Hydrogen sulfide inhibits inflammatory responses induced by acute myocardial ischemia in isolated rat hearts

AIM：To investigate whether hydrogen sulfide (H2S) protects the hearts against inflammatory responses induced by acute myocardial ischemia in isolated rat hearts. METHODS：Rat acute myocardial ischemia injury was induced by ligation of the left anterior descending coronary artery for 4 h, and the normal perfusate was replaced with NaHS (5 μmol/L, 10 μmol/L and 20 μmol/L) perfusate accordingly in NaHS groups 2 h after ischemia. The changes of cardiac function in the myocardial ischemic injury rats were observed. The mRNA expression of TNF-α, IL-1β, IL-6, IL-10 and ICAM-1 was detected by real-time PCR. The protein level of nuclear factor-κB (NF-κB) in the myocardial tissues was detected by Western blotting. RESULTS：The cardiac function in ischemia group was lower than that in sham group (P<0.01). Compared with ischemia group, perfusion of NaHS resulted in the improvement of the cardiac function (P<0.05 or P<0.01). Compared with sham group, the mRNA expression of TNF-α, IL-1β, IL-6 and ICAM-1 in the cardiac tissues was significantly increased, and the mRNA expression of IL-10 in the cardiac tissues was significantly decreased in ischemia group (P<0.01). Compared with ischemia group, the perfusion of NaHS significantly decreased the mRNA expression of TNF-α, IL-1β, IL-6 and ICAM-1 (P<0.05 or P<0.01). The perfusion of NaHS at concentrations of 10 μmol/L and 20 μmol/L significantly increased the mRNA expression of IL-10 (P<0.01). The protein level of NF-κB in ischemia group was markedly higher than that in sham group (P<0.01). Compared with ischemia group, the perfusion of NaHS at concentrations of 10 μmol/L and 20 μmol/L significantly decreased the expression of NF-κB (P<0.05 or P<0.01). CONCLUSION：H2S protects the hearts against acute ischemia injury through inhibition of NF-κB activation and subsequent down-regulation of NF-κB-dependent inflammatory gene expression.     

Propofol inhibits LPS-induced inflammatory response in microglia via TRPV1 ion channels

AIM:To investigate the effects of propofol (P) on the inflammatory response of microglia induced by lipopolysaccharide (LPS) and the mechanisms. METHODS:Mouse microglia BV2 cells were treated with LPS at 100 μg/L to establish a neuroinflammatory injury model. The BV2 cells were divided into 4 groups:control group (C group), model group (L group), L+P group and LPS+AMG517 group (L+A group). The level of tumor necrosis factor-α (TNF-α) in the cell culture supernatant was measured by ELISA. The mRNA expression of transient receptor potential cation channel subfamily V member 1 (TRPV1) was detected by real-time PCR. The protein levels of TRPV1, TNF-α, interleukin-1β (IL-1β), interleukin-6 (IL-6) and phosphorylated calcium/calmodulin-dependent protein kinase Ⅱ (p-CaMKⅡ) were determined by Western blot. The content of free Ca²⁺ in the microglia BV2 cells was detected by Fluo-3 AM assay. RESULTS:Compared with C group, the level of TNF-α was significantly increased in L group (P<0.01), but that in P group was not changed. Compared with L group, the level of TNF-α was significantly lower than that in L+P group within 4 h (P<0.01). Compared with C group, the mRNA expression of TRPV1 was significantly increased in L group (P<0.01). Compared with L group, the mRNA expression of TRPV1 was significantly down-regulated in L+P group (P<0.01).Compared with L group, the protein levels of TNF-α, IL-1β, IL-6 and p-CaMKⅡ and intracellular Ca²⁺ concentration were significantly lower than those in L+P group and L+A group (P<0.01). CONCLUSION:Propofol inhibits the inflammatory response of microglia by reducing the expression of TNF-α, IL-1 and IL-6, which may be related to the down-regulation of TRPV1 and p-CaMKⅡ and the reduction of intracellular Ca²⁺ concentration.     

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 patchouli oil on lipopolysaccharide-induced fever in rabbits

AIM:To investigate the antipyretic effect of patchouli oil on lipopolysaccharide (LPS)-induced fever in rabbits. METHODS:Male rabbits (n=42) were randomly divided into 7 groups according to their body weight and basal body temperature, including control group, model group, western medical positive group, traditional Chinese medical positive group, and high, middle and low doses (2%, 1% and 0.5%) of patchouli oil groups. Subsequently, except the controls, the rabbits were injected with LPS at a dose of 1 mL/kg (2 mg/L) through marginal ear vein to establish rabbit fever model and the rabbits in control group received the same volume of NS. The rabbits in control group and model group were injected with 0.5% Tween-80 0.5 h late, and the rabbits in the other groups were treated with correspoonding drugs. The effect of patchouli oil on the body temperature was observed, and the levels of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in the serum, and prostaglandin E2 (PGE2) and cyclic adenosine monophosphate (cAMP) in the hypothalamus were measured by radioimmunoassay. RESULTS:The body temperature and the levels of IL-1β, TNF-α, cAMP and PGE2 in model group were significant higher than those in control group. Patchouli oil notably inhibited the body temperature in the febrile rabbits. From 1.5 h to 5.5 h after administration, the body temperatures were increased by (1.06±1.55), (1.62±1.36), (1.38±1.22), (0.98±0.98) and (0.48±0.95) ℃ in high patchouli oil group, respectively. From 3.5 to 5.5 h after administration, the body temperatures were elevated by (1.47±0.73), (1.15±0.68) and (0.63±0.54) ℃ in middle patchouli oil group, respectively. A tendency of downregulation of the elevated body temperatures was observed at every time point after administration in low patchouli oil group. Patchouli oil significantly decreased the levels of TNF-α in the serum and cAMP content in the hypothalamus, and attenuated the elevated tendency of the IL-1β level in the serum and PGE2 level in the hypothalamus.CONCLUSION: Patchouli oil evidently has antipyretic effect on LPS-induced fever in the rabbits. The antipyretic mechanism might be related to the inhibition of TNF-α level in serum and cAMP content in the hypothalamus.     

α7nAChR is involved in anti-inflammation of physiological concentrations of glucocorticoids

AIM: To explore the role of α7 nicotinic acetylcholine receptor (α7nAChR) in anti-inflammation of glucocorticoids (GCs) at physiological concentrations. METHODS: MTT assay was used to measure the viability of BV-2 cells, which were processed by hydrocortisone at different concentrations. On the basis of inflammatory model induced by LPS in BV-2 cells, experimental groups were divided as follows: (1) control; (2) LPS; (3) GCs＋LPS; (4) methyllycaconitine (MLA)＋GCs＋LPS. The levels of TNF-α and IL-1β in the cell supernatants were detected by ELISA. RESULTS: Hydrocortisone at concentrations of 2 000 and 1 000 nmol/L decreased the cell viability to (76.9±5.5)% and (90.8±7.3)%, respectively, indicating the cellular injury by GCs at over-physiological doses. LPS significantly induced the releases of TNF-α and IL-1β in a time- and dose-dependent manner in BV-2 cells. Hydrocortisone at physiological concentrations (500 and 250 nmol/L) reduced the releases of TNF-α and IL-1β in BV-2 cells stimulated by LPS, and MLA at concentration of 10 nmol/L antagonized the anti-inflammatory effect of GCs. CONCLUSION: α7nAChR is involved in the anti-inflammatory effect of the physiological concentrations of GCs.     

Effects of Radix Angelicae Sinensis on changes of IL-6, TNF-α and bFGF in renal ischemia/reperfusion injury in rabbits

AIM: To determine the effect of Radix Angelicae Sinensis(RAS) on renal ischemia/reperfusion injury in rabbits and to explore its mechanism. METHODS: Twenty-five rabbits were divided randomly into the sham operated group(Control group), renal ischemia/reperfusion injury group(IR group) and RAS+IR group. At the time point of reperfusion 48 h after renal ischemia 1 h, the renal tissue were observed by electron-microscope and the contents of creatinine(Cr) in serum, tumor necrosis factor-α(TNF-α), interleukin-6(IL-6)and basic fibroblast growth factor(bFGF) in the renal tissue were measured. RESULTS: A remarkably degenerative changes in renal tissue were showed under electronmicroscope in IR group, but the changes in RAS+IR group were slight. The contents of Cr, TNF-α and IL-6 in IR group were higher than those in Control group, these parameters in RAS+IR group were lower than those in IR group, the difference between these groups was significant(P< 0.05 or P< 0.01). At the same time, the content of bFGF in IR group was lower than that in Control group(P< 0.01), while the content of bFGF in RAS+IR group was higher than that in IR group(P< 0.01) and Control group(P< 0.05). CONCLUSION: RAS has an effect of alleviating the renal ischemia/reperfusion injury by modulating the production or release of TNF-α, IL-6 and bFGF.     

Palmitate triggers inflammatory response by upregulating fatty acid translocase in THP-1 macrophages

AIM: To investigate the role of fatty acid translocase (FAT/CD36) on palmitate-induced inflammation in human monocyte-derived macrophage THP-1.METHODS: THP-1 cells were treated with palmitate (0, 0.1 and 0.2 mmol/L) for 24 h. Transwell chamber assay was used to examine the migration ability of THP-1 cells. The mRNA expression of CD36, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and monocyte chemotactic protein 1 (MCP-1) was measured by real-time PCR. The protein levels of TNF-α and IL-6 in the supernatant of cultured cells were measured by ELISA. The protein level of CD36 was examined by Western blot. Small interfering RNA (siRNA) targeting CD36 (siCD36) was used to inhibit the expression of CD36 in the THP-1 cells, and the changes of the cell migration and inflammatory response were monitored as mentioned above. RESULTS: Palmitate increased the expression of CD36 in the THP-1 cells (P<0.05). Palmitate also up-regulated inflammatory cytokine and chemokine levels, and the differences were statistically significant (P<0.05). Compared with control group, palmitate promoted migration of THP-1 cells. siCD36 was transfected into the THP-1 cells and the silencing efficiency was approximately 54%. The protein levels of TNF-α and IL-6 were also decreased in siCD36 group compared with scrambled RNA (scrRNA) group, and the differences were statistically significant (P<0.05). The migrated cells in siCD36 group were significantly less than those in scrRNA group (P<0.05).CONCLUSION: Palmitate promotes migration ability and triggers inflammatory response in the THP-1 macrophages by upregulating CD36 expression.     

Effects of renal denervation on inflammatory factors in a rabbit model of early atherosclerosis

AIM: To evaluate the effects of renal denervation (RDN) on the expression of tumor necrosis factor-α (TNF-α), interleukin-1α (IL-1α) and interleukin-6 (IL-6) in a rabbit model of early atherosclerosis. METHODS: New Zealand male rabbits were divided into control group, RDN+ high-fat diet (HFD) group (RDN group), sham+HFD group (sham group) and HFD group. The rabbits in later 3 groups were fed with 2% cholesterol for 8 weeks to establish an early atherosclerosis model. The blood samples were collected to test the levels of lipids, norepinephrine (NE), TNF-α, IL-1α and IL-6. The protein expression of angiotensin Ⅱ (Ang Ⅱ) was detected by the method of immunohistochemistry. The levels of nuclear factor-κB (NF-κB) and Ang II 1 type receptor (AT1R) were evaluated by Western blot. The mRNA expression of TNF-α, IL-1α and IL-6 was determined by real-time PCR. RESULTS: After 1 d of RDN procedure, the NE level was lower in RDN group than that in sham group (P<0.01). After 8 weeks, the NE level was lower in RDN group than that in sham group and HFD group (P<0.05), and triglyceride (TG) was lower in RDN group than that in HFD group (P<0.05). The protein expression of Ang II was decreased in RDN group compared with sham group and HFD group (P<0.01). The protein expression of NF-κB was lower in RDN group than that in sham group (P<0.05). The plasma levels of TNF-α and IL-1α were reduced in RDN group compared with sham group and HFD group (P<0.05). The mRNA expression of TNF-α, IL-1α and IL-6 was reduced in RDN group compared with sham group (P<0.05). CONCLUSION: RDN inhibits sympathetic activity, decreases the plasma level of TG, and alleviates inflammatory reactions in the rabbits with atherosclerosis.     

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.     

Hypoxia-inducible factor-1α attenuates myocardial inflammatory injury induced by ischemia and reperfusion in rats

AIM:To investigate the role of hypoxia-inducible factor-1α (HIF-1α) stable expression in myocardial inflammatory injury induced by ischemia and reperfusion (I/R) in rats. METHODS:Male Wistar rats were randomly divided into 4 groups:sham operation (sham) group, I/R group, HIF-1α stabilizer dimethyloxalyl glycine (DMOG)+I/R group and HIF-1α inhibitor YC-1+I/R group. The protein expression of myocardial Toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB) was determined by Western blot. The mRNA levels of interleukin (IL)-1β, tumor necrosis factor-α (TNF-α), IL-6, TLR4 and NF-κB were detected by real-time PCR. The myeloperoxidase (MPO) activity in the myocardial tissues was measured. HE staining was used to observe the infiltration of inflammatory cells. RESULTS:HIF-1α decreased the infiltration of inflammatory cells, the MPO activity, and the mRNA levels of inflammatory factors IL-1β, IL-6 and TNF-α in the myocardial tissues. HIF-1α also reduced the expression of TLR4 and NF-κB at mRNA and protein levels (P<0.05). CONCLUSION:The stable expression of HIF-1α has an anti-inflammatory effect on the myocardial tissues after I/R injury in rats. The mechanism may be related to the inhibition of TLR4/NF-κB signaling pathway.     

Effects of immunoglobulin on circulating proinflammatory cytokines in children with hand-foot-mouth disease

AIM：To study the mechanism of intravenous administration of immunoglobulin for treatment of hand-foot-mouth disease. METHODS：Sixty-four children with hand-foot-mouth disease were randomly divided into treatment group and control group. The children in control group (n=32) were treated with ribavirin and given normal supportive therapy. The children in treatment group (n=32) were given ribavirin and normal supportive therapy plus intravenous administration of immunoglobulin (500 mg·kg-1·d-1) for 3 d. The levels of TNF-α, C-reactive protein (CRP) and IL-6 in venous blood were observed. RESULTS：The levels of TNF-α, CRP and IL-6 in treatment group and control group were all higher than those in the normal children. The levels of TNF-α, CRP and IL-6 in treatment group were similar to those in control group before treatment. The levels of TNF-α, CRP and IL-6 in treatment group were significantly lower than those in control group after treatment with immunoglobulin for 3 d. CONCLUSION：The systemic inflammatory response syndrome is one of the possible mechanisms of hand-foot-mouth disease. Intravenous administration of immunoglobulin decreases the proinflammatory cytokines in the patients with hand-foot-mouth disease.     

Expression of calprotectin in rats with renal ischemia-reperfusion injury

AIM: To investigate the expression of calprotectin(CALP) in the rats with renal ischemia-reperfusion injury(IRI). METHODS: Male Sprague-Dawley rats were randomly divided into sham operation and IRI group(n=25 in each group). Blood samples and the kidneys were obtained at 6 h, 12 h, 24 h, 48 h and 72 h after reperfusion. The pathological changes of the kidneys were observed. The serum concentrations of blood urea nitrogen(BUN) and serum creatinine(SCr) were measured. The serum levels of CALP, tumor necrosis factor-α(TNF-α) and interleukin-6(IL-6) were detected by ELISA, and the expression of CALP, Toll-like receptor 4(TLR4) and NF-κB p65 in the renal tissues were determined by the methods of immunohistochemistry and Western blot. RESULTS: Different serial ischemia changes were observed in the renal tissues, mainly in the renal tubular epithelial cells and the mesenchyma, with the infiltration of inflammatory cells. The serum levels of BUN, SCr, CALP, TNF-α and IL-6 in IRI group were markedly increased as compared with sham group(P<0.05). The protein expression of CALP, TLR4 and NF-κB p65 in the renal tubular epithelial cells in IRI group was greatly enhanced in comparison with that in sham group(P<0.05). CONCLUSION: The serum concentrations of CALP, TNF-α and IL-6, and the protein expression levels of CALP, TLR4 and NF-κB p65 in the renal tissue are significantly increased in the rats with IRI, suggesting that calprotectin plays an important role in the inflammation in rats with IRI.     

Experimental study on anti-endotoxin activity of a tetrahydropyrimidine derivative,ZL-5015

AIM: To investigate the protective effect of 1, 3-dicyclopentyl-1, 2, 3, 6-tetrahydropyrimidine-4, 5-dicarboxylic acid diethyl ester (ZL-5015) on lethal endotoxin-challenged mice and to explore the underlying mechanism. METHODS: Mouse model of lethal endotoxin challenge and endotoxemia were established by intraperitoneal administration of lipopolysaccharide (LPS) at a dose of 70 mg/kg to the C57BL/6J mice. Mouse peritoneal macrophages stimulated with LPS (10 mg/L) were used as an in vitro inflammatory model. The levels of interleukin-1β (IL-1β), interleukin-10 (IL-10) and tumor necrosis factor-α (TNF-α) were measured by enzyme-linked immunosorbent assay (ELISA). Real-time PCR was used to evaluate the mRNA expression of the cytokines. RESULTS: Prophylactic treatment of the mice with ZL-5015 (100 and 200 mg/kg, ig) slightly increased the survival rate, extended the survival time, decreased the serum levels of IL-1β and TNF-α, and increased the serum level of IL-10 in the early stage of endotoxemia as compared with model group. The results of in vitro study demonstrated that treatment of the endotoxin-stimulated mouse peritoneal macrophages with ZL-5015 (10, 20 and 40 μmol/L) inhibited the expression of IL-1β and TNF-α at both mRNA and protein levels but promoted the expression of IL-10 at both mRNA and protein levels. CONCLUSION: The tetrahydropyrimidine derivative ZL-5015 shows a moderate anti-endotoxin effect by increasing the survival rate and extending the survival time of the mice challenged by endotoxin, which may result from inhibition of the expression of pro-inflammatory cytokines such as IL-1β and TNF-α, and promotion of the expression of anti-inflammatory cytokine IL-10.     

Effects of atorvastatin on expression of PAPP-A induced by TNF-α and IL-1β in rat aortic endothelial cells

AIM: To investigate the effects of atorvastatin on the expression of pregnancy-associated plasma protein A(PAPP-A)induced by TNF-α and IL-1β in endothelial cells. METHODS: The rat aortic endothelial cells were isolated from thoracic aortas and cultured by the tissue explant method. The cells in passage 3-4 were used in the experiment and were randomly divided into 4 groups: blank control group: the cells were treated without any intervention; atorvastatin concentration groups: the cells were incubated with atorvastatin at the concentrations of 0.1, 1 and 10 μmol/L for 24 h; atorvastatin time groups: the cells were incubated with atorvastatin at the concentration of 10 μmol/L for 6 h,12 h and 24 h; atorvastatin+inflammatory factors groups: the cells were pre-incubated with 60 μg/L TNF-α or 20 μg/L IL-1β for 1 h, then different concentrations of atorvastatin (0.1, 1.0, 10 μmol/L) were added for 6 h,12 h and 24 h. MTT reduction assay was used to observe the cell proliferation. The mRNA expression of PAPP-A was detected by RT-PCR. The protein level of PAPP-A in the supernatants of cultured cells was measured by ELISA. RESULTS: Compared with blank control group, no significant change of cell proliferation was observed after the intervention of atorvastatin and TNF-α/IL-1β for 3 h, 6 h, 12 h, 24 h and 48 h, indicating that the drugs had no toxic effects on the cells. No significant difference of PAPP-A expression between atorvastatin groups and blank control groups was found. Compared with TNF-α groups and IL-1β groups, PAPP-A expressions in atorvastatin intervention groups significantly decreased. The protein level of PAPP-A was gradually decreased with the raised concentration of atorvastatin and the prolonged time in a concentration- and time-dependent manner. CONCLUSION: Atorvastatin doesn't influence the PAPP-A expression, but inhibits the expression of PAPP-A activated by inflammatory factors in a concentration- and time-dependent manner in primary cultured rat aortic endothelial cells.     

Effects of ursodeoxycholic acid on proinflammatory cytokines in children with infantile hepatitis syndrome

AIM: To observe the effect of ursodeoxycholic acid (UDCA) on the treatment of infantile hepatitis syndrome (HIS) and to investigate its mechanism. METHODS: The children with infantile hepatitis syndrome were divided into conventional treatment group and the UDCA treatment group. Twenty healthy children were selected as normal control. The children in conventional therapy group were given antiviral and hepatoprotective treatments. The children in UDCA treatment group were given ursodeoxycholic acid (10 mg·kg^-1·d^-1) in addition to the conventional treatment group for 2 to 3 weeks. The levels of total bilirubin (TBIL), direct bilirubin (DBIL), alanine aminotransferase (ALT), glutamyltransferase (GGT), total bile acids (TBA) and TNF-α, IL-6 were detected before admission and 2 weeks later.RESULTS: The levels of TNF-α and IL-6 were significantly higher in the children with IHS than those in the normal control (P<0.01). The levels of TBIL, DBIL, ALT, GGT, TBA, TNF-α and IL-6 in conventional treatment group were reduced after therapy (P<0.01). All the above index in UDCA treatment group were decreased compared with conventional treatment group (P<0.01). CONCLUSION: On the basis of conventional therapy, ursodeoxycholic acid effectively alleviates the systemic inflammatory response in the children with IHS, reduces the liver damages.     

Effects of IL-6 and IL-1α on the peripheral blood polymorphonuclear neutrophil apoptosis postburn in rats

AIM:To study the effects of IL-6 and IL-1α on the blood polymorphonuclear-neutrophils(PMN) apoptosis postburn.METHODS:Wistar rats inflicted by 30% total body surface area (TBSA) Ⅲ degree scalding were employed as the model. PMN were isolated by density gradient centrifugation using Percoll-hypaque and labeled with TdT-mediated and dUTP nick end labeling (TUNEL) and analyzed by flow cytometric analysis. The intracellular caspase-3 activation and the serum levels of IL-6 and IL-1α were analyzed by fluorometric immunosorbent enzyme assay and enzyme-linked immunosorbent assay, respectively.RESULTS:The serum IL-6 levels (μg/L) in groups of 3, 6, 12, 24 and 48 h postburn (9.14±1.16, 12.49±1.14, 3.01±0.75, 1.41±0.28 and 1.56±0.43 in turn) and IL-1α (ng/L) in groups of 3, 6, 12 h postburn (90.08±8.39, 320.93±14.48 and 47.84±5.19) were much higher than IL-6 (0.24±0.07) and IL-1α (27.65±4.86) in control group (P＜0.05), respectively. The relative proportions of apoptotic PMN(%) in groups postburn were 9.89±2.00, 4.98±1.35, 1.31±0.72, 2.49±1.87 and 6.88±1.13 in turn, which were obviously less than 13.66 ± 3.88 in the control group. The results of intracellular caspase-3 activation in PMN were observed to be consistent with the results of apoptotic PMN analysis in experimental groups.CONCLUSION:IL-6 and IL-1α are the important factors to induce PMN apoptosis delay that occurred obviously postburn. And decrease in the activity of intracellular caspase-3 of PMN may be involved in their mechanisms.