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1.
AIM: To study the role of heme oxygenase (HO)-1 in the mechanism of cholecystokinin-octapeptide (CCK-8) for attenuation of acute lung injury (ALI) induced by lipopolysaccharide (LPS).METHODS: Adult male rats were randomly divided into five groups: control group,LPS group,CCK-8+LPS group,LPS+ Hm (hemin,HO-1 donor) group and LPS+ZnPP (zinc protoporphyrin,specific inhibitor of HO-1) group.PMN number in bronchoalveolar lavage fluid (BALF),the structure of the lung,MDA content,HO-1 activity,the expressions of HO-1 mRNA and protein in the lung were detected respectively.RESULTS: The lung injury in LPS group was observed,at the same time the numbers of PMN,the content of MDA,the activity and the expression of HO-1 were all higher than those in control group (all P<0.05).The degree of lung injury,PMN numbers and MDA content were lower,while the activity and the expression of HO-1 in CCK-8+LPS and LPS+Hm group were higher than those in LPS group (all P<0.05).However,the degree of lung injury,PMN numbers and MDA content were higher,the activity and the expression of HO-1 were lower in LPS+ZnPP than those in LPS group respectively (all P<0.05).CONCLUSION: CCK-8 attenuates the LPS-induced ALI by means of anti-oxidation and inhibits PMN aggregation,which are both mediated by HO-1 partly.  相似文献   

2.
AIM: To study the role of carbon monoxide (CO) in the mechanism of cholecystokinin-octapeptide (CCK-8) for attenuation of acute lung injury (ALI) induced by lipopolysaccharide (LPS). METHODS: Fifty-six adult male rats were randomly divided into seven groups: control group, LPS group, LPS+ZnPP (a specific inhibitor of HO-1) group, LPS+Hemin (Hm， CO donor) group, CCK-8+LPS group, CCK-8+LPS+ZnPP group and CCK-8 group (n=8 for each). Bronchoalveolar lavage was performed 2 h, 6 h and 12 h respectively after treatments. The numbers of polymorphonuclear leukocytes (PMN) in bronchoalveolar lavage fluid (BALF) was detected. The mortality of rats and the structure of lung tissues were observed. MDA and CO contents in lung tissues were also measured. RESULTS: The mortalities of rats were both zero 2 h and 6 h after agent administration. The mortality of rats was higher than control group 12 h after LPS administration. The mortality of rats in LPS+Hm and CCK-8+LPS group were lower than that in LPS group, and its in LPS+ZnPP and CCK-8+LPS+ZnPP group were lower than that in LPS and CCK-8+LPS group, respectively. Lung injury was observed in LPS group. At the same time the number of PMN, MDA and CO content were higher than those in control group. The degree of lung injury, PMN numbers and MDA content were lower, while CO content in LPS+Hm and CCK-8+LPS group were higher than those in LPS group. However, the degree of lung injury, PMN number and MDA content were higher, CO content were lower in LPS+ZnPP and CCK-8+LPS+ZnPP group than those in LPS and CCK-8+LPS group, respectively. CONCLUSION: CCK-8 attenuates the LPS-induced acute lunginjury by means of anti-oxidation and inhibition of PMN aggregation, which are both mediated by CO.  相似文献   

3.
AIM: To investigate the relationship of p38 mitogen-activated protein kinases (p38MAPK), nuclear factor-kappa B (NF-κB) and heme oxygenase-1 (HO-1) in acute lung injury (ALI) in rats.METHODS: Forty male Wistar rats were divided into 5 groups (n=8) at random: control group or normal saline group (NS group), lipopolysaccharide group (LPS group), Hemin (inducer of HO-1)+LPS group, ZnPPIX (inhibitor of HO-1)+LPS group and SB203580 (inhibitor of p38MAPK)+LPS group (SB+LPS group). Six hours after endotracheal instillation of LPS or NS, the ratio of neutrophils and the protein contents in bronchoalveolar lavage fluid (BALF) of right lung, the ratio of wet/dry weight (W/D) of the superior lobe of right lung, and arterial blood gas analysis (ABG) were examined. The protein levels of p38MAPK and NF-κB in the lower lobe of right lung were detected by Western blotting. The protein expression of HO-1 in the middle lobe of right lung was measured by the method of immunohistochemisty. The structure of the lung was evaluated under light microscope. RESULTS: Compared with NS group, the ratio of neutrophils and protein contents in BALF, the ratio of W/D, the protein levels of HO-1, p38MAPK and NF-κB were obviously higher, and arterial oxygen pressure (PaO2), partial pressure of carbon dioxide in artery (PaCO2) and bicarbonate content (HCO-3) were significantly lower in LPS group, Hemin+LPS group, ZnPPIX+LPS group and SB+LPS group (P<0.05 or P<0.01). The ratio of neutrophils and proteins in BALF, the ratio of W/D, the protein levels of p38MAPK and NF-κB were significantly lower, the protein level of HO-1 was obviously higher in Hemin+LPS group and SB+LPS group than those in LPS group (P<0.05), while the changes of the parameters in ZnPPIX+LPS group were in a contrary manner (P<0.05). No significant difference of the parameters between Hemin+LPS group and SB+LPS group (P>0.05) was found. The structures of the lung tissues in LPS group were severely damaged and even severer damages were observed in ZnPPIX+LPS group. The structural changes of the lung tissues in Hemin+LPS group and SB+LPS group were slighter. CONCLUSION: p38MAPK/NF-κB and HO-1 are inhibited by each other and the effects of them are independent on the acute lung injury.  相似文献   

4.
AIM: To examine the role of glucocorticoid receptor (GR) in regulation of lipopolysaccharide (LPS)-induced lung injury. METHODS:Male Sprague-Dawley rats were divided into six groups randomly: control group (n=6), LPS group (n=6 each), Dex+LPS group (n=6 each), RU486 group (n=6), RU486+LPS group (n=6 each) and RU486+Dex+LPS group (n=6 each). All groups were subjected into 1 h, 3 h, 6 h and 12 h time point subgroups after LPS administration, except of control group and RU486 group. The concentrations of TNF-α and IL-6 in bronchoalveolar lavage fluids (BALF) were detected by ELISA. The histopathologic changes of lung tissues, the activation of p38MAPK and the expression of MKP-1 in lung tissue were also observed. Further, to confirm the role of GR in this model, the mortality of rats in LPS group vs RU486+LPS group and in Dex+LPS group vs RU486+Des+LPS group was compared. RESULTS: LPS induced lung injury and the secretions of TNF-α and IL-6 in BALF, which were significantly enhanced by pretreatment of RU486 (P<0.05). RU486 pretreatment also significantly increased the LPS-induced lethality (P<0.05). Dexamethasone attenuated LPS-induced lung damage, cytokine release and mortality rates, and the protective effects might be mediated by GR. Western blotting analysis showed dexamethasone inhibited the phosphorylation of p38MAPK in lung tissues by induction of MKP-1, and these actions were also GR dependent. CONCLUSION: GR plays an essential role in regulation of LPS-induced acute lung injury. Anti-inflammatory effects of hormone-activated GR may be mediated by inhibition of p38MAPK phosphorylation/activation, which is associated with the induction of MKP-1.  相似文献   

5.
AIM and METHODS:The animal model of acute lung injury (ALI) caused by intratracheal instillation of lipopolysaccharides(LPS) in vivo and human peripheral blood polymorphonuclear neutrophil (PMN) in vitro were used to study the effects of sodium nitroprusside (SNP), nitric oxide (NO) donor, on LPS-induced PMN accumulation, microvascular permeability and PMN apoptosis. RESULTS:①In vivo, PMN accumulation in lung, the protein content in bronchoalveolar lavage fluid (BALF) and the Evans blue dye and monastral blue dye extravasation in lung tissue of LPS group were markedly higher than those of both sham operation group and LPS+SNP group. ②In vitro, the apoptotic percentage of SNP group was much higher than that of control group, while compared with LPS group, SNP+LPS group has significantly higher apoptotic percentage. CONCLUSIONS:SNP intratracheal instillation attenuated LPS-induced microvascular permeability and alleviated ALI. PMN apoptosis induced by SNP may be one of the potential mechanisms underlying the decrease of PMN accumulation in lung tissue.  相似文献   

6.
AIM:To investigate the role of HO-1 in pro tection of rat hearts against anoxia/reoxygenation-induced injury and its under lying mechanism.METHODS:Cardiac contractility,lactate dehydrogenase (LDH) and infarct area were analyzed by the Langendorff method in isolated rat hearts.RESULTS:After intraperitoneal injection of HO-1 inducer hemin,CO concentration in rat blood enhanced (P<0.01 vs control group).Pretreatm ent with hemin prevented the increase in LVEDP and decrease in LVDP,±dp/d tmax during the anoxia and reoxygenation period in hearts.Hemin had n o effect on changes of coronary flow,but it really inhibited the release of LDH from anoxia/reoxygenation hearts.Hemin also reduced the infarct area in anoxia heart after 2 h reoxygenation (P<0.01).CO concentration in rat blood redu ced after intraperitoneal injection of HO-1 inhibitor ZnPP (P<0.01 vs contr ol group).ZnPP aggravated the decrease in LVDP and ±dp/dtmax.Co mpared with anoxia/reoxygenation heart,pretreatment of ZnPP enhanced the LDH re lease and enlarged the infarct area (P<0.05).GC inhibitor methylene blue a nd cyclooxygenase-2 (COX-2) inhibitor celecoxib both partly abolished the protec tion effect of hemin on LVEDP,LVDP and ±dp/dtmax.Pretreatment o f methylene blue or celecoxib also cancelled the inhibition of LDH release and r eduction of infarct area caused by hemin (P<0.05).CONCLUSION:HO-1 inducer hemin protects heart from anoxia/reoxy genation-induced injury.The cardiac protection of HO/CO might be through GC pathway,and the activation of COX-2 might be also involved in this process.  相似文献   

7.
AIM: To investigate the effects and mechanisms of sphingosine-1-phosphate receptor-2 (S1P2R)on lipopolysaccharide (LPS)-induced acute lung injury (ALI). METHODS: ALI model was induced by intratracheal administration of LPS in both wild-type mice and S1P2R -deficient mice. The pathological changes in the lung tissues were observed, and the protein concentration, total cell number, neutrophil ratio, TNF-α level and IL-6 level were determined in the bronchoalveolar lavage fluid (BALF) 24 h after LPS injection. In order to investigate the mechanisms of S1P2R in LPS-induced ALI, 10 min before LPS injection, both wild-type mice and S1P2R -deficient mice were injected with nitric oxide synthase inhibitor by tail vein injection, the pathological changes of the lung tissues were observed, and the protein concentration and total cell number in BALF were determined 12 h after LPS injection. RESULTS: Compared with wild-type mice, S1P2R -deficient mice showed more severe LPS-induced ALI, and the protein concentration, neutrophils and inflammatory cytokines in BALF were significantly increased in S1P2R -deficient mice. Administration of nitric oxide synthase inhibitor Nω-L-nitro-arginine methyl ester protected S1P2R -deficient mice from aggravation of ALI. CONCLUSION: S1P2R mediates the protection from LPS-induced ALI possibly through inhibiting nitric oxide synthase.  相似文献   

8.
AIM: To investigate the effect of heme oxygenase-1 (HO-1)/carbon monoxide (CO) system on pulmonary ischemia-reperfusion injury (PIRI) in rabbits. METHODS: Single lung ischemia and reperfusion animal model was used in vivo. The rabbits were randomly divided into three groups (n=10 in each), control group (C), PIR group (I-R), PIR+ hemin group (H) and PIR+zinc protoporphyrin IX (ZnPP) group (Z). Changes of several parameters which included plasma carboxyhemoglobin (COHb) at different time points, wet to dry ratio of lung tissue weight (W/D), the injured alveoli rate (IAR) and the HO-1 enzymatic activity were measured at 180 min after reperfusion in lung tissue. The tissue slides were also stained by immunohistochemistry (IHC) and in situ hybridization (ISH) for HO-1 to detect the expression of HO-1 in lung and to analyze the optical density. The lung tissue was prepared for electron microscopic observation at 180 min after reperfusion. RESULTS: The plasma content of COHb in I-R, H, and Z group increased in a time-dependent manner after I-R. But the increment of H group was higher than that of I-R group, while that of Z group was lower. The HO-1 activity in lung tissue was highest in H group, followed by IR group, Z group, and C group (P<0.05 and P<0.01). Except C group, HO-1 was upregulated in all other groups in the pulmonary endothelial cells, part of pulmonary vascular smooth muscle cells, extima of vessels and epithelial cells of airway. H group had the highest average optical density value, then the IR group, Z group and C group (P<0.05 and P<0.01). The value of W/D and IAR was highest in Z group, the second was in IR group, then the H group and C group (P<0.05 and P<0.01). The abnormal changes of the lung tissue in morphology in I-R group, Hemin treatment mitigated the injury of I-R in H group and ZnPP exacerbated the impairment of ultrastructure in Z group were also observed. CONCLUSION: HO-1/CO system possesses notable protective effects on lung during pulmonary ischemia-reperfusion injury in rabbits.  相似文献   

9.
AIM:To investigate the mechanisms by which berberine attenuates LPS-induced acute lung injury, and provide a new strategy for the treatment of the lung injury due to LPS. METHODS:BALB/c mice were randomly assigned into three groups (control, LPS group, and berberine treatment group). Mice were administered intragastrically with distilled water (0.1 mL/10 g) or neutral sulfate berberine (50 mg/kg) once a day for 3 days, 1 h after intragastrical treatment on day 3, LPS (20 mg/kg) or normal saline was injected intraperitoneally (ip). All animals were sacrificed 12 h after LPS injection, the left lung tissue sections were prepared for histology analysis and the right lung were used to determine the ratio of wet to dry lung tissue weight (W/D). In another experiment, bronchoalveolar lavage fluid (BALF) was collected, and then the total protein content, and the amounts of white blood cells (WBC) and polymorphonuclear neutrophils (PMN) in BALF were determined. Furthermore, the phosphorylation of cytosolic phospholipase A2 (cPLA2) was detected with immunohistochemical analysis by using phospho-cPLA2(Ser505) antibody, and the contents of thromboxane B2 (TXB2) in BALF, malondialdehyde (MDA) in the lungs, and activity of superoxide dismutase (SOD) in lung tissues were also determined.RESULTS:LPS induced acute lung injury, activated cPLA2, and increased TXB2 content in the BALF and MDA level in the lung tissue. The pretreatment with berberine significantly attenuated lung injury, lung edema and protein leakage induced by intraperitoneal injection of LPS. The expression of phospho-cPLA2 in the lung tissues and TXB2 content in the BALF in the berberine treatment group were lower than those in LPS group (P<0.05). In addition, the content of MDA in the lung tissue was lower in the berberine treatment group than LPS group (P<0.05), but there was no significant difference in activity of lung SOD between the berberine treatment and LPS group (P>0.05). CONCLUSION:Pretreatment with berberine remarkably reduces the LPS-induced lung injury, which is, at least in part, through inhibiting phosphorylation of cPLA2 and decreasing lipid peroxidation. These findings provide a new strategy for the prevention and treatment of LPS-induced acute lung injury.  相似文献   

10.
AIM: To investigate the effects of Auricularia auricular-judae polysaccharide(AAP) on pulmonary tissues of rats with LPS-induced acute lung injury(ALI) and its mechanisms.METHODS: Adult Sprague-Dawley rats were randomly divided into control group, LPS group,low-dose AAP group, middle-dose AAP group, high-dose APP group, and dexamethasone group. The rats were injected with LPS(8 mg/kg, ip) to induce ALI. The rats in the AAP groups were treated with AAP for 7 d before the induction of ALI. The protein concentration in the bronchoalveolar lavage fluid(BALF) was measured. The lung edema degree was measured by detecting the wet/dry weight ratio. The myeloper-oxidase(MPO), total antioxidant capacity(T-AOC), total superoxide dismutase(T-SOD), nitric oxide synthase(NOS) and malondialdehyde(MDA) levels were determined. The pathological changes of the lung tissues were evaluated by HE staining.RESULTS: Treatment with AAP significantly improved LPS-induced lung pathological changes, attenuated the protein concentration in the BALF and wet/dry weight ratio, inhibited the activities of MPO and NOS, reduced MDA level and increased the activities of T-AOC and T-SOD.CONCLUSION: AAP protects against LPS-induced acute lung injury in rats.  相似文献   

11.
AIM:To explore the delayed protection of heme oxygenase-1 (HO-1) in the exercise preconditioning (EP) from the myocardial relative ischemia reperfusion injury (rI/R). METHODS:40 Wistar Rats were divided into 5 groups randomly:control group (CN), rI/R group (IR), EP+rI/R group (EI), HO-1 inductor hemin+rI/R group (HE) and HO-1 inhibitor ZnPP+EP+rI/R group (EZ). The following indexes were detected, including the HO-1activity in myocardium, the cardiac function parameter-pressure-rate product (heart rate × left ventricular developed pressure, PRP) and the content of MDA in coronary effluent. RESULTS:After myocardial rI/R, HO-1 activity increased significantly. Moreover, EP or HO-1 inductor could enhance this effect manifestly. Nevertheless, when the HO-1 inhibitor was administered before EP，HO-1 activity decreased. In addition, there was no distinct difference in the HO-1 activity between EI group and HE group. At the 30 min point of reperfusion, the PRP recovery rate of EI group was higher clearly than that of IR group. However, there was reverse effect between the EZ group and the EI group. The MDA in coronary effluent of EI group, EZ group and HE group were lower obviously than that of IR group and there was significant difference between EI group and EZ group. CONCLUSION:EP could protect the heart from the rI/R injury occurring 24 hours later, which might be performed through activating the HO-1.  相似文献   

12.
AIM: To explore the role of endogenous hydrogen sulfide (H2S) in the mechanism of cholecystokinin octapeptide (CCK-8) to alleviate acute lung injury (ALI) induced by lipopolysaccharide (LPS). METHODS: Eighty-four Sprague-Dawley rats were randomly divided into seven groups: control, LPS (instilled intratracheally to reproduce the model of ALI), NaHS (H2S donor) +LPS, propargylglycine ［inhibitor of cysathionine-γ-lyase (CSE), PPG］+LPS, CCK-8+LPS, PPG+CCK-8+LPS and CCK-8 group. Animals were sacrificed at 4 h and 8 h after agent instillation. The wet and dry ratio (W/D) of the lung weight was measured and calculated. Morphological changes of lung tissues were observed. H2S concentration in plasma, malondialdehyde (MDA) content, myeloperoxidase (MPO) and CSE activities in the lung were determined. Furthermore, the level of P-selectin of lung tissue was measured by radioimmunoassay, the CSE mRNA expression in the lung was detected by RT-PCR, and the protein content in bronchoalveolar lavage fluid (BALF) was detected. RESULTS: Compared with control, severe injury of lung tissues and increase in W/D, protein content in BALF, MDA content, MPO activity and P-selectin level in the lung were observed in rats treated with LPS. LPS also lead to a drop in plasma H2S concentration, lung CSE activity and CSE mRNA expression. Administration of NaHS before LPS could attenuate the changes induced by LPS, while H2S concentration, CSE activity and CSE mRNA expression were higher than those in LPS group. However, pre-treatment with PPG exacerbated the lung injury induced by LPS, H2S concentration, CSE activity and CSE mRNA expression were lower than those in LPS and CCK-8 +LPS group, respectively. CONCLUSION: CCK-8 attenuates LPS-induced acute lung injury by means of anti-oxidation and inhibition of PMN adhesion and aggregation, both of which are mediated by endogenous H2S.  相似文献   

13.
AIM: To investigate the effect of sodium nitrite (SN) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) and its underlying mechanism in mice. METHODS: All male Institute of Cancer Research (ICR) mice were randomly divided into five groups: Control group; LPS group; and SN 4.8 nmol/L, SN 48 nmol/L, SN 480 nmol/L (ip) groups. Lung wet weight/dry weight (W/D) ratio and permeability were detected. Neutrophil infiltration in bronchoalveolar lavage fluid (BALF) was measured by cel1 counting and morphological changes in lung tissues were assayed by hematoxylin-eosin staining. The 1evels of interleukin-10 (IL-10) and tumor necrosis factor-α (TNF-α) in lung were detected. Nitric oxide (NO) level and nitric oxide synthase (NOS) activity in lung were measured according to the specification. RESULTS: Compared to lung in LPS-induced ALI mice, at doses of 4.8 nmol/L and 48 nmol/L, not 480 nmol/L, SN markedly decreased the lung W/D ratio, total leukocyte number and neutrophil percentage in the BALF, lung permeability, and TNF-α/IL-10 ratio, in lung. SN at dose of 480 nmol/L markedly increased the lung NO level compared to control group. In addition, SN decreased the total NOS and inducible NOS (iNOS) activities compared to LPS-induced ALI mice. CONCLUSION: These results indicate that the protective effect of SN against LPS-induced ALI in mice is associated with the low dose SN-induced NO, as well as the subsequent decrease in iNOS activity and TNF-α/IL-10 ratio.  相似文献   

14.
AIM: To study the signal pathway involved in up-regulation of LPS-induced HO-1 expression by CCK-8. METHODS: Forty-two SD rats were divided into 7 groups (six rats each) randomly as follows: control group, LPS group, LPS+SP600125 (JNK-specific inhibitor) group, CCK-8+LPS group, CCK-8+LPS+SP600125 group, CCK-8 group and CCK-8 +SP600125 group. Lungs from the rats in these 7 groups were excised 6 h after the agents were administered. HO-1 mRNA expression was examined by RT-PCR. The protein expression of HO-1 was detected by Western blotting and immunofluorescence flow cytometry (FCM). RESULTS: There were significant positive expression of HO-1 mRNA in LPS group compared to control group. CCK-8 enhanced LPS-induced HO-1 mRNA expression and CCK-8 alone induced HO-1 mRNA expression as well. The mRNA expressions of HO-1 in LPS group, CCK-8+LPS group and CCK-8 group were 3.01 (P<0.01), 5.88 (P<0.01) and 3.45 (P<0.01) times as many as that in control group, respectively. SP600125 inhibited the mRNA expression of HO-1 induced by CCK-8 and (or) LPS. The change of HO-1 protein expression was in accordance with that of HO-1 mRNA expression by Western blotting and immunofluorescence FCM. CONCLUSION: These results suggest that JNK/c-Jun signal pathway plays an important role in the up-regulation of LPS-induced HO-1 expression by CCK-8.  相似文献   

15.
AIM: To study the protective effect of heat shock factor1 (HSF1) on the mice with lipopolysaccharide (LPS)-induced acute lung injury (ALI), and to screen the relevant differentially-expressed genes. METHODS: ALI mouse model was established by LPS intracheal instillation. The macroscopic and pathological changes of the lung tissue were observed, and the concentrations of total protein, TNF-α, IL-β, IL-6 and VEGF in the bronchoalveolar lavage fluid (BALF) were analyzed. Differentially-expressed genes in the lung tissues of HSF1+/+ mice and HSF1-/- mice with ALI induced by LPS were screened by gene chips. The key gene was verified by real-time qPCR. RESULTS: The macroscopic and pathological changes of the lung injury in HSF1-/-+LPS mice were more serious than those in HSF1+/++LPS mice. The concentrations of total protein, VEGF, TNF-α, IL-1β and IL-6 in the BALF of HSF1-/-+LPS mice were significantly higher than those of HSF1+/++LPS mice (P<0.05). Compared with the HSF1+/+ mice, a total of 918 differentially-expressed genes were indentified in the HSF1-/- mice, among which the expression levels of 65 genes had obvious diffe-rence, with 28 genes up-regulated, including Atg7, ccr1, cxcr2, Tbl1xr1, Mmp9, Pparg, Plcb2, Arrb2, Cntn1, Col4a6, etc, and 37 genes down-regulated, including Fgfr1, Fgfr2, Map4k4, Ddx58, Tfg, Stat3, Smad4, Lamc1, Sdc3, etc. The results of real-time qPCR showed that the mRNA level of CXCR2 in HSF1-/-+ LPS mice was significantly higher than that in HSF1+/++ LPS mice, which was consistent with the results of gene chips. CONCLUSION: HSF1 has protective effect on the mice with LPS-induced ALI. CXCR2 may be involved in the protective effect of HSF1 on this process.  相似文献   

16.
AIM: To investigate the mechanisms by which paeoniflorin (Pae) attenuates lipopolysaccharide(LPS)-induced acute lung injury in mice. METHODS: Male BALB/c mice were randomly divided into 4 groups: control,LPS, Pae+LPS, and Pae. Mice were administered intragastrically with double distilled water or Pae (20 mg/kg) once a day for 3 days. One hour after intragastrical treatment on the third day, LPS (20 mg/kg) or normal saline was injected intraperitoneally. Twelve hours after LPS challenge, the histological changes of the lung were observed, and histology score was also assessed. The myeloperoxidase (MPO),cytosolic phospholipase A2 (cPLA2) and phosphorylated cytosolic phospholipase A2 (phospho-cPLA2) in lung tissues were detected by Western blotting.RESULTS: LPS challenge resulted in acute lung injury, activated cPLA2 and increased MPO content in lung. Pretreatment with paeoniflorin significantly attenuated lung injury induced by intraperitoneal injection of LPS. The levels of MPO and phospho-cPLA2 in the lung tissues of the mice in Pae+LPS group were lower than those in LPS group (P<0.05).CONCLUSION: Pretreatment with paeoniflorin remarkably reduces LPS-induced acute lung injury through inhibiting phosphorylation of cPLA2 and decreasing neutrophil infiltration in the lung. These findings provide a new strategy for the prevention and treatment of LPS-induced acute lung injury.  相似文献   

17.
AIM: To explore the cytokines level and the discrepancy of reaction to dexamethasone (Dex) in ALI rats induced by hydrochloric acid (HCl) and lipopolysaccharide (LPS). METHODS: Ninety-six SD rats were divided into six groups at random (n=16 in each group): NS group, HCl group, LPS group, NS+Dex group, HCl+Dex group and LPS+Dex group. Every group was divided into two subgroups: the bronchoalveolar lavage (BAL) subgroup and no bronchoalveolar lavage (NBAL) subgroup. The total leukocytes, PMN%, macrophage%, lymphocyte%, total protein in BALF and the wet/dry of the lung weight were measured. The concentrations of TNF-α, IL-1β, IL-4 and IL-10 in serum and BALF in every group were compared. RESULTS: (1) In the groups of LPS and HCl, the total leukocytes, PMN numbers, the protein concentration in the BALF and W/D were higher than those in control group (P<0.05). Compared to LPS groups, the percentage of macrophage increased in LPS+Dex group (P<0.05). (2) In serum and BALF of both LPS group and HCl group, the concentrations of TNF-α, IL-4 and IL-10 were higher than those in the control (P<0.01). The content of IL-1β in serum of all the groups was undetected. Compared to LPS groups, the concentrations of TNF-α and that of IL-1β decreased in LPS+Dex group (P<0.05). The concentration of IL-10 in LPS+Dex group was higher than that in LPS group (P<0.01). CONCLUSION: The permeability and the inflammatory cytokines in these two models were not consistent. Glucocorticoids play an effective role for resisting ALI induced by LPS but not HCl.  相似文献   

18.
TANG Xu-mao  QI Di  WANG Dao-xin 《园艺学报》2016,32(7):1252-1258
AIM: To investigate the effect of adipolin/CTRP12 in LPS-induced acute respiratory distress syndrome(ARDS) and its potential regulation on alveolar epithelial sodium channel(ENaC) in mice. METHODS: C57BL/6J mice(n=40) were randomly divided into control group, LPS group, adipolin group and wortmannin(PI3K inhibitor) group with 10 mice in each group using random number table. The pathological changes of the lung tissues were evaluated by HE staining. The alveolar fluid clearance(AFC) was measured by Evans blue-marked albumin, and the concentrations of total protein in bronchoalveolar lavage fluid(BALF) were assessed by bicinchoninic acid(BCA) method. In BALF, the levels of IL-1β and TNF-α were determined by ELISA, and the activity of myeloperoxidase(MPO) was detected by an MPO assay kit. The total cell counts and polymorphonuclear neutrophil(PMN) counts in the BALF were analyzed by Giemsa staining. The mRNA levels of α-ENaC were assessed by qPCR, while the protein levels of α-ENaC and p-Akt were determined by Western blot. RESULTS: Compared with control group, the classic ARDS pathological changes were observed in the mice in LPS group, manifesting by severe pathological lung injury(P<0.05), increases in W/D weight ratio, total protein levels, cell counts, MPO activitiy, and IL-1β and TNF-α levels in the BALF, and decrease in AFC(P<0.05), accompanied by down-regulated levels of α-ENaC and p-Akt in the lung tissues(P<0.05). The deteriorating effects triggered by LPS were significantly reversed by administration of adipolin. However, PI3K inhibitor wortmannin canceled the beneficial effects of adipolin on LPS-induced ARDS, as evidenced by aggravated lung injury, increased levels of W/D weight ratio, protein levels, cell counts, MPO activity, and IL-1β and TNF-α levels in the BALF(P<0.05), and decreased levels of AFC, α-ENaC and p-Akt in the lung tissues. CONCLUSION: Adipolin protects against LPS-induced ARDS in the mice by up-regulating α-ENaC and enhancing AFC via PI3K/Akt signal pathway.  相似文献   

19.
AIM:To explore the effects of bone marrow-derived mesenchymal stem cells-conditioned medium (MSCs CdM) on lipopolysaccharide (LPS)-induced acute lung injury. METHODS:Lung injury was induced in mice by intraperitoneal injection of LPS. The mice were given a tail vein injection of MSCs CdM or normal saline 1 h after LPS administration. The mice were killed by an intraperitoneal injection of pentobarbital 6 h after LPS injection for either bronchoalveolar lavage fluid (BALF) and serum collection or lung histological analysis. RESULTS:Compared with control group, the BALF levels of protein, interleukin-10 (IL-10) and keratinocyte growth factor (KGF), the serum levels of tumor necrosis factor α (TNF-α) and IL-6, and the myeloperoxidase (MOP) activity in the lung tissues were significantly higher in LPS group, and severe pathological damages in the lung tissues were also observed. Treatment with MSCs CdM significantly reduced the BALF prtein level, the seum TNF-α and IL-6　levels and the lung MPO activity, and attenuated the lung pathological damages, but further increased the levels of IL-10 and KGF in the BALF. CONCLUSION:Treatment with MSCs CdM attenuates the lung injuries induced by LPS, which may be via regulating the expression of TNF-α, IL-6, IL-10 and KGF.  相似文献   

20.
AIM: To study the role of polymorphonuclear neutrophile(PMN) in lipopolysaccharide (LPS)- induced acute lung injury (ALI) and the protective effect of interleukin -10(IL-10) on ALI. METHODS: LPS alone (100μg) or LPS+ IL-10 (l ug) was instilled intratracheally into rats. PMN numbers, protein content and malondialdehyde (MDA) content in bronchoalveolar lavage fluid (BALF) were measured. Histological change of lung was also observed. RESULTS: LPS increased significantly PMN numbers, protein content and MDA content in BALF. Histological finding shows PMN accumulation in lung. IL - 10+LPS reduced remarkably PMN numbers ,pro- tein content and MDA content in BALF than those caused by LPS. PMN decreasing was also identified by light microscopy. CONCLUSION: LPS instilled intratracheally causes PMN accumulation in lung and ALI, while IL - 10 could alleviate ALI through reducing PMN accumulation.  相似文献   

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