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Objective: To investigate the expression of IL-38 and MIP-2 in lung tissue of rats with pulmonary fibrosis induced by bleomycin, and to explore the significance of IL-38 and MIP-2 in pulmonary fibrosis in rats. Methods: 45 Wistar rats were randomly divided into saline control group ( group N), bleomycin group ( group B) and dexamethasone group ( group D) according to the random and control principle. On the 7 th, 14 th, and 28 th day, 5 rats were killed in each group. The pathological changes of lung tissue were observed by hematoxylin-eosin ( HE) staining in lung tissue. The expression of IL-38 and HYP in lung tissue of rats was measured by enzyme linked immunoassay ( ELISA) and the expression of MIP-2 in lung tissue of rats was measured by RT-PCR method. Results: (1) HE staining showed that the lung tissue from group B and group D developed from normal to inflammatory changes to pulmonary fibrosis. (2) The expression of IL-38 in group B and D decreased gradually, and the decrease was most obvious at 28 th day, which was lower than that in group N ( P＜0. 05), and the expression of IL-38 in group B was lower than that in D group, and the difference was statistically significant ( P＜0. 05). (3) The expression of MIP-2 and HYP increased gradually in group B and D, which were higher than those in group N, and the difference was statistically significant ( P＜0. 05). The MIP-2 and HYP expressions in group B were higher than those of group D in the same period, and the difference was statistically significant ( P＜0. 05). Conclusion: IL-38 and MIP-2 play an important role in the occurrence and development of bleomycin induced pulmonary fibrosis in rats. The application of dexamethasone can improve the degree of pulmonary fibrosis in rats. The effect may be related to the up-regulation of IL-38 and the downregulation of MIP-2.
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Objective: To observe the effect and mechanism of Jiedu Hugan decoction on drug-induced liver injury in rats by detecting serum liver function, serum biomarkers, inflammatory factors, macrophage inflammatory protein-2 (MIP-2) and macrophage inflammatory protein-1β (MIP-1β). Method: The rat model of drug-induced liver injury was induced by acetaminophen (1 g·kg-1) orally once daily for 30 days. The sixty male adult Wistar rats were divided into five groups, control group,model group,administered silybin group(44.1 mg·kg-1), Jiedu Hugan decoction high, medium and low dose groups (63,31.5,15.75 g·kg-1), normal group and model group were given normal saline gavage, and the other groups were given corresponding liquid gavage for 30 days. After the experiment, the abdominal aorta separation take blood serum aspartate amino transferase (AST), alanine aminotransferase (ALT), total bilirubin (TBIL), direct bilirubin (DBIL), malate dehydrogenase (MDH), enzyme for oxygen p1 (PON1) and glutamate dehydrogenase (GLDH), arginine (ARG), purine nucleotide phosphorylase (PNP), tumor necrosis factor-α(TNF-α), interleukin-6(IL-6) content. Pathological morphological changes of liver tissues were observed by hematoxylin-eosin (HE) staining. The protein expression of MIP-1β was observed by immunohistochemistry. The protein expression of MIP-2 was observed by single fluorescence immunohistochemistry, and the contents of TNF-α and IL-6 in liver homogenate were detected by enzyme-linked immunosorbent assay (ELISA). Result: Compared with normal group, levels of AST, ALT, DBIL, PON1, ARG, GLDH, MDH, PNP and TNF-α in model group were significantly increased (PPPPα in liver injury rats(PPβ protein expression, detoxification protect liver soup effect of the optimal dose group, the pathological morphology of liver cell dosage group were with different degree of protection. Conclusion: The effect of Jiedu Hugan decoction in medium dose group is better, and its mechanism may affect the chemotaxis of neutrophils induced by MIP-2 and MIP-1β by reducing the content of TNF-α, thus inhibiting the release of inflammatory factors and preventing inflammation.
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Objective To investigate the expression and variation of MIP 1β,MIP-2,and IL-12p70 in mice with bloodstream infection caused by 4 kinds of bacteria.Methods CD-1 (ICR) mouse models of bloodstream infection with Staphylococcus aureus (S.aureus),Enterococcus f aecalis (E.f aecalis),Escherichia coli (E.coli),and K lebsiella pneumoniae (K.pneumoniae) were established.After mice in each trial group and PBS control group were infected by bacteria for 0.5h,1h,3h,6h,12h,24h,and 48h,concentrations of MIP-1β,MIP-2,and IL-12p70 were detected by Luminex liquid suspension chip system.Results Concentrations of MIP-1β increased significantly 1h after bacteria was in blood,S.aureus,E.faecalis,E.coli,K.pneumoniae,and control groups were (134.5 ± 18.3),(61.5 ± 15.4),(3 354.0 ±809.0),(6 888.4 ± 1 100.2),and (28.9 ± 4.6) pg/mL respectively;the peak values of IL-12p70 were (389.3 ± 118.1),(127.6 ± 10.0),(42.2 ± 3.5),(62.8 ± 8.4),and (4.8 ± 0.3) pg/mL respectively.Concentrations of MIP-1β and MIP-2 in E.coli and K.pneumoniae groups were significantly higher than other trial groups and control group (all P＜0.01),while concentrations of IL-12p70 in S.aureus and E.faecalis groups were both significantly higher than E.coli,K.pneumoniae,and control groups (all P＜0.01).Conclusion Concentrations of MIP-1β and MIP-2 in E.coli and K.pneumoniae groups were both significantly higher than those in S.aureus and E.faecalis groups,while concentrations of IL-12p70 in S.aureus and E.faecalis groups were both significantly higher than those in E.coli and K.pneumoniae groups.The combination detection of multiple cytokines or chemokines are valuable in predicting gram-positive or gram-negative bacterial infection,and can provide basis for treatment of early infection.
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Objective To investigate the effect of naftopidil in the treatment of prostatitis in the elderly on MIP-2 and MIP-1αin serum and succus prostaticus.Methods 78 elderly patients with chronic prostatitis were randomly divided into the control group and the observation group, 39 cases in each group.The control group were treated with Diosmin routine treatment, the observation group were treated on the basis of the control group combined with naftopidil tablets in the treatment,2 groups were treated continuous for 8 weeks.MIP-2 and MIP-1αin serum and prostatic fluid before and after treatment were compared, and the maximum urine flow rate and clinical efficacy were compared after the treatment.Results compared with pre-treatment, MIP-2, MIP-1αin serum and prostate fluid in 2 groups after treatment decreased, NIH-CPSI and QOL scores in 2 groups decreased, the maximum urinary flow rate increased (P<0.05);compared with the control group, the levels of MIP-2, MIP-1αin the serum and prostatic fluid, NIH-CPSI and QOL of observation group were lower, and the maximum urine flow rate was higher (P<0.05);Compared with the control group, the total efficiency of the observation group was higher (P<0.05).Conclusion Naftopidil can significantly reduce the elderly patients with chronic non bacterial prostatitis and serum of patients with prostatic fluid MIP-2, MIP-1αlevel and improve pain in urination, dysuria symptoms.
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Objective To explore effect of diosmin on serum and prostatic fluid immune mediated factors and clinical effect in patients with chronic prostatitis.Methods 89 cases of old male patients with chronic non bacterial prostatitis were selected, and divided into two groups.The control group were treated with universal tablets, the experiment group were treated on the base of the control group with diosmin.12 weeks as a course.Clinic effect, adverse reaction rate, prostatic fluid MIP-2 and MIP-1αwere compared after treatment.Results Compared with control group, MIP-1αand MIP-2 in serum and prostatic fluid were lower(P<0.05),NIH-CPSI score and QOL scores were lower(P<0.05), total effective rate was higher than control group(P<0.05),the incidence of adverse reactions was lower(P<0.05).Conclusion Diosmin can reduce MIP-1α, MIP-2 in serum and prostate fluid of patients with chronic none bacterial prostatitis, and improve the pelvic pain, dysuria, sexual dysfunction and other symptoms, and has less adverse reaction.
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BACKGROUND: High mobility group box 1 (HMGB1) is a novel, late mediator of inflammation. This study compared the pro-inflammatory effects of LPS and HMGB1. The transcriptional factors that play an important role in mediating the HMGB1-induced stimulation of IL-8 were also evaluated. METHODS: RAW264.7 cells were stimulated with either LPS (100 ng/ml) or HMGB1 (500 ng/ml). The TNF-alpha, MIP-2 and IL-1beta levels in the supernatant were evaluated by ELISA at 0, 2, 4, 8, 12 and 24h after stimulation. An acute lung injury was induced by an injection of LPS (5 mg/kg) or HMGB1 (2.5 mg/kg) into the peritoneum of the Balb/c mice. The lung cytokines and MPO activity were measured at 4h (for LPS) or 24h (for HMGB1) after the injection. The transcriptional factor binding sites for NF-IL6, NF-kappaB and AP-1 in the IL-8 promoter region were artificially mutated. Each mutant was ligated with pIL-6luc and transfected into the RAW264.7 cells. One hour after stimulation with HMGB1 (500 ng/ml), the cell lysate was analyzed for the luciferase activity. RESULTS: The expression of MIP-2, which peaked at 8h with LPS stimulation, increased sequentially until 24h after HMGB1 stimulation. An intraperitoneal injection of HMGB1, which induced a minimal increased in IL-1beta expression, provoked the accumulation of neutrophils the lung. A mutation of AP-1 as well as NF-kappaB in the IL-8 promoter region resulted in a lower luciferase activity after HMGB1 stimulation. CONCLUSION: The proinflammatory effects of HMGB1, particularly on IL-8, are mediated by both NF-kappaB and AP-1.
Assuntos
Animais , Camundongos , Lesão Pulmonar Aguda , Sítios de Ligação , Proteína beta Intensificadora de Ligação a CCAAT , Citocinas , Ensaio de Imunoadsorção Enzimática , Proteína HMGB1 , Inflamação , Injeções Intraperitoneais , Interleucina-8 , Luciferases , Pulmão , Negociação , Neutrófilos , NF-kappa B , Peritônio , Regiões Promotoras Genéticas , Fator de Transcrição AP-1 , Fator de Necrose Tumoral alfaRESUMO
The pulmonary recruitment and activation of inflammatory cells, in particular, neutrophils is thought to contribute to lung injury resulting from dust exposure. MIP-2 (macrophage inflammatory protein-2) which is a member of C-X-C chemokine plays a key role in neutrophil recruitment to sites of tissue injury. Especially, mineral fiber induced pulmonary response is as a model for the neutrophil recruitment. Therefore, we evaluated the distribution of MIP-2 expression in lung tissue of mineral fiber exposed rat using immunohistochemical study and the relationship between degree of inflammation of lower respiratory tract and MIP-2 expression. Total cell counts in bronchoalveolar lavage (BAL) fluid in mineral fiber-exposed group were markedly increased compared with each control group even not in ceramic fiber group. Number of neutrophil in BAL fluid in mineral fiber-exposed group were markedly increased compared with each control group until 4th week but except ceramic fiber group. In chrysotile group, number of neutrophil in BAL fluid were markedly increased compared with control group at 8th week. Lung tissue instilled with all kinds of mineral fibers showed remarkable developments of bronchus associated lymphoid tissue (BALT) and small multiple granulomas but not for ceramic fiber group. In chrysotile group, multiple granuloma and inflammatory change were more profuse response compared with other groups. MIP-2 was predominently expresses in epithelial cells of bronchioles and bronchus and was express also found in macrophages with lung section at 1 week after fiber instillation. Small amount of epithelial cell associated MIP-2 was present in chrysotile at 8 week group. But MIP-2 was not seen in epithelial cells and macrophages in the lung tissue instilled with crocidolite, ceramic fiber and glass fiber at 8 weeks. Our finding suggest that MIP-2 is predominantly expressed in bronchial epithelial cells of lung from mineral fiber-exposed rat and correlated with inflammatory cell, especially neutrophil, recruitment and tissue reaction. And we documented that MIP-2 expression and neutrophil recruitment in man-made vitreous fiber-exposed rat, especially glass fiber, less than chrysotile.