Observation of cardiomyocytes stimulated by TNF-α, IL-1β, LPS in vitro

AIM: To observe the changes of cardiomyocytes after stimulation by TNF-α, IL-1β, LPS.METHODS: Cardiac ventricular myocytes were cultured in vitro. Different doses of TNF-α, IL-1β, LPS were added to stimulate the cardiomyocytes, the hypertrophy of cardiomyocytes 8 h, 24 h, and 48 h after stimulation was determined and the apoptosis were also observed 24 h, 48 h, 72 h after stimulation. RESULTS: Compared to the normal myocytes, the cardiomyocytes were hypertrophied after stimulation by 10 μg/L, 15 μg/L of TNF-α, 20 μg/L, 100 μg/L of IL-1β and 10 mg/L, 15 mg/L, 20 mg/L of LPS, and the effect was dose-dependent, the strongest effect was showed in 24 h. Moreover, 20 μg/L of TNF-α, 100 μg/L of IL-1β and 30 mg/L of LPS caused cardiomyocyte apoptosis, especially in 72h. CONCLUSION: TNF-α, IL-1β, LPS induced the cardiomyocyte hypertrophy and apoptosis, suggesting the inflammation may be the main cause of cardiovascular disease.     

Atorvastatin inhibits IL-1β and IL-18 releases via lowering the expression of NLRP1 inflammasome

AIM: To explore the role of nucleotide-binding oligomerization domain-like receptor protein 1 (NLRP1) inflammasome in atorvastatin-induced reduction of interleukin-1β (IL-1β) and interleukin-18 (IL-18) releases from the THP-1 macrophages. METHODS: Lipopolysaccharide (LPS, 10 μg/L) was used to trigger the secretion of IL-1β and IL-18 in the THP-1 macrophages. The cells were incubated with different concentrations of atorvastatin (1, 10 and 20 μmol/L) for 24 h, or treated with 10 μmol/L atorvastatin for different time (12 h, 24 h and 48 h). NLRP1 siRNA was transfected into the THP-1 cells. The mRNA expression of NLRP1 inflammasome was detected by RT-PCR. The protein expression of NLRP1 inflammasome was determined by Western blot. The secretion of proinflammatory cytokines IL-1β and IL-18 was quantified by ELISA. RESULTS: Atorvastatin inhibited the mRNA and protein expression of NLRP1 inflammasome in the THP-1 macrophages in a dose- and time-dependent manner. Transfection of NLRP1 siRNA significantly decreased the protein expression of NLRP1 and promoted the suppressive effect of atorvastatin on IL-1β and IL-18 secretion in the THP-1 macrophages. CONCLUSION: Atorvastatin inhibits the production of IL-1β and IL-18 in the macrophages through decreasing NLRP1 inflammasome expression, possibly contributing to the anti-inflammatory effect of atorvastatin on atherosclerosis.     

Aortic expression of HSP22, TNF-α and eNOS in rats with hyperlipidemia and effects of atorvastatin

AIM:To establish a rat hyperlipidemia model for studying the aortic expression of heat shock protein 22 (HSP22), tumor necrosis factor alpha (TNF-α) and endothelial nitric oxide synthase (eNOS) and the effect of atorvastatin intervention. METHODS:Hyperlipidemia model was established in SD rats. Afterwards, the rats were divided into normal control group, high fat group and high fat+atorvastatin intervention group. The expression of HSP22 and TNF-α in the rat aortas was detected by immunohistochemical assay and the expression of eNOS was assessed by Western blotting. RESULTS:No detectable expression of HSP22 and TNF-α in the normal control group was observed. However, the expression of HSP22 and TNF-α was positive in the high fat group and the atorvastatin intervention group. The mean densities of HSP22 and TNF-α positive particles were significant lower in the atorvastatin intervention group as compared with high fat group (both P＜0.05). The expression of eNOS protein in the high fat group and atorvastatin intervention group was significantly lower than that in normal control group (P<0.01). However, no marked difference of eNOS protein expression between high fat group and atorvastatins intervention group was observed. CONCLUSION: The expression of HSP22 and TNF-α in the rat aortas is increased in the hyperlipidemia rat model. This effect can be restored by atorvastatin treatment. The expression of eNOS in the rat aortas is decreased in the hyperlipidemia rat model, but this tendency could not be attenuated by atorvastatin.     

Effects of resveratrol on TNF-α-induced injury and expression of MCP-1 in isolated rat pulmonary artery endothelial cells

AIM: To investigate the possible mechanism of resveratrol (Res) on tumor necrosis factor-α (TNF-α)-induced monocyte chemoattractant protein-1 (MCP-1) expression in primary rat pulmonary artery endothelial cells (RPAECs).METHODS: RPAECs were randomly divided into 4 groups:control group, solvent (1% DMSO) group, TNF-α group and Res group. Each group was divided into 1 h, 4 h and 8 h subgroups (n=6 per time point). The TNF-α+C1142 (a rodent chimeric mAb that neutralizes rat MCP-1) group was set up at the 8 h time point. At each time point, the protein and mRNA expression of MCP-1 was measured by Western blot and real-time PCR.RESULTS: Pretreatment of the RPAECs with C1142 significantly down-regulated the expression of MCP-1 (P<0.05). The protein and mRNA expression of MCP-1 was markedly increased in TNF-α group (P<0.05). Notably, incubation with Res down-re-gulated the protein and mRNA expression of MCP-1, which was significantly lower than that in TNF-α group (P<0.05).CONCLUSION: MCP-1 was involved in the process of TNF-α-induced injury of RPAECs. Res down-regulates the expression of MCP-1 in RPAECs, thus attenuating cell injury.     

Extract of Ginkgo Biloba decreased expression of lectin-like oxidized low density lipoprotein receptor-1 induced by TNF-α in bovine aortic endothelial cells

AIM: To investigate the effects of extract of Ginkgo biloba (EGB) on the expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) induced by tumor necrosis factor a(TNF-α) in bovine aortic endothelial cells(BAECs). METHODS: The BAECs were incubated with TNF-α, followed by EGB treatment. The effect of EGB on LOX-1 expression was investigated by RT-PCR and Western blotting. The content of endothelial nitric oxide synthase (eNOS) was determined by Western blotting. Potential involvement of signaling pathways of the effects was explored by using related inhibitors of the signal molecules. The concentration of NO^-₂/NO^-₃ was also tested. RESULTS: Increased LOX-1 expression was induced by TNF-α. EGB markedly prevented the increase of LOX-1 expression induced by TNF-α (P<0.05), and this effect was inhibited by inhibitor of NOS (P<0.05). EGB significantly prevented the decrease of eNOS expression induced by TNF-α (P<0.05). EGB also significantly prevented the decrease of NO^-₂/NO^-₃ production induced by TNF-α (P<0.05). CONCLUSION: EGB markedly prevents the increase of LOX-1 expression induced by TNF-α and the effect is mediated by eNOS.     

Effects of oxidized low density lipoprotein and vitamin E on the levels of IL-6,IL-8 and TNF-α in cultured human umbilical vein endothelial cells

AIM:To investigate effects of OX-LDL and VitE on the levels of IL-6,IL-8 and TNF-α in human umbilical vein endothelial cells(HUVEC).METHODS: Human umbilical vein endothelial cells were obtained by in vitro culture. HUVEC treated with or without Vit E was incubated with OX-LDL, and the levels of IL-6, IL-8 and TNF-α were determined by enzyme-linked immunosorbent assy technique. RESULTS:50 μg/L,100 μg/L, 200 μg/L OX-LDL induced the release of IL-6,IL-8 and TNF-α by HUVEC in a dose-dependent manner. Compared with the control group , the levels of IL-6 and IL-8 were significantly increased at 6-12 h of stimulation with OX-LDL . Maximal levels of IL-6 and IL-8 occurred after 24-36 h, reaching a plateau maintained for at least 48 h. TNF-α rose after 2-6 h in HUVEC, and reached a maximum after 12 h. In contrast to IL-6 and IL-8, TNF-α declined after 48 h. However, when VitE (50 mg/L,100 mg/L,200 mg/L)was added, it can significant inhibited the release of IL-6, IL-8 and TNF-α in a dose-dependent manner, and after 48 h these cytokines have no diference between OX-LDL+VitE groups and OX-LDL groups. CONCLUSION: OX-LDL can obviously stimulate the production of IL-6,IL-8 and TNF-α in vascular endothelial cells, which can significantly be inhibited by VitE in a short time.     

Effect of recombinant rat CC16 protein on LPS-induced expression of TNF-α, IL-6 and IL-8 in rat tracheal epithelial cells

AIM: To explore the effect of recombinamt rat CC16 protein (rCC16) on LPS-induced expression of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and IL-8 in the rat tracheal epithelial (RTE) cells.METHODS: The RTE cells were incubated with rCC16 at concentrations of 0.5, 1.0 and 2.0 mg/L in serum-free media for 2 h prior to LPS (0.1 mg/L) treatment for further 24 h. The cells were harvested for assessing the mRNA levels of TNF-α, IL-6 and IL-8 by RT-qPCR. The cell culture supernatants were collected for analyzing the protein levels of TNF-α, IL-6 and IL-8 by ELISA. In addition, the nuclear translocation of nuclear factor-κB (NF-κB) p65 was tested by Western blot.RESULTS: rCC16 inhibited LPS-induced IL-6 and IL-8 expression at both mRNA and protein levels in the RTE cells in a concentration-dependent (0~2 mg/L) manner, as demonstrated by RT-qPCR and ELISA. However, no concentration-dependent manner between the dose of rCC16 and TNF-α expression was observed, and rCC16 inhibited LPS-induced TNF-α expression at lower concentration (0.5 mg/L). rCC16 concentration-dependently inhibited the effects of LPS on the level of nuclear translocation of NF-κB p65.CONCLUSION: rCC16 suppresses LPS-mediated TNF-α, IL-6 and IL-8 production through inactivation of NF-κB activity in RTE cells.[KEY WORDS] CC16 protein; Airway inflammation; LPS; Inflammatory mediators; Nuclear factor-κB     

Effect of NOD8 on production of nitric oxide,IL-1β and TNF-α in LPS-treated macrophages

AIM: To investigate the effect of NOD8 on lipopolysaccharide (LPS)-induced releases of nitric oxide (NO), tumor necrosis factor α (TNF-α) and interleukin-1β (IL-1β) in RAW264.7 cells. METHODS: The plasmids of pEGFP-C2 and pEGFP-NOD8 were transfected into RAW264.7 cells respectively. The transfected and non-transfected cells were stimulated by LPS for 0, 6, 12 and 24 h. NO production was evaluated by Griess reagent assay, and the levels of IL-1β and TNF-α were measured by ELISA. The protein expression of NOD8 and the nuclear translocation of nuclear factor κB (NF-κB) p65 subunit were detected by Western blotting. The level of activated caspase-1 was determined by fluorimetric method. RESULTS: Compared with pEGFP-C2 group, the protein expression of NOD8 was significantly elevated in pEGFP-NOD8+LPS group. The releases of NO, IL-1β and TNF-α were obviously increased after RAW264.7 cells were treated with LPS for 6 h, 12 h and 24 h, and while the secretion of NO was significantly reduced in the cells transfected with pEGFP-NOD8 and induced by LPS for 12 h and 24 h, and the release of IL-1β was also significantly reduced at 6 h, 12 h and 24 h. However, no significant difference of TNF-α release was observed between pEGFP-C2+LPS group and pEGFP-NOD8+LPS group. The activation of caspase-1 in RAW264.7 cells stimulated with LPS for 6 h, 12 h and 24 h was markedly increased, and the expression of NF-κB p65 subunit in the cytoplasm was significantly decreased, indicating that p65 nuclear translocation was increased. In addition, the activation of caspase-1 and the nuclear translocation of p65 were significantly inhibited in pEGFP-NOD8+LPS group. CONCLUSION: NOD8 suppresses the releases of LPS-induced NO and IL-1β in RAW264.7 cells by inhibiting the activation of caspase-1 and NF-κB.     

Effects of atorvastatin on cardiac myocyte hypertrophy of neonatal rat induced by angiotensinⅡ in vitro and TLR4 expression

AIM: To assess effects of atorvastatin (Ator) on cardiac myocytes (CM) hypertrophy of neonatal rat induced by angiotensinⅡ (AngⅡ) in vitro and Toll like receptor 4 (TLR4) expression for theoretical bases of preventing and treating myocardial hypertrophy.METHODS: CM of neonatal Sprague-Dawley (SD) rats were isolated with trypsin digestion method and those growth-arrested cells were stimulated with 10^-7 mol/L AngⅡ in the presence of various concentrations of Ator.The method of coomassie brilliant blue was adopted to evaluate the protein contents of CM.The changes in β-MHC,AT₁ receptor and TLR4 mRNA expression were observed by RT-PCR.RESULTS: ① AngⅡ increased the protein content of CM and β-MHC mRNA expression significantly,upregulated AT₁ receptor and TLR4 gene expression.② In a dose-dependent manner,Ator inhibited the increases in the protein contents of CM and β-MHC mRNA expression induced by AngⅡ.③ In a dose-dependent manner,Ator downregulated the AT₁ receptor and TLR4 mRNA expression of CM hypertrophy of neonatal rat induced by AngⅡ.CONCLUSION: Ator inhibits CM hypertrophy,downregulates the AT₁ receptor and TLR4 gene expression.     

Pretreatment with external trigeminal nerve electrostimulation inhibits seizures and decreases expression of IL-1β and TNF-α in hippocampus with status epilepticus induced by pentylenetetrazol in rats

AIM:To observe the effect of pretreatment with external trigeminal nerve electrostimulation (eTNS) on behavioral changes and the expression of interleukin-1β (IL-1β) and 　tumor necrosis factor α (TNF-α) in hippocampus of pentylenetetrazol (PTZ)-treated rats. METHODS:The rats were randomly divided into control group, PTZ group and eTNS group, and kindled by PTZ after administered 7 d, 14 d and 28 d of consecutive fake electrostimulation or eTNS. Subsequently, the severity and duration of seizure were quantitatively evaluated. The concentrations of IL-1β and TNF-α in hippocampus were detected by the methods of ELISA and immunohistochemisty. RESULTS:Compared with PTZ group, treatment with eTNS significantly inhibited the severity and duration of seizure (P<0.05), and significantly reduced the content of IL-1β and TNF-α in the hippocampus after status epilepticus (P<0.05 or P<0.01). CONCLUSION:Pretreatment with eTNS may provide a new approach for prevention and treatment of epileptogenesis.     

Serum levels of TNF-α, IL-6, IL-10, CRP and D-dimer in patients with multiple organ dysfunction syndrome

AIM: To determine the changes of the serum levels of tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), IL-10, C reactive protein (CRP) and D-dimer in the patients with multiple organ dysfunction syndrome (MODS) and compare the relationship between the levels of cytokines in early stage and MODS. METHODS: The serum values of TNF-α, IL-6, IL-10, CRP and D-dimer were measured in 27 patients with MODS in 1 d, 3 d and 5 d after undergoing disease, and compared with the adult peripheral blood of 15 normal controls. The levels in the first undergoing day between the lived group (n=19) and died group (n=8) were compared. RESULTS: The serum levels of TNF-α, IL-6, IL-10, CRP and D-dimer in MODS group were higher than that in control (P<0.05). With the development of the MODS, the levels of TNF-α, IL-6, IL-10, CRP and D-dimer were higher gradually. The level of IL-10 was increased at the third day. The levels of TNF-α, IL-6, IL-10, CRP and D-dimer in the first day of MODS in died group were higher than those in lived group, especially IL-6 and D-dimer (P<0.01). CONCLUSION: Determining the serum levels of TNF-α, IL-6, IL-10, CRP and D-dimer in MODS patients is helpful to guide the diagnosis and outcome.     

Effect of HMGB1 expression knockdown on invasion ability of breast cancer cells induced by TNF-α

AIM:To investigate the effect of high-mobility group box-1 (HMGB1) expression knockdown on the invasion ability of breast cancer cells induced by tumor necrosis factor-α (TNF-α). METHODS:HMGB1 siRNA was used to transfect into the breast cancer MDA-MB-231 cells. The expression of HMGB1 at mRNA and protein levels was determined by RT-qPCR and Western blot. After the MDA-MB-231 cells with HMGB1 expression knockdown were treated with TNF-α, the apoptosis rate was analyzed by flow cytometry, the cell invasion ability was measured by Transwell assay, and the cell migration ability was detected by cell scratch test. The protein expression of E-cadherin, MMP-2, N-cadherin, MMP-9 and Bax was determined by Western blot. RESULTS:The expression of HMGB1 at mRNA and protein levels in the MDA-MB-231 cells transfected with HMGB1 siRNA was significantly lower than that in the non-transfected cells (P<0.05). The apoptosis rate in the cells was increased after TNF-α treatment, and the cell invasion and migration abilities were also increased. The protein level of E-cadherin in the cells was decreased, the protein level of N-cadherin was increased, and the protein levels of MMP-2, MMP-9 and Bax were also increased (P<0.05). After the MDA-MB-231 cells with HMGB1 expression knockdown were induced by TNF-α, the apoptotic rate was increased, the invasion and migration abilities were decreased, the protein levels of E-cadherin and Bax were increased, and the protein levels of N-cadherin, MMP-2 and MMP-9 were decreased, as compared with the cells only induced by TNF-α without knockdown of HMGB1 expression (P<0.05). CONCLUSION:Knockdown of HMGB1 expression enhances the apoptosis of breast cancer cells induced by TNF-α, and inhibited the cell invasion, migration and epithelial-mesenchymal transition induced by TNF-α. The mechanism may be related with the changes of protein expression of MMP-2, MMP-9 and Bax.     

Expression of IL-1α and TNF-α modified by Toll-like receptor 4 genetic polymorphism is associated with colorectal carcinoma

AIM: To investigate the association of D299G, T399I and A896G polymorphisms of Toll-like receptor 4 (TLR4) and colorectal carcinoma (CRC). METHODS:
The genotypes of these 3 loci among 268 patients with CRC and 268 healthy controls were determined by polymerase chain reaction-restriction fragment lengthy polymorphism (PCR-RFLP). The protein levels of IL-1α, IL-8, TGF-β and TNF-α in the homogenate of CRC biopsies were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: No significant difference of the genotype frequencies of TLR4 A896G and D299G between the cases and the controls was observed. CT combined TT genotype of T399I was significantly associated with increased CRC risk. The individuals with the T allele of T399I showed a 1.843-fold increase in CRC risk as compared with the C allele. The concentrations of IL-1α and TNF-α in CRC biopsies were significantly elevated in the individuals with the genotype of T399I CT combined with TT as compared with the genotype of CC. CONCLUSION: TLR4 T399I promotes the development of CRC by modifying the expression of IL-1α and TNF-α in CRC tissues.     

Intracellular calcium alterations induced by endotoxin and IL-1β in rabbit hypothalamic neurons

AIM: To investigate intracellular free calcium ( [Ca²⁺]i ) alterations in hypothalamus of febrile rabbits induced by endotoxin (ET), and compare with the effect of ET and IL-1β on i in hypothalamic neurocytes from normothermia rabbits. METHOD: The concentration of [Ca²⁺]i was determined by using spectrofluorometer and fluorescent Ca²⁺ probe fura-2 /Am. RESULTS: 1. A minute dose of ET (2 ng/mL) induced a significant rise in [Ca²⁺]i in hypothalamic neurocytes from normothermia rabbits. The rise in [Ca²⁺]i in hypothalamic neurocytes from febrile rabbits induced by intravenous injection of ET was also observed. 2. In hypothalamic neurocytes from normotheria rabbits, IL-1β failed to affect [Ca²⁺]i at concentrations of 100, 500, 1 000ng/mL, respectively. CONCLUSION:The action site of low concentration of calcium that plays a regulatory role during fever seems unlikely to be in cytosolic compartment of hypothalamic neurons. The change of [Ca²⁺]i in hypothalamic neurocytes by ET can not be considered the direct effect of IL-1β.     

Expression of IL-1β and IL-17 on mast cells in human periapical diseases

AIM：To identify and quantify the expression of IL-1β and IL-17 in mast cells (MCs) in different types of human pericapical diseases using double immunofluorescence staining. METHODS：The specimens (n=102), including healthy control (n=35), periapical cyst (n=35) and periapical granuloma (n=32), were involved in the present study. The tissue samples were fixed in 10 % buffered formalin for at least 48 h and then embedded in paraffin. Serial 5-μm-thick sections were deposited onto SuperFrost/Plus microscope glasses. Routine staining of the sections using hematoxylin & eosin (HE) was performed for morphological evaluation. The number of IL-1β and IL-17 positive MCs was identified by double immunofluorescence staining. RESULTS：Compared with the healthy controls, the inflammation score of periapical lesions was significantly increased in the periapical patients (P<0.01). The density of IL-1β and IL-17 positive MCs in the periapical lesions were obviously higher than that in the healthy controls (P<0.01). However, no significant difference between periapical cyst and periapical granuloma was observed. The Pearson correlation analysis showed that there was a positive correlation between the density of IL-1β and IL-17 double positive MCs and inflammation score in different groups of specimens (P<0.01). CONCLUSION：There is significantly increased number of MCs, along with increased density of IL-1β and IL-17 positive MCs in human periapical lesions. The increased density of IL-1β and IL-17 positive MCs has the similar tendency as the severity of tissue inflammation in human periapical lesions, suggesting that IL-1β and IL-17 positive MCs may play an important role in the pathogenesis of human periapical diseases.     

Effects of β-ME and RA on expression of GFAP in mesenchymal cells derived from mouse fetal liver

AIM: To investigate the effects of β-mercaptoethanol (β-ME) and all-trans rentinal acid (RA) on glial fibrillary acidic protein (GFAP) expression in mesenchymal cells derived from mouse fetal liver in vitro. METHODS: Cells suspension from 14.5-days-old mouse fetal liver were cultured in DMEM/HEPES/F12 supplemented with 20％ FCS and mesenchymal cells were acquired after discarding nonadherent cells. The 5th passage cells were induced by β-ME and RA. The characteristics of treated cells were assayed by immunocytochemistry staining at 5 hours and 5 days after induction. β-actin as an internal control, GFAP gene expression of mesenchyal cells was detected with semi-quantitative RT-PCR. RESULTS: After being inducted by β-ME and RA, 80％ approximately of the cells exhibited typical neural morphology and about 85％ expressed GFAP phenotype. Semi-quantitative RT-PCR showed that mRNA expression of GFAP increased in treated cells versus untreated cells (P<0.01). CONCLUSION: GFAP expression in mesenchymal cells derived from mouse fetal liver in vitro increases after being treated with β-ME and RA.     

Effects of statin reloading before percutaneous coronary intervention on circulatory endothelial progenitor cells and inflammatory cytokines

AIM:To investigate the effects of atorvastatin reloading in pre-percutaneous coronary intervention (PCI) period on endothelial progenitor cell (EPC) count and inflammatory cytokine expression in the stable angina pectoris patients who had previously received long-term statin treatment. METHODS:The patients with stable angina pectoris that had received long-term statin therapy and planned to accept PCI were randomized into 3 groups: 80 mg atorvastatin 12 h and 40 mg 2 h before coronary angioplasty (80 mg reloading), pre-operatively with 40 mg/d atorvastatin for 7 d (40 mg reloading), and without atorvastatin reloading (no reloading). CD45-/CD133+/CD34+, CD45-/CD34+/KDR+ and CD45-/CD144+/KDR+ EPCs in 100 μL peripheral blood were determined by flow cytometry 1 h prior to PCI and 1 h, 6 h and 24 h after PCI. The serum concentrations of soluble intercellular adhesion molecule 1 (sICAM-1), C-reactive protein (CRP) and troponin I (TnI) were analyzed immediately prior to and 24 h after PCI. RESULTS: (1) In 80 mg reloading group, the numbers of circulating CD45-/CD133+/CD34+ and CD45-/CD34+/ KDR+ early differentiation stage EPCs 1 h and 6 h after coronary angioplasty was significantly elevated compared with those before PCI (P<0.05). (2) In control group, the serum concentrations of sICAM-1 and CRP 24 h after PCI were significantly elevated (P<0.05) compared with preoperative values. (3) The rise in serum TnI concentration from pre- to post-operation in 80 mg reloading group was lower than that in control group. CONCLUSION: The method of atorvastatin reload before PCI affects the number of EPCs in peri-operative period. High dose of atorvastatin application before PCI triggers early EPC circulation. The serum levels of post-operative inflammatory cytokine sICAM-1 as well as CRP are reduced by atorvastatin reloading before PCI.     

Effects of atorvastatin on release of endothelial microparticles and myocardial apoptosis in rats with acute myocardial infarction

AIM: To investigate the effect of atorvastatin(AT) on the release of endothelial microparticles(EMP) and myocardial apoptosis in the rats with myocardial infarction. METHODS: SD male rats(n=24) were randomly divided into 3 groups:sham operation(sham) group, myocardial infarction(MI) group and MI+AT group. The rat model of acute myocardial infarction was prepared by coronary artery ligation. At 2 h and 24 h after modeling, the peripheral blood was collected to detect creatine kinase-MB(CK-MB) and cardiac troponin T(cTnT). The circulating levels of EMP were measured by flow cytometry. The myocardial apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL) assay. RESULTS: At 2 h after modeling, the level of CK-MB was significantly increased in MI group compared with sham group, and the level of EMP and the myocardial apoptotic rate were significantly increased in MI group and MI+AT group compared with sham group. At 24 h after modeling, the level of EMP was significantly increased in MI group compared with sham group. The levels of CK-MB, cTnT, EMP and the myocardial apoptotic rate were significantly decreased in MI+AT group compared with MI group. Moreover, the level of CK-MB in MI group was significantly increased at 24 h compared with that at 2 h after modeling. The levels of CK-MB, cTnT and EMP were significantly decreased in MI+AT group at 24 h compared with those at 2 h after modeling. CONCLUSION: Ator-vastatin may reduce the level of EMP and the myocardial apoptotic rate in the rats with acute myocardial infarction, indicating that atorvastatin plays a role in protecting endothelium.