. METHODS: Thirty adult Sprague-Dawley (SD) rats were randomized into 3 groups (n=10), and the following grafts: both SCs and FN, FN, and basal medium were implanted respectively into the lumbar of spinal cords hemisected at vertebra T(12). RESULTS: At 6 weeks postoperation, the latencies of spinal cord evoked potential (SCEP) P(1) wave in the three groups were 1.57 ms, 1.84 ms, and 2.03 ms, respectively. The differences between SCs/FN group and the other two groups were statistically significant. The number of regenerated axons in SCs/FN group was significantly greater than that in FN group. The number of survival neurons in L(4) and L(5) left dorsal root ganglia (DRG) in SCs/FN group was significantly greater than that in the rest two groups respectively. The latencies of P(1) wave were significantly correlated with axon counts in both SCs/FN and FN groups. CONCLUSIONS: SCs/FN grafted to the hemisected lumbar of spinal cords can produce robust axon regeneration and promote partial repair of their conduction. Surface recording of SCEP technique has been proved to be a reliable and less-traumatic method for assessment of recovery of afferent conduction in hemisected spinal cord.