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Objective To explore the effects of prostaglandin E1 (PGE1) on the expression of Apaf-1 and TLR4 in rats with cerebral ischemia-reperfusion(CIR) injury.Methods 32 healthy adult male Wistar rats were randomly divided into four groups,which were sham operated group (n=8),CIR model group (n=8) and PGE1 pretreated groups (low dose,12 μg · kg-1;high dose,24 μg · kg-1,n =8).Rat model of cerebral ischemia/reperfusion was established by bilateral common carotid artery ligation.The expression of Apaf-1 and TLR4 was detected with immunohistochemical staining method in hippocampus and epencephalon.Results After 20 min of ischemia and reperfusion for 24 h,compared with sham operated group (Apaf-1:hippocampus (0.87±0.78),epencephalon (0.67 ±0.43);TLR4:hippocampus (2.43 ± 1.17),epencephalon (1.97± 1.033)),the number of positive cells of Apaf-1 (hippocampus (11.83± 2.26);epencephalon(5.80±1.30) and TLR4 (hippocampus(16.90±2.86);epencephalon(12.90±2.66)) was increased in CIR model group (P＜0.05).Compared with CIR model group,the positive cell numbers of Apaf-1 (hippocampus:low dose(9.83±2.12),high dose(5.50± 1.17);epencephalon:low dose(4.87± 1.38),high dose(2.73±1.172)) and TLR4 (hippocampus:low dose (11.53± 2.40),high dose (9.13 ± 2.54);epencephalon:low dose (9.07 ± 2.07),high dose (4.47 ± 1.68)) were reduced dose-dependently in PGE 1 pretreatment all group (all P ＜0.05).Conclusion PGE1 can inhibit the expression of Apaf-1 and TLR4 in hippocampus and epencephalon of rat with cerebral ischemia-reperfusion injury.
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Functional Science Lab.Of Jining Medical College has attempted to reform the management system,share the resource,improve the resource utilization,exceed the limits of science,modify the contents of experimental courses,innovate the teaching methods,pay attention to teacher training.Through longtime research and practice,we have gained the significant achievements.
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Aim To study the effects of smoking and glonoine on intracellular free Ca2+ concentration([Ca2+]i) in vascular smooth muscle cell in rabbits with atherosclerosis,and to explore the effects of smoking on atherosclerosis and biologic action of glonoine.Methods An atherosclerosis in rabbits was produced.The vascular smooth muscle cells were isolated.The cells were loaded by Fluo-3/AM.[Ca2+]i in vascular smooth muscle cell was measured by flow cytometer(FCM).The spatial distribution and the dynamic changes of [Ca2+]i in single vascular smooth muscle cells were determined by laser scanning confocal microscopy(LSCM).Results Atherosclerosis plaques in arteriae aorta were observed and the degrees were different in various groups.[Ca2+]i in vascular smooth muscle cells in rabbits with atherosclerosis markedly increased[(48.45?5.31) vs that in saline control(38.09?2.57),P
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<p><b>OBJECTIVE</b>To investigate the antagonistic effect and mechanism of the effect of cyproheptadine (Cyp) on endotoxic shock in rats.</p><p><b>METHODS</b>Endotoxic shock was produced in rats by i.v. injection of lipopolysaccharides (LPS) (5 mg/kg). Tumor necrosis factor (TNF(alpha)) mRNA expression was assessed by Northern blot. Plasma TNF(alpha) content was measured by radioimmunoassay. Plasma superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were measured. The intracellular free calcium concentration ([Ca(2+)](i)) in single endothelial cells was determined by laser scanning confocal microscopy (LSCM).</p><p><b>RESULTS</b>Cyp 5 mg/kg injected immediately after i.v. LPS raised the mean arterial blood pressure (MABP) of shocked rats and improved their 24 h survival rate. Meanwhile, Cyp markedly decreased TNF(alpha) mRNA levels in rat liver (18 +/- 10 vs. LPS + saline 38 +/- 10, P < 0.01) as well as plasma TNF(alpha) content [(7.8 +/- 2.4) microg/L vs. LPS + saline (21.5 +/- 3.2) microg/L, P < 0.01)]. It enhanced plasma SOD activity [(1037.2 +/- 112.8) NU/L vs LPS + saline (615.4 +/- 92.6) NU/L, P < 0.01], reduced the MDA content [(5.2 +/- 1.1) micromol/L vs. LPS + saline (9.8 +/- 1.5) micromol/L, P < 0.01], and inhibited TNF(alpha)-induced [Ca(2+)](i) elevation.</p><p><b>CONCLUSION</b>Cyp exerts an anti-endotoxic shock effect by inhibiting TNF(alpha) gene expression, enhancing SOD activity, reducing lipid peroxidation, and preventing [Ca(2+)](i) overload.</p>
Subject(s)
Animals , Rats , Cyproheptadine , Pharmacology , Histamine H1 Antagonists , Pharmacology , Malondialdehyde , Blood , Rats, Wistar , Shock, Septic , Drug Therapy , Metabolism , Superoxide Dismutase , Blood , Tumor Necrosis Factor-alpha , GeneticsABSTRACT
AimTo establish a model of the injury of the vascular endothelial cell(VEC) in rats and observe the function of Chinese herbs of Li Qi Huo Xue(LQHX) will prevent and treat the VEC injury. Methods30 SD rats weredivided into the control, the model and LQHX groups. The model of the VEC injury was established. It tried to demonstrate the effect of LQHX for the coagula tion and fibrinolysis function of the VEC by the C EC count,t-PA, PAI activity, 6-keto-PGF1αcontent and PAgTmax. Results In LQHX group as compared with those of the medol group, The CEC count was redued obviously(P＜0.01). t-PA activity was increased(P＜0.01), so did the percentage of active t-PA(P＜0.01), but PAI activity decreased (P＜0.05), 6-keto-PGF1α content increased (P＜0.01)α the PAgTmax decreasd (P ＜0.01) Conclution LQHX can enhance the anticoagulation and fibrinolysis activities. It is a more effective measure for the VEC protection.
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AIM: To study the effects of cyproheptadine (Cyp) and anisodamine (Ani)on the changes of intracellular free Ca 2+ concentration ([Ca 2+ ] i) induced by tumor necrosis factor (TNF ?) in single endothelial cells, and to explore the mechanisms of TNF ?-mediated shock and antishock actions of Cyp and Ani. METHODS: Human umbilical vein endothelial cell strains(ECV304) were seed in 35 mm tissue culture dish with 2 mL DMEM culture medium. The cultured cells were loaded by Fluo-3/AM. The spatial distribution and the dynamic changes of [Ca 2+ ] i in single endothelial cell was determined by laser scanning confocal microscopy(LSCM). RESULTS: [Ca 2+ ] i in single endothelial cell after stimulation of TNF ? rapidly increased in a dose-dependent manner and approached the peak value within 60 seconds, afterwards, decreased and kept above the basal level. The confocal scanning image showed that [Ca 2+ ] i elevation was more obvious in nuclear than in cytoplasma, and decreased slowly. Cyp (3?10 -5 , 6?10 -5 mol/L) and Ani (2?10 -5 , 4?10 -5 mol?L -1 ) markedly inhibited TNF ? (1.2?10 -9 mol?L -1 )-induced [Ca 2+ ] i elevation. CONCLUSIONS: TNF ? markedly induces elevation of [Ca 2+ ] i in single endothelial cell, it may be an important mechanism of TNF ?-induced shock and tissue injury. Cyp and Ani obviously suppress TNF ?-induced [Ca 2+ ] i elevation, which probably is one of the mechanisms of their antishock effects.