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1.
The effects of Wumeiwan (WMW) on TNF-α, IL-6, IL-8, IL-10 and NF-κBp65 in rats with ulcerative colitis (UC) were investigated, the curative effectiveness of WMW vs salicylazosulfapyridine (SASP) was compared, and the action mechanism was analyzed. Fifty-Six Sprague-Dawley (SD) rats were randomly divided into four groups (n=14 in each group, with equal ratio of male and female): normal control group, model group, SASP group, and WMW group. Except normal control group, the rat UC models in the remaining three groups were established using the method of 2.4-dinitrochlorobenzene (DNCB) immunization and acetic acid local enema. The rats in model group, SASP group, and WMW group were treated with distilled water, SASP, and WMW respectively. The changes in the symptoms and signs were observed, and levels of IL-6, IL-8, TNF-α, IL-10 and the expression of NF-κBp65 in the colonic tissues were statistically analyzed. The results showed that the levels of IL-6, IL-8, and TNF-α were significantly increased (P〈0.01), while those of IL-10 significantly reduced (P〈0.01) after establishment of rat UC models as compared with normal control group. The levels of IL-6, IL-8, and TNF-α were obviously lower, but the level of IL-10 was obviously higher in WMW and SASP groups than those in model group (P〈0.05). The levels of IL-6, IL-8, and TNF-α were lower, while the level oflL-10 was higher in WMW group than in SASP group. NF-κBp65 was expressed negatively or weakly in normal colonic tissues. The positive expression rate of NF-κBp65 in WMW group and SASP group was obviously lower than in model group (P〈0.01), and there was significant difference between WMW group and SASP group (P〈0.05). It was concluded that rat UC model was established successfully. WMW could up-regulate the expression of IL-10, down-regulate the expression of TNF-α, IL-6, IL-8, and inhibit the NF-κBp65 activity to adjust immune function, indicating WMW had better curative effects on UC in rats. 相似文献
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Activation of NF-κB and its regulation on IL-6 expression during LPS-induced liver injury 总被引:2,自引:0,他引:2
Objective: To explore the kinetics of the activation of nuclear factor-kappa B (NF-κB) and its regulation of interleukin-6 (IL-6) expression during LPS induced liver injury. Methods: Kunming mice were randomly divided into 4 groups in order to observe the does effect relationship at 3h: normal saline solution (control) group, low (1 mg/kg), middle (5 mg/kg), and high (10 mg/kg) LPS-induced groups; 6 groups in order to observe the time-effect relationship of 5 mg/kg LPS injection: normal saline solution (control) group, 0.5, 1, 3, 5 and 8 h groups ; pyrrolidine dithiocarbamate (PDTC) intervened groups (3 h): normal saline solution (control) group, 5 mg/kg LPS, 200 mg/kg PDTC, and 200 mg/kg PDTC+5 mg/kg LPS groups. NF-κB activities of Kupffer cells were determined with electrophoretic mobility shift assay (EMSA) and expression levels of IL-6 were measured with enzyme-linked immunosorbent assay (ELISA). Results: Does-effect of NF-κB activities in Kupffer cells after LPS injection 3 h: NF-κB activation could be detected in 1 mg/kg LPS group, reached the highest level in 5 mg/kg LPS group, and persisted in 10 mg/kg LPS group; time-course after 5 mg/kg LPS injection: the DNA-binding activity was observable at 0.5 h after LPS injection, increased significantly at 3 h, and persisted for at least 8 h; in addition, antioxidant PDTC could inhibit the activation of NF-κB significantly. The kinetics of IL-6 level in liver tissues during LPS-induced liver injury were that IL-6 level after 3 h of injection increased first and then reduced; the same trend was observed in the time-course on IL-6 level after LPS injection; PDTC could significantly inhibit the release of IL-6. Correlation analyses revealed that IL-6 level was significantly and positively correlated with the activation of NF-κB. Conclusion : NF-κB in Kupffer cells can be activitied during LPS-induced liver injury to some extent, and NF-κB may have some regulation on the expression of IL-6. 相似文献
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Objective: To explore the role of activated liver X receptor α (LXRα) on the expressions of interleukin-1 receptor associated kinase-4 (IRAK-4) and NF-kappaB (NF-κB) in the inflammatory response which induced by LPS in the Kupffer cells and to investigate the possible mechanisms of LXRα negative regulation of inflammatory response. Methods: The Kupffer cells were isolated from male Kunming mice by collagen perfusion in situ. And these cells were divided into 4 groups: normal control group, LPS treatment group, LXRct agonist T0901317 treatment group, LPS and T0901317 combined treatment group. The LPS treatment group were treated with a final concentration of 1 μg/ml LPS in RPMI 1640 and cultured for 6 h, the T0901317 treatment group were treated with a final concentration of 5 μg/ml in RPMI 1640 and cultured for 24 h, and the combined treatment group received pre-culture for 24 h with a final concentration of 1μg/ml T0901317 in RPMI 1640 and then cultured for 6 h with a final concentration of 5 μg/ml LPS in RPMI 1640. All groups were cultured for 30 h. The expression of LXRα, IRAK-4 and NF-κB at mRNA and protein levels were detected by real-time PCR and Western blotting, and the TNF-α and IL-1β levels were detected by ELISA. Results: The levels of LXRα mRNA and protein were highest in T0901317 group, and lowest in LPS group (P〈0.05). The level of IRAK4 and NF-κB mRNAs and proteins were evidently lower in the Combined-treated group than in LPS group (P〈0.05). And the level of TNF-α and IL-1 were observed highest in LPS group (P〈0.05), but no difference among the Control group, T0901317 group and Combined-treated group (P〉0.05). Conclusion: These date suggest that the LXR agonists can effectively up-regulate the expressions of LXRα mRNA and protein and inhibit the inflammatory response. This may be via down-regulating the expressions of IRAK4 and NF-κB at mRNA and protein levels. 相似文献
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Role of Shenfu Injection (参附注射液) in rats with systemic inflammatory response syndrome 总被引:1,自引:0,他引:1
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Objective: To investigate the role of Shenfu Injection (参附注射液, SFI) in rats with systemic inflammatory response syndrome (SIRS). Methods: The SIRS rat model was induced by the intravenous injection of lipopolysaccharide (LPS). Forty-five male Wistar rats were randomly divided into 3 groups, the sham operative control group (control group, n=5), the SIRS model group (model group, n=20) and the SFI treatment group (SFI group, n=20). LPS was injected through the external jugular vein (12 mg/kg, 6 mg/mL) to all rats except for those in the control group, and SFI (10 mL/kg) was given to those in the SF group only once through intraperitoneal injection, while the normal saline (10 mL/kg) was given to those in the model group. For those in the control group, normal saline was given through the external jugular vein (2 mL/kg) and intraperitoneal injection (10 mL/kg). Then, rats in the model group and SFI group were divided into 4 subgroups according to the time points, i.e., 1 h, 2 h, 4 h and 6 h subgroups, 5 rats in each group. The activity of nuclear factor of κB (NF-κB) of in blood mononuclear cells and the plasma levels of tumor necrosis factor- α (TNF- α ) and interleukin 6-(IL-6) were determined using enzyme-linked immunoabsordent assay (ELISA) at 1 h, 2 h, 4 h and 6 h after modeling. Histopathologic changes of the lung and liver were observed under a light microscope. Results: Compared with the control group, the activity of NF-κB in mononuclear cells and the plasma level of TNF-α were obviously increased at each time points (all P〈0.01), reaching the peaks at 2 h after modeling. The plasma level of IL-6 increased gradually as time went by in the model group (P〈0.01). Pathological examination showed pulmonary alveoli hemorrhage, edema and inflammatory cell infiltration in the lung tissue, and angiotelectasis, congestion, and local necrosis in the liver tissue in the model group. Compared with the model group, the activity 相似文献
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To investigate the effect of TGF-β1 on the expressions of IL-12, IL-15, IL-18, IL-4 and IL-10 in heart transplantation rejection in rats, a model of rat cervical heterotopic heart transplantation was set up and the model rats were randomly divided into three groups: control group, transplant group and TGF-β1 group. The mRNA expression levels of IL-12, IL-15, IL-18, IL-4 and IL-10 were determined by RT-PCR at the 5th day after the transplantation. The mRNA expression levels of IL- 12, IL-15, IL-18 were increased obviously and those of IL-4, IL-10 were significantly decreased in the transplant group as compared with the control group (P〈0.01). In the TGF-β1 group, the mRNA ex- pression levels of IL- 12, IL- 15, IL- 18 were significantly decreased and those of IL-4, IL- 10 were significantly increased as compared with the transplant group (P〈0.01). The immunosuppressive effect of TGF-β1 on heart transplantation rejection was related to its inhibition of the expressions of Th1-type cytokines (IL-12, IL-15, IL-18 etc) and its promotion of the expressions of Th2-tpye cyto- kines (IL-4, IL-10). 相似文献
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Xue-rong CHEN Ya-li LIU Dun-zhen XIAO Jun GAO Reproductive Medicine Center Research Institute of Family Planning Tongji Medical College Huazhong University of Science Technology Wuhan China 《生殖与避孕(英文版)》2007,18(4):253-260
Objective To investigate the possible role of estrogen in the pathogenesis of vulvovaginal candidiasis(VVC). Methods Estrogen-dependent experimental murine model of C. albicans vaginal infection was established by injecting subcutaneously with estradiol benzoate and then 5×106 stationary-phase C. albicans blastoconidia was inoculated intravaginally to mice (group EI), and other 3 groups were set up: estrogen-treated but not infected (group E); estrogen-untreated but infected (group I); normal control (group C). The dynamic change of colony-forming unit (CFU) of cervivovaginal lavage fluid was observed. Vaginal tissues at different time points (d 2, d 4, d 7 and d 14) after inoculation of C. albicans were obtained. In situ hybridization staining was used to detect expression of cyclooxygenase-2 (COX-2) mRNA and expression of nuclear factor-κB (NF-κB) was examined by immuohistochemistry. ELISA was applied to determine the interlenkin-1β (IL-1β) level. Results The constitutional high level expression of COX-2 mRNA in the vaginal tissue of group E was significantly higher than that in group C on d 4 and d 7 (P<0.01), and the optical density (OD) in group EI was higher than that in the other 3 groups (P<0.05). There were higher IL-1a levels in vaginal tissues from d 4 to d 7 postin- oculation in group EI and group I than group C (P<0.01). Furthermore, IL-1β in group EI was markedly elevated on d 4 and d 7 compared with group I (P<0.01). Compared with group C, the expression of NF-κB in group E was increased obviously on d 4 (P<0.01), and there was significant difference between group EI and group Ion d 4 and d 7 (P<0.01). Conclusions In the murine model of estrogen-dependent experimental VVC, estrogen promotes the infection establishment by up-regulating expression of COX-2 via activating NF-κB signal pathway, and the high expression of COX-2 promoted by the interaction of IL-1β and NF-êB after infection formation was involved in persistence of infection. 相似文献
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This study investigated the effects of propofol on the mRNA expression of Toll-like receptor-4 (TLR4) in BV-2 cells during mimic ischemia-reperfusion (I/R) injury in vitro. BV-2 cells, a mouse microglia line, were cultured and divided into 4 groups at random: control group (group C), ischemia/reperfusion group (group I/R), low-dose propofol (25 μmol/L) intervention group (group PF25) and high-dose propofol (100 μmol/L) intervention group (group PF100). The mRNA expression of TLR4 and NF-κB was measured by means of RT-PCR. TNF-α levels in the supernatants of BV-2 cells were detected by ELISA. The results showed that the mRNA expression of TLR4 and NF-κB was significantly higher in groups I/R, PF25 and PF100 than in group C (P〈0.01). And the TNF-α level in the supernatants was elevated in groups I/R, PF25 and PF100 as compared with that in group C (P〈0.01). After pre-treatment with propofol, the mRNA expressions of TLR4 and NF-κB and the TNF-α level were significantly decreased in groups PF25 and PF100 in comparison to those in group I/R (P〈0.01). And the decrease in those indicators was more significant in group PF100 than in group PF25 (P〈0.01). It was concluded that propofol exerted brain-protecting effects during I/R injury by suppressing the mRNA expressions of TLR4 and NF-κB and deceasing the TNF-α level. 相似文献
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This study examined the effects of Bangdeyun on the expressions of nuclear factor-kappaB (NF-κB), interferon-gamma (IFN-y) and interleukin-10 (IL-10) in the endometrium of mice with embryo implantation dysfunction (EID) during the implantation time (namely on pregnancy day 5, 6, 7 and 8) and explored the local immune regulatory effects of Bangdeyun. The gestational mice were randomly divided into normal group, model group and Bangdeyun-treated group. EID models of mice were established by using indomethacin. The endometrial expression of NF-κB was detected by immunohistochemistry and Western blotting. IFN-γ and IL-10 were measured by enzyme-linked immunosorbent assay (ELISA). The results showed that in the normal group, NF-κB and IFN-γ were weakly expressed and IL-10 was strongly expressed in the endometrium during the whole implantation period. In the model group, the expressions of NF-κB and IFN-T were increased on pregnancy day 5, 6 and 7, and IL-10 expression decreased during the whole implantation time when compared with those in the normal group (P〈0.01 for all). In the Bangdeyun-treated group, little amount of NF-κB and IFN-γ was expressed and IL-10 expression was strong, much the way they were expressed in the normal group (P〉0.05). The expressions of NF-κB and IFN-T were much lower in the Bangdeyun-treated group than those in the model group on pregnancy day 5, 6 and 7 (P〈0.01 for all), while the expression of IL-10 was much higher than in the model group during the whole implantation time (P〈0.01). It was suggested Bangderun may favor a shift from Thl- to Th2-type immune response, therefore inhibiting the maternal immune rejection, inducing the immune tolerance and improving the fetal implantation. 相似文献
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Objective: To study the effect of TP chemotherapy regimen combined with Kanglaite in the treatment of cervical carcinoma and its effect on the serum level of CYFRA21-1 and CK19. Methods: 74 patients with cervical carcinoma were admitted in our hospital from October 2015 to May 2017 and were randomly divided into observation group and control group according to random digital table method, 60 cases in each group. The control group was treated with TP chemotherapy and the observation group was treated with TP chemotherapy regimen combined with Kanglaite. The clinical efficacy, the quality of life, serum CYFRA21-1 and CK19 levels and adverse reactions were compared between the two groups before and after treatment. Results: After treatment, the clinical effective rate(83.78%) in the observation group was significantly higher than that of control group (62.16%), u=4.390,P=0.036, with statistical significance(P<0.05). The KPS scores of the two groups were significantly decreased, and the KPS scores in the observation group were significantly higher than those in the control group(u=6.538,P=0.000). After treatment, the serum levels of CYFRA21-1 and CK19 were significantly decreased in both groups, and the levels in the observation group were significantly lower than those in the control group (u = 6.659, 8.647, P=0.000). The adverse reactions were mainly myelosuppression, gastrointestinal reaction and phlebitis. The incidences of myelosuppression and gastrointestinal reaction of grade III-IV in the observation group were significantly lower than that in the control group, while the incidence of phlebitis was significantly higher in the observation group than in the control group ((u = 2.160, 2.000, 4.16, P = 0.030, 0.045, 0.041, respectively). Conclusion: The effect of TP chemotherapy regimen combined with Kanglaite on cervical carcinoma is significantly. It can effectively reduce serum CYFRA21-1 and CK19 levels, improve the quality of life and safety, which is worth popularizing in clinical application. 相似文献
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The protective effects of diallyl trisulfide on liver were examined in rats with sepsis. Sepsis was reproduced in rats by cecum ligation and puncture (CLP). Fifty-six male Wistar rats were randomly divided into sham-operated group (group S, n=8), sepsis model group (group C, n=24), diallyl trisulfide (DATS)-treated group (group D, n=24). Animals in groups C and D were further divided into three subgroups according to different observation time points, with 8 rats in each sub-group.Rats in group D and C were intravenously injected with normal saline or DATS respectively at a dose of 20 mg/kg after the establishment of sepsis model. Eight rats in groups C and D were sacrificed at 3, 6 and 24 h post-CLP and their livers were harvested for detection of interleukin (IL)-1 receptor associated kinase-4 (IRAK-4), nuclear factor-κB (NF-κB), c-fos, c-jun, malondialdehydethhe (MDA) and superoxide dismutase (SOD), tumor necrosis factor alpha (TNF-α) and for pathological examination. The results showed that the levels of serum IRAK-4, NF-κB and TNF-α in hepatic tissues were higher in group C than group S (control group) (P<0.05). After DATS treatment, the levels of IRAK-4 and NF-κB in the hepatic tissues and serum TNF-α in group D were lower than those in group C (P<0.05). The levels of c-fos and c-jun and MDA in the hepatic tissues were higher in group C than in group S (P<0.05). After DATS treatment, the levels of c-fos and c-jun and MDA in the hepatic tissues were significantly lower in group D than in group C (P<0.05). When compared with group S group, concentration of SOD in the hepatic tissues in group C was significantly lower (P<0.05). After DATS treatment, the concentration of SOD in the hepatic tissues was higher in group D than in group C (P<0.05). These findings suggested that treatment with DATS could ameliorate sepsis-induced liver injury in rats. The protective effect might be related to its ability to inhibit the signal pathway of IRAK-4 and NF-κB, thereby decreasing the production o 相似文献
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Objective:To explore the effects of IL-10 on acute leukemic immune evasion. Methods: Plasma concentrations of IL-10 were measured by ELISA in 56 first-visit acute leukemic patients. And expressions of IL-10 on leukemic cells in 30 patients were measured by indirect immunofluorescence technique.Results: Compared with those in control group,IL-10 concentrations increased significantly in first-visit acute leukemic patients. And there was a slight but not significant decrease of IL-10 in patients with acute lymphocytic leukemia(ALL) compared with those with acute non lymphocytic leukemic(ANLL). After intensive chemotherapy,there was a significant decrease of IL-10 in completely remitted (CR) patients ,especially in those with ANLL,but there was still a significant increase compared with those in control group.The positive rate of cells giving out yellow-green bright fluorescence on membranes was 10%-80% ;there were 18 patients expressing IL-10(18/30,60%) positively:among them 11 with ANLL(11/19,58%) and 7 with ALL(7/11,64 %) respectively while that of peripheral mononucleate cells in control group was 13%.Compared with that in control group,there was a significant increase of positive rate in ANLL and ALL but with no significant difference between ANLL and ALL. Conclusion: Probably as one of important mechanisms of acute leukemic immune evasion,IL-10 secreted by leukemic cells,contributing to the immunosuppressive state at the tumor site ,increase significantly in acute leukemic patients. 相似文献
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Effects of therapeutic hypercapnia on inflammation and apoptosis after hepatic ischemia-reperfusion injury in rats 总被引:1,自引:0,他引:1
Background Therapeutic hypercapnia (TH) has been demonstrated to protect several organs ischemia-reperfusion injury.The study aimed to investigate the effects of therapeutic hypercapnia on hepatic ischemia-reperfusion injury (HIRI).Methods Thirty adult male Wistar rats weighing (250 ± 20) g were randomized into 3 groups (n=10 in each), group C (control group), group A (hypercapnia group) and group B (CO2 preconditioning group).A segmental ischemia of the liver was induced by interrupting the blood vessels including the bile duct to the median and left lateral lobes for 60 minutes and all the animals were sacrificed after 240 minutes observation period of reperfusion.Mean arterial pressure (MAP)and the blood gases were measured before ischemia (baseline) and at 30, 60, 120, 180 and 240 minutes after reperfusion.Arterial blood samples were obtained for determination of serum levels of TNF-α, IL-10, serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT).The histopathology of liver tissues was evaluated by light microscopy.The NF-κB expression and apoptotic hepatocytes were respectively determined by immunohistochemistry and TUNEL assay.Results The serum levels of liver enzymes and TNF-α were significantly decreased while the IL-10 level was significantly increased in groups A and B than in group C (P 〈0.05), and group B surpassed group A (P 〈0.05).The histopathological scores, the NF-κB immunohistochemical score (IHS) and apoptotic index were significantly lower in groups A and B than in group C (P 〈0.05), and the decrease in group B was more obvious than in group A (P〈0.05).Conclusion Therapeutic hypercapnia attenuates ischemia-reperfusion injury to the liver.Moreover, the effects of CO2preconditioning are outstandingly notable. 相似文献
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This study investigated the effects of propofol on the mRNA expression of Toll-like receptor-4 (TLR4) in BV-2 cells during mimic ischemia-reperfusion (I/R) injury in vitro. BV-2 cells, a mouse microglia line, were cultured and divided into 4 groups at random: control group (group C), ischemia/reperfusion group (group I/R), low-dose propofol (25 μmol/L) intervention group (group PF25) and high-dose propofol (100 μmol/L) intervention group (group PF100). The mRNA expression of TLR4 and NF-κB was measured by means of RT-PCR. TNF-α levels in the supernatants of BV-2 cells were detected by ELISA. The results showed that the mRNA expression of TLR4 and NF-κB was significantly higher in groups I/R, PF25 and PF100 than in group C (P<0.01). And the TNF-α level in the supernatants was elevated in groups I/R, PF25 and PF100 as compared with that in group C (P<0.01). After pre-treatment with propofol, the mRNA expressions of TLR4 and NF-κB and the TNF-α level were significantly decreased in groups PF25 and PF100 in comparison to those in group I/R (P<0.01). And the decrease in those indicators was more significant in group PF100 than in group PF25 (P<0.01). It was concluded that propofol exerted brain-protecting effects during I/R injury by suppressing the mRNA expressions of TLR4 and NF-κB and deceasing the TNF-α level. 相似文献
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Background Hyperglycemia in brain and spinal cord could aggravate neurologic impairment. Recent studies showed that L-lysine monohydrochlonde (LMH) could increase the insulin secretion and regulate the blood glucose level. The aim of the present study was to investigate the effects of LMH on pancreatic islet B cells, the levels of endogenous insulin and blood glucose in spinal cord injured rats.Methods Forty male Wistar rats were divided into four groups, namely, normal control group, model group, high-dose LMH group (621.5 mg/kg equal to LMH 1/8 LD50), and low-dose LMH group (310.8 mg/kg equal to LMH 1/16 LD50). The model of spinal cord injured rat was established by hemi-transection at the lower right thoracic spinal cord. LMH was administered via intraperitoneal injection once spinal cord injury was produced in rats. All rats were sacrificed 48 hours after spinal cord injured. The effects of LMH on pancreatic islet B cells, the content of endogenous insulin, end the level of blood glucose were observed with immunohistochemical method, radioimmunoassay method, end biochemical analyzer, respectively. Results The insulin immunohistochemical intensities of islet B cells were significantly weaker in model group then those in normal control group (P 〈0.01). The levels of endogenous insulin were significantly lower and the blood glucose levels were significantly higher in model group than those in normal control group (P 〈0.01). The insulin immunohistochemical intensities of islet B cells were significantly stronger in high-dose LMH group then those in model group (P〈0.05). In addition, we found that the levels of endogenous insulin were significantly higher and the blood glucose levels were significantly lower in high-dose LMH group then those in model group (P 〈0.05). There were no significant differences in the insulin immunohistochemical intensities of islet B cells, the levels of endogenous insulin and the blood glucose between low-dose LMH group and model group (P 〉0.05). Conclusion LMH, but dose-dependent, might participate in the regulation of pancreatic islet B cells, and then reduce the blood glucose levels in the spinal cord injured rats. 相似文献
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Summary: The expression of TNF-α in the liver at different periods post Schistosoma japonica infection and the effect on liver fibrosis after supplementary injection of these cytokines were investigated. The mice infected with schistosome cercariae were divided into 3 groups., normal control group, TNF-α-untreated infection group and TNF-α-treated infection group. ABC immunohistochemistry and pathologic image multimedia quantification system were applied to dynamically detect the activity of TNF-α. The results showed that the levels of TNF-α in the liver in TNF-α-untreated infection group were slowly decreased with prolongation of infection time (from 8th, 11th, 14th to 18th week), while in the TNF-α-treated infection group, those were increased significantly after intraperitoneal injection of TNF-α at 6th week after infection. At first to 8th week after the final injection of TNF-α, the intrahepatic TNF-α levels in the TNF-α-treated infection group were significantly higher than in the other two groups (P〈0.01), and the granulomatous inflammation and fibrosis in the liver were also milder in the normal control group. It was concluded that at the early stage of Schistosoma japonica infection mouse liver mainly released Thl cytokine and TNF-α from Thl activated macrophages. Six weeks after infection (post egg deposition), exogenous supplement with intraperitoneal injection of TNF-α could induce the enhanced expression of Thl cytokines and alleviate the liver granulomatous inflammation and fibrosis. 相似文献
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Regulatory effect of Langchuang serial recipes on T-lymphocyte subsets Th and Tc in patients with systemic lupus erythematosus
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Objective: To study the principle of clearing Fei (肺), cooling blood, and detoxification as well as nourishing yin and moisening Fei (abbr. as CCD-NM) in regulating the levels of peripheral T-lymphocyte subsets Th and Tc cells to explore its mechanism for lowering the incidence of infection in patients with systemic lupus erythematosus iSLE). Methods: Sixty SLE patients without complicated infection were assigned to the treatment group and the control group, 30 in each group. The control group was treated with Western medicine alone, while the treatment group was treated with the same program of Western medicine, but additionally administered with either Langchuang No.1 (狼疮 Ⅰ号) or 2 (狼疮 Ⅱ 号), serial concerted Chinese recipes, applied respectively in patients in the active stage or in the resting stage. The total time of treatment for both groups was 1 year. Further, a healthy control group was set up with 20 healthy subjects. The expressions of Thl, Th2, and Tcl and Tc2 cells in peripheral blood were detected and compared with those in the healthy control group. Results: (1) As compared with the healthy control group, ratios of Thl/Th2 and Tcl/Tc2 in SLE patients, whether complicated with infection or not, were significantly lower (P〈0.05 or P〈0.01). (2) Comparison between patients with complications and those uncomplicated with infection showed that the two ratios and Thl expression were lower and Tc2 was higher in the former than those in the latter (all P〈0.05). (3) Ratios of Thl/Th2 and Tcl/Tc2 increased after treatment in patients of both the treatment group and the control group (P〈0.05 and P〈0.01), but the changes in the treatment group were more significant (P〈0.05). Conclusion: The principle of CCD-NM could regulate the Th and Tc subsets toward equilibrium in SLE patients, which might be one of the mechanisms of action for alleviating complicated infection. 相似文献
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Structural and functional changes of immune system in aging mouse induced by D-galactose 总被引:6,自引:0,他引:6
Deng HB Cheng CL Cui DP Li DD Cui L Cai NS 《Biomedical and environmental sciences : BES》2006,19(6):432-438
Objective To investigate the role of D-galactose, especially in the structural and functional changes of the immune system in aging. Methods Serum levels of advanced glycation end-products (AGE) were determined by ELISA method. Ultra-structures of thymus and spleen were detected by transmission electron microscopy. MTT method was used to determine the lymphocyte proliferation. IL-2 activity was determined by bioassay. Northern blot was used to detect the IL-2 mRNA levels. Results Serum AGE levels of D-galactose- (P〈0.01) and AGE-treated (P〈0.05) mice (n=8) were increased significantly. The ultra-structures of thymus and spleen in D-galactose- and AGE-treated mice showed regressive changes similar to those in the aged control group. The lymphocyte mitogenesis and IL-2 activity of spleen were also decreased significantly (P〈0.01, n=8). The change of IL-2 activity shown by Northern blot resulted from the change of mRNA expression. The AGE plus aminoguanidine group, however, showed no significant change in these parameters in comparison with the young control group (P〈0.01 or P〈0.05, n=8). Conclusion D-galactose and AGE lead to a mimic regression change of aging in the immune system in vivo. 相似文献