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Aim To study the antiviral anrl antipyretic mechanism of Phillvrin in vitro and in vivo.Methods By respiratory virus infection cell model, SI index and antiviral activity of forsythia glycosides virus activity in vitro were detected.A mouse model of influenza virus infection was established, and hemagglutination titer, lung index, lung histopathology pathology were detec¬ted.Hemagglutination titer, lung index, lung histopa¬thology pathology were observed and in vivo anti-influ¬enza virus and pneumonia effects were investigated.Dry yeast induced rat fever model was established, temperature and plasma and hypothalamus thermoregu¬lation and inflammation of the related factors were test¬ed , and its antipyretic mechanism was investigated.By AutoDock Vina software for molecular docking, the docking results were plotted with PyMol software.Re¬sults Phillyrin had certain inhibitory effects on H3N2, RSV, E71 , ADV-3, HSV-1 and HSV-2 (SI >2).Phillyrin could reduce hemagglutination titer of infected lung tissue, decrease lung index, and alleviate lung lesions, especially interstitial pneumonia.Phill- vrin could also significantly reduce the body tempera¬ture of rats with fever, and its antipyretic mechanism might he related to the decrease of PGE2 and IL-ip levels in plasma and hypothalamus of rats.Molecular docking results showed that the binding energies of Phillyrin with a-MSH, IL-lp, PEG2, A VP, cAMP and other proteins were all less than - 5 kcal • mol 1.Conclusions Phillyrin has obvious antiviral, antipy-retic and improvement of pulmonary inflammatory le¬sions, and it is speculated that it can play an anti-in¬fluenza effect through "treating both symptoms and root causes".
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Resumen Leptospirosis es una enfermedad re-emergente de distribución mundial ocasionada por espiroquetas patogénicas del género Leptospira que afectan humanos, animales domésticos o silvestres. Las manifestaciones clínicas de la enfermedad son diversas y son el resultado de la interacción de la respuesta inmune del hospedador y las condiciones de virulencia propias de las especies patógenas. Aunque se desconocen muchos aspectos de la inmunidad en la infección por Leptospira spp, es reconocido que los hospe deros susceptibles presentan diferencias en su respuesta inmune, como la activación/evasión del sistema del complemento, la activación de sub poblaciones celulares, la producción de citoquina y el desarrollo de anti cuerpos. El estudio del perfil inmunológico en pacientes con leptospirosis ha sido documentado y contribuye en la identificación de biomarcadores asociados con severidad. Esta revisión presenta algunos de los eventos relacionados con la respuesta inmune desde el ingreso de la bacteria en la fase inicial de la infección hasta su multiplicación y generación de enfer medad en el humano.
Abstract Leptospirosis is a re-emergent disease of worldwide distribution caused by pathogenic spirochetes of the Leptospira genus that affect humans, do mestic and wild animals. The clinical manifestations of the disease are diverse and are the result of the interaction of the immune response of the host and the virulence conditions of the pathogenic species. Although many aspects of immunity in infection with Leptospira spp are unknown, it is recognized that susceptible hosts show differences in their immune res ponse, such as activation / evasion of the complement system, activation of cellular subpopulations, production of cytokines, development of anti bodies. Study of the immunological profile in patients with leptospirosis has been documented and contributes in the identification of bio-markers associated with severity. This review presents updated events related to the immune response from the entry of the bacteria in the initial phase of the infection to its multiplication and generation of human disease.
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Objective To investigate the relationship between cellular immune response which is related with Th1/Th2 cells and the different severities of tuberculosis pleural effusion adhesion.Methods A total of 66 in-patients diagnosed with different severities of tuberculosis pleural effusion adhesion by internal thoracoscope were enrolled from August 2014 to December 2016.ELISA was used to determine levels of INF-γ,TNF-α,IL-2 and IL-4. The ratio of Th1 and Th2 cells was detected by flow cytometry. Results All the patients were divided into 3 groups:9 cases without pleural adhesion,32 cases with mild pleural adhesion,25 cases with severe pleural adhe-sion. The levels of 4 cytokines in pleural fluid were significantly higher than those in serum in each group(P <0.05,respectively).The concentrations of INF-γ and TNF-α were increased with the severity of tuberculosis pleu-ral effusion adhesion. The levels of INF-γ and TNF-α in the severe pleural adhesion group were markedly higher than those in the other two groups(P<0.05,respectively).The proportion of Th1 cells in the severe pleural adhe-sion group was significantly higher than that in the none pleural adhesion group and in the mild pleural adhesion group(P<0.05,respectively).Conclusions The proportion of Th1 cells and levels of INF-γ and TNF-α are pos-itively related with pleural adhesion severity. Cellular immune response which is related with Th1 cells contributes to pathological immune pleural damage and intensify the severity of pleural adhesions.
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Objective To investigate the regulation mechanism of silencing the DUSP1 gene on the release of proinflammatory cytokines in mice with acute pancreatitis(AP). Methods Two DUSP1 - siRNA and one scramble siRNA sequences were designed,and the sequence with higher silence efficiency was selected. Mice models with AP were established,and KM mice were divided into 6 groups:control group,AP group,AP + PD98059 group,AP + scram-ble group,AP + siRNA group and AP + PD98059 + siRNA group. Expressions of proinflammatory cytokines tumor necro-sis factor - α(TNF - α),interleukin(IL)- 1β and IL - 6 in serum were detected by using enzyme linked immunosor-bent assay(ELISA)after 12 h,24 h,48 h of modeling. Serum amylase levels were detected. The mRNA expression levels of DUSP1,TNF - α,IL - 1β and IL - 6 in pancreatic tissues were detected by using quantitative real time poly-merase chain reaction (qPCR). The protein expression levels of DUSP1,extracellular regulated protein kinases(ERK), c - Jun N - terminal kinase(JNK),p38,p - ERK,p - JNK and p - p38 in pancreatic tissues were detected by using Western blot. Results Compared with the control group,the other 5 groups displayed the increased expressions of TNF - α,IL - 1β,IL - 6 and amylase in serum,and expressions of DUSP1,TNF - α,IL - 1β,IL - 6,p - ERK,p -JNK,p - p38 in tissues,and there was a statistical significance (all P < 0. 05). Compared with the AP group,the AP +PD98059 + siRNA group showed the decreased DUSP1 expression in tissues,and there was a statistical significance (all P < 0. 05);the AP + PD98059 group had decreased expressions of TNF - α,IL - 1β,IL - 6 and amylase in serum,and expressions of TNF - α,IL - 1β,IL - 6,p - ERK,p - JNK,p - p38 in tissues,and there were statistical significances (all P < 0. 05);while the opposite results were observed in the AP + siRNA group with DUSP1 expression decreased. Conclusions The results support that silencing the DUSP1 gene promotes the release of proinflammatory cytokines through activating the mitogen - activated protein kinase signaling pathway in mice with AP.
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Tumor metastasis is one of the most important biologi-cal characteristics of malignant tumor, and it is also the main factor resulting in poor prognosis and leading to failure of treat-ment. In recent years, studies have shown that the extracellular matrix ( ECM) of tumor microenvironment plays a critical role in tumor metastasis. Tumor ECM fibrogenesis could form the cross-linked network structure, which not only provides nutrition and support to tumor, also it is necessary to tumor growth and inva-sion. These research results indicate that blocking ECM fibro-genesis may exert an inhibitory effect on tumor metastasis. Therefore, targeting ECM fibrogenesis has become a particularly attractive strategy as it can be used in the treatment of metasta-sis-related diseases. The ECM fibrogenesis in tumor is reviewed in this paper as well as the treatment strategies on tumor metas-tasis by targeting ECM fibrogenesis, which may provide refer-ences for follow-up research and clinical treatment.
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Aim Tostudytheinfluencesofsulfated polysaccharides ( SPPM60-D) on the regulation of free calcium concentration ( [ Ca2+] i ) of T lymphocytes of mice in vitro and explore the mechanisms involved. Methods Polysaccharides(PPM60)wereextracted from masson pine pollen with hot water and 60% etha-nol. PPM60-D was separated and purified from PPM60 with Sephacryl S-400HR. Sulfated polysaccharides ( SPPM60-D ) were derivated by chlorosulfonic acid-pyridine method and the [ Ca2+] i of T lymphocytes were measured by fluorescence spectrophotometer. IL-2 and IL-4 were measured by ELISA kits. Results ConAandSPPM60-Dcouldincrease[Ca2+]iinT lymphocytes by 211. 5% and 201. 8% respectively ( P<0. 01). 2-APB, LY294002, U73122 and verapamil rather than TAK-242 could significantly inhibit the in-crease of [ Ca2+] i induced by SPPM60-D. SPPM60-D could significantly increase the level of IL-2 and IL-4 in supernatant ( P <0. 01 ) . 2-APB rather than TAK-242 could significantly inhibit the increase of cyto-kines.Conclusion ItisspeculatedthatSPPM60-D could increase [ Ca2+ ] i via TCR/CD3-PI3K-PLC-IP3 R-Ca2+ signal pathway through TCD/CD3 receptor in T lymphocytes so that it could improve the level of IL-2 and IL-4 in supernatant in T lymphocytes.
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<0.01). It was suggested Bangderun may favor a shift from Th1-to Th2-type immune response, therefore inhibiting the maternal immune rejection, inducing the immune tolerance and improving the fetal implantation.
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Objective To determine the diversity of Porphytomonas gingivalis lipopolysaccharide (LPS)induced IL-1β,TNF-αand IL-6 levels in THP-1 cells and the associated Toll-like receptors(TLR).Methods P.gingivalis strain ATCC33277 LPS (Pg-LPS)was prepared using phenol-water method and then identified by both infrared spectrometry and limulus test.The levels of IL-1β,TNF-α and IL-6 secreted by THP-1 cells under inducement of Pg-LPS were quantitatively detected using commercial ELISA kits.The bloc-king test using TLR2 or TLR4 monoelonal antibody(McAb)plus the ELISA were used to determine the types of Pg-LPS binding TLR on the surface of target cells.In this study.a commercial LPS from E.coli strain O111:B4(E-LPS)was used as the contr01.Results When 1彬ml ofPg.u,s induced THP.1 ceHs for0.5,6 and 6 h.or l∥rnl ofE-LPs induced for 6,24 and 24 h,respectively,tIIe levels ofTNF.a,IL-1B and IL广6 were in.creased obviously(P<0.01).However,the maximal concentration of tlle t11ree cytokines induced by Pg.LP$ were similar to that induced by E-LPS(P>0.05).tLR2 or TLR4 McAb could block the effects of Pg-LPS in-ducing THP-1 cells to secrete IL-1β and IL-6(P<0.05),where as only TLR2 McAb displayed the inhibition of TNF-α secretion(P<0.05).On the contrast,only TLR4 McAb showed the effects blocking the three cytokines secretion in the THP-1 cells under inducement of E-LPS(P<0.05).Conclusion Pg-LPS shows a slight high-er activity inducing THP-1 cells to secrete IL-1β,TNF-α and IL-6 than E-LPS.TLR2,but not TLR4,is the major receptor of Pg-LPS on the target cells to mediate the secretion of the three cytokines.
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Residual renal function rapidly declines after the initiation of hemodialysis and its mechanisms are supposed to be associated with frequent hypotensive episodes during hemodialysis and subsequent ischemic injury to remnant nephron, but blood-membrane interaction might play an important role because of its ability to activate complement system and other various humoral and cellular mechanisms. Blood monocytes are activated by complements, bacterial contaminants and activated monocytes are known to secrete multiple proinflammatory cytokines such as TNF-alpha, IL-1 beta. The expression of TNF-alpha and IL-1 beta in mRNA and protein level were examined by RT-PCR and ELISA respectively in patients with ESRD after the initiation of hemodialysis. Author also investigated the mRNA expression of Fas in human proximal tubular cell culture in the presence of TNF-alpha and PBMC culture supernatant before and after the initiation of hemodialysis. Compared to PBMC separated before the initiation of HD, the amount of cytokine mRNA from PBMC separated after the initiation of HD showed increased tendency from 0.97+/-0.2 to 1.12+/-0.28 for TNF-alpha(p=0.29), from 1.03+/-0.18 to 1.10+/-027 for IL-1 beta (p=0.54). TNF-alpha and IL-l beta protein level in PBMC culture supernatant also showed increased tendency from 2.25+/-0.5 to 4.254+/-3.77 for TNF-alpha (p=0.10), from 3.5+/-2.08 to 4.0+/-4.3 for IL-1 beta(p=0,25). TNF-alpha increased Fas mRNA expression dose-dependently compared to control but it was not statistically significant(p=0,37, 0.22). Compared to the the level of Fas expression in HPTC cultured in the presence of pre HD PBMC supernatant, the level of Fas expression increased significantly in the presence of post HD PBMC supernatant (0.64+/- 057 vs 1.05+/- 0.12, p=0.01). As a conclusion, cytokine gene expression and secretion can increase as a result of blood-membrane interaction and these might have some influence on the loss of residual renal function in CRF patients maintained on hemodialysis.