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The inflammation and apoptosis were vital important in the progress and recovery in myocardial infarction. Apoptosis was regulated by inflammation though TNF-α,CHOP,IL-10 andα7nAChR signal pathways and influenced the se-verity of the inflammation via feedback regulation.Inflammation and apoptosis affected myocardial infarction size and cardiac function recovery together.Inhibition of inflammation,reducing apoptosis had been proved to be the important parts in preven-tion of ventricular remodeling and regulating cardiac dysfunction after myocardial infarction,which had broad prospects.
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Monocyte locomotion inhibitory factor(MLIF)was an anti‐inflammatory pentapeptide produced by Entamoeba histolytica .In vivo and in vitro study showed that MLIF displayed anti‐inflammatory and immune protection effects and MLIF had protective effects on rheumatoid arthritis ,nerve injury ,myocardial ischemia ,cerebral ischemia and Alzheimer′s disease . Studies had shown that MLIF regulated inflammatory response and immune protection through NF‐κB and MAPK signal path‐ways .The sources and biological activities of MLIF were reviewed in this paper .
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Objective Lox-1 ( lectin-like oxidized low-density lipoprotein receptor-1 ) was one of the main receptor of ox-LDL, which took an important role in vascular endothelial dysfunction , the formation of foam cells , and the stability of atherosclerotic plaques .To investigate the role of Lox-1 in cardiovascular diseases .Methods The literatures of Lox-1 in cardiovascular diseases retro-spectively were reviewed .Results As a new ox-LDL scavenger receptor , Lox-1 played an important role in cardiovascular diseases . Conclusion Lox-1 might provide new ideas for cardiovascular diseases .
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This study is to investigate the protein and mRNA expressions of pro-inflammatory and anti-inflammatory cytokines in U937 foam cells and effects of Ginkgo biloba extract (GbE) on the cytokines.U937 cells were cultured with different concentrations of GbE (0.1,1,and 10 μg·L-1),and stimulated by 100 mg·L-1 oxidized low density lipoprotein (ox-LDL) for 24 h.The expressions of interleukin-1β (IL-1β),tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) in culture solution were detected by enzyme-linked immunosorbant assay (ELISA) and reverse transcriptase polymerase chain reaction (RT-PCR).The results showed that incubated with 100 mg·L-1 ox-LDL for 24 h,the U937 cells became foam cells,the protein or mRNA expressions of IL-1β,TNF-α,IL-10,and its receptor IL-10R in U937 foam cells were higher markedly than those in normal U937 cells.When the cells were pretreated with GbE (0.1,1,and 10 μg·L-1),the increases of IL-1β and TNF-α in U937 foam cells were remarkably inhibited,but IL-10 expression increased greatly.Especially when cells were pretreated with 10 μg·L-1 GbE,the protein and mRNA expressions of IL-1β and TNF-α were markedly lower than those in U937 foam cells.The protein expression of IL-10 and mRNA expressions of IL-10 and its receptor IL-10R were markedly higher than those in U937 foam cells.GbE inhibited production of pro-inflammatory cytokines IL-1β and TNF-α,but up-regulated the production of anti-inflammatory cytokine IL-10 and its receptor IL-10R in U937 foam cells,which might be related with its anti-atherosclerotic actions.
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OBJECTIVE: To evaluate the effects of madecassoside (MC) on the depression behavior of mice and the activities of monoamine oxidase (MAO) in different rat brain regions. METHODS: Imipramine as the positive contrast medicine, effects of MC on the depression behavior of mice were observed by forced swimming test and reserpine antagonist test. Moclobemide and pargyline as the positive controlled medicines, the activities of monoamine oxidase-A (MAO-A) and monoamine oxidase-B (MAO-B) in different rat brain regions were determined after intragastric administration of MC in 3 different dosages for 3 days or 21 days. RESULTS: (1) The low, middle and high dosages of MC (i.g.) significantly reduced the immobility time of mice in forced swimming test (P0.05). (3) With acute administration (3 days), the low, middle and high dosagey of MC (i.g.) significantly inhibited the activity of MAO-A in hippocampus (P0.05). With chronic administration (21 days), MC in 3 dosages had no significant effects on the activities of MAO-A in cortex and hypothalamus (P>0.05), and the high dosage (40 mg/kg) significantly enhanced the activity of MAO-A in hippocampus (P0.05), and MC in dosage of 10 mg/kg significantly inhibited the activity of MAO-B in hypothalamus (P0.05). CONCLUSION: These results support the idea that MC produces antidepressant effects through MAO inhibition in rat brain, which seems stronger with acute administration than chronic administration, while its mechanism remains to be further studied.
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Objective: To establish an experimental model of atherosclerosis in rats and to study the atherosclerotic lesions in the aorta,heart and liver.Methods: The rats in experimental groups were injected with a single dose of vitamin D (600 000 IU/kg) and loaded with high fat diet;control group was given saline and basic food.The pathological changes were observed in the aorta,heart and liver after 2,4,6 weeks.The scores were evaluated according to the pathological degrees.Results: No changes were observed after 2 weeks,but after 4 weeks atheroslerotic plaques were seen in the aorta and the score of the lesions were 0.50?0.39; a little lipid were found in coronary arteries;deposition of lipid was seen in the myocardium; many positive red pellets were found in the plasma of cells in the liver.After 6 weeks,more atheroslerotic plaques were observed in the aorta,and atheroslerotic plaques in coronary arteries were formed (pathological score 1.12?0.48); abundant positive red pellets were found in the plasma of the cardiac myocyte.The pathological changes occurred in rats were very similar to that of man.Conclusion: The experimental model of atherosclerosis in rat may be conveniently established by injection of vitamin D with loading of high fat diet,which can be used for the pathological and pharmacological study of atherosclerosis.
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Antigen challenge of sensitized isolated guinea-pig mesentery perfused under constant pressure resulted in a significant flow reduction which was induced by the release of leukotrienes bioassayed on guinea-pig ileum. 3 min after challenge, the mescnteric perfusion rate dropped to a minimum of 32?12% ( P
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The effects of imperatorin (Imp) and iso-imperatorin(Isi) on tumor necrosis factor (TNF) release from mouse peritoneal macrophages were investigated. It was found that Imp and lsi significantly inhibited TNF release from mouse peritoneal macrophages. At the concentration of 10-6～10-4 mol?L-1, the inhibitory effects were presented by Imp and Isi in a dose dependent manner. At 10-4 mol/L TNF release was entirely inhibited by each drug.
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27 rabbits were divided into normal group(n = 4),control group (n = 5), silybin group (n = 6), hyperbaric oxygen (HBO) group (n = 6), and HBO combined with silybin group (n = 6). Circulation of hindlimb was interrupted completely for 6 h and reperfused for 1 h. Malondialdehyde (MDA) and superoxide dismutase(SOD) in plasma from ischemic-reperfused injured limb were measured. Adenosine triphosphate (ATP) and creatine phosphate (CP) in samples taken from anterior tibial muscle were determined. Ultrastructural changes of injured muscle were observed. The results showed that HBO combined with silybin treatment had a favourable effect on ischemic and reperfused injured limb muscle with reduction of the lipid peroxidated injury, increase of the SOD activity and the high energy phosphate compounds (ATP and CP), and a promoting recovery of injured muscle cells. HBO and silybin had a synergistic action. It suggests that HBO combined with silybin is an effective method for treatment of ischemic and reperfused injured limb.
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The release of platelet activating factor (PAF) induced 14C-arachidonic acid (14C-AA) in the bovine cerebral microvascular endothdial cells (CMEC) and arterior cerebral artery smooth muscle cells (ACASMC) and the antagonism of SZ-1 are described. The results showed that 14C-AA incorporated into the cells rapidly and PAF 0.1-20?mol/L dose-dependently stimulated the AA release significantly. It indicated that the action of PAF on the cerebrovascular system was associated with the stimulation of AA release. SZ-1 0.2-20?nol/L dose-dependently inhibited the PAF induced AA release in CMBC and ACASMC, and PAF induced aggregation of washed rabbit platelets, but did not inhibited ADP or AA induced aggregation of platelet-rich plasma(PRP), and PAF production in CMEC, indicating the specific antagonism of SZ-1 on PAF receptor.
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Specific receptors for leukotriene C4 LTC4 have been identified on intact smooth muscle cells derived from bovine cerebral microvasculatures. Specific pHJLTC4, binding at a fixed input at 25 ℃ was rapid , reaching the maximum at 20min With incremental inputs of radioligand and a constant cell number, specific [3H]LTC4 binding reached a plateau indicative of a saturable binding site. Analysis of Scatchard plots demonstrated a single high affinity binding site with a dissociation constant (Kd) of 2.01?0.4 nmol/L and Bmax = 156.6?13.1 fmol/106 cells. The specific [3H]LTC4 binding could be inhibited by unlabted LTC4, LTD4 and FPL-55712 with an inhibitory rate of 96.9%, 73.9% and 44.9% at 10-5 mol/L, respectively.
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The mechanism of hypotensive effect of siiybin was studied in anesthetized cats and rats. The results show that the hypotensive action caused by siiybin is not central in origin, and not related to the effect of autonomic nervous system and the release of histamine and prostagiandin, but is mainly due to vasodilation.