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1.
AIM:To investigate the mechanism of tetramethylpyrazine (TMP) in treating collagen-induced arthritis (CIA) in rats. METHODS:The rat model of type II collagen-induced arthritis was established and the rats were randomly divided into normal control group, CIA group and TMP treatment group. The protein expression of matrix metalloproteinase 13 (MMP-13) in paw tissues was detected by immunohistochemical staining and Western blotting. The histopathological changes of the skin in the rat paws were observed with HE staining. The levels of vascular endothelial growth factor (VEGF), interleukin 17 (IL-17) and interleukin 23 (IL-23) in the serum of CIA rats were detected by ELISA. RESULTS:Compared with CIA group, TMP at a dose of 100 mg/kg significantly reduced the weight loss in CIA rats and decreased the protein expression of MMP-13 by 31.82%. TMP also attenuated the pathological changes of the paw subcutaneous tissues. TMP obviously decreased the levels of VEGF by 33.33%, IL-17 by 27.40% and IL-23 by 33.33% in the serum. CONCLUSION:TMP significantly inhibits the development of CIA by decreasing the protein expression of MMP-13, inhibiting the inflammatory cell infiltration and vascular proliferation, and reducing the production of VEGF, IL-17 and IL-23 in CIA rats.  相似文献   

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AIM To investigate the effect of bortezomib, a protease inhibitor, on the treatment of rheumatoid arthritis (RA) and it mechanism, based on interleukin-33 (IL-33)/suppression of tumorigenicity 2 (ST2) signaling pathway. METHODS A total of 40 Wistar rats were randomly divided into 4 groups: control group, model group, and low- and high-dose bortezomib groups, with 10 rats in each group. In addition to control group, the rats in other groups were used to construct RA model. Bortezomib was given intraperitoneally at 0.2 mg/kg and 0.5 mg/kg in low- and high-dose bortezomib groups, respectively, while the rats in control group and model group were injected with the same amount of saline, once a day for 21 d. The general situation of the rats in each group was observed, the swelling degree of the foot was calculated, and the inflammation score was evaluated. HE staining was used to observe the pathological changes of ankle joint. The automatic biochemical analyzer was used to detect blood hemoglobin content, the total number of platelets (PLT), serum creatinine (SCr) level and blood urea nitrogen (BUN) level. The serum levels of IL-6, tumor necrosis factor-α (TNF-α), IL-33 and ST2 were measured by ELISA. The protein expression of IL-33 and ST2 in ankle tissues of each group was determined by Western blot. RESULTS On the 7th, 14th and 21th days after modeling, compared with control group, the degree of paw swelling in model group was significantly increased (P<0.05). Compared with model group, the swelling degree of paw in low- and high-dose groups was decreased (P<0.05). At the end of administration, compared with control group, the synovial cells in model group were increased and in disorder, with a lot of inflammatory exudates in the articular cavity, and the inflammatory score, the levels of PLT, SCr and BUN, the serum levels of IL-6, TNF-α, IL-33 and ST2, and the protein expression of IL-33 and ST2 in ankle tissues were significantly increased (P<0.05). Compared with model group, the inflammatory exudates in the articular cavity of the rats in low- and high-dose bortezomib groups were decreased, and the inflammatory score, the levels of PLT, SCr and BUN, the serum levels of IL-6, TNF-α, IL-33 and ST2, and the protein expression of IL-33 and ST2 in ankle tissues were decreased (P<0.05). CONCLUSION Bortezomib may reduce the inflammation and swelling of the joints in RA rats by regulating the IL-33/ST2 signaling pathway.  相似文献   

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AIM: To investigate whether and how AT1 receptor blocker, valsartan, attenuates left ventricular remodeling and failure in a rat model of adriamycin(ADR)-induced dilated cardiomyopathy. METHODS: Weight-matched adult male Wistar rats were randomly divided into 3 groups as follows: 1) the ADR group, in which 2.5 mg/kg of ADR was weekly injected via a tail vein for 10 weeks (n=25); 2) concomitant AT1 receptor blocker valsartan and ADR, in which valsartan was administered by daily gavage at a dose of 30 mg·kg-1·d-1 (n=10); 3) control group (n=10). Hemodynamics and echocardiographic measurements were obtained at 12 weeks after treatment. Finally, left ventricle (LV) samples were collected at 12 weeks. The hydroxyproline content was determined by the methods of chloramines T. The expression of MMP-2, MMP-9 and tissue inhibitors of metalloproteinase-1 (TIMP-1) were measured by Western blotting. MMP-2 and -9 gelatinolytic activities were measured by gelatin zymography. RESULTS: Mortality was significantly lower in valsartan -treated rats than that in ADR rats (20% versus 40%, P<0.01). The dilatation of LV cavity was significantly attenuated in ADR-induced dilated cardiomyopathy rats given valsartan. Valsartan partially normalized LV contractile function, which was significantly reduced in ADR rats. The hydroxyproline content was increased in ADR-DCM group and significantly reduced by valsartan treatment (P<0.01). The protein levels of LV MMP-2 and MMP-9 were increased in ADR rats and attenuated by valsartan treatment (both P<0.01). However, no change in TIMP-1 was observed (P>0.05). The activities of LV myocardial MMP-2 and -9 gelatinolytic were increased significantly in ADR rats (both P<0.01) and attenuated by valsartan treatment (both P<0.01). CONCLUSION: Pretreatment with AT1 receptor blocker valsartan attenuates left ventricular remodeling and failure in a rat model of adriamycin-induced dilated cardiomyopathy.  相似文献   

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AIM: To determine whether triptolide induce apoptosis of synovial cells in collagen-induced arthritis (CIA) in rats. METHODS: The male Wistar rats were used to make CIA models by immunized with Bovine collagen Ⅱ (BCⅡ) in Freund's complete adjuvant (FCA). A total of 20 CIA rats were randomly divided into 2 groups, triptolide group (10 rats) and CIA control group (10 rats). Triptolide group were administered with triptolide at 40 μg/kg body weight intramuscularly every three days. CIA control group and another 10 age-matched normal rats were given normal saline instead. The rats were sacrificed on the 31st day after the triptolide administration. The pieces of synovium of the rat knee joints were harvested. The synovium was examined by HE staining and electron microscope. The apoptosis was tested by TUNEL and flow cytometer. RESULTS: The earlier phase of apoptotic synoviocytes were observed under the electron microscope. The flow cytometry showed that the percentage of the apoptotic cells was (3.98±1.16)% in the triptolide group, (1.83±0.82)% in the CIA control group, and (0.87±0.24)% in the normal group (P<0.01: triptolide vs control group). While the percentage of the cells in DNA synthesis phase was (3.3±1.2)% in the triptolide group, (8.0±1.4)% in the CIA control group, and (3.4±0.7)% in the normal group. There is significantly different in the apoptosis changes between the triptolide group and the CIA control group (P<0.01: triptolide vs CIA control group). The TUNEL labeling demonstrated that the percentage of the apoptotic cells was (4.5±1.0)% in the triptolide group, (2.2±1.0)% in the CIA control group, and (1.0±0.4)% in the normal group. The difference of apoptotic rate between the triptolide group and the CIA control group is significant (P<0.01). CONCLUSION: This study demonstrates that triptolide can induce apoptosis in CIA rats, which may be one of the mechanisms that triptolide treats the rheumatoid arthritis.  相似文献   

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AIM:To investigate the effects of IL-13 on expression of IL-1β in acute renal ischemia/reperfusion injury.METHODS:Fifty-seven male Wistar rats were randomly divided into 8 group: normal group, sham operation group, ischemia group, ischemia/reperfusion injury group(I/R), normal saline(NS)-treated group 1(C-1), NS-treated group 2(C-2), IL-13-treated group1(T-1)and IL-13-treated group 2(T-2).Rats were subjected to 45 min bilateral renal ischemia followed by reperfusion. rmIL-13 (1.5 μg/50 g body weight )was injected into the renal arteries through the abdominal aorta before ischemia(T-1) or immediately afterischemia(T-2).The serum level of IL-1β and the renal expression of IL-1β were determined in each group at 24 h post-ischemia. In addition, BUN, Cr and renal histology were also measured.RESULTS:(1)The serum level of IL-1β, gene expression and protein production of IL-1β in kidney decreased markedly in IL-13-treated groups.(2)Renal function and histology were significantly improved in IL-13-treated groups, renal injury scores decreased significantly.(3)A positive correlation were found between the serum level of IL-1β and BUN, SCr(r=0.708, P<0.01;r=0.770, P<0.01).CONCLUSION:These data suggest that IL-13 inhibit the expression of IL-1βand improve func-tion and histology of kidney in acute renal ischemia/reperfusion injury.  相似文献   

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AIM: To investigate the liver protective effects of polysaccharides of Dicliptera chinensis (L.) Nees. on fulminant hepatitis caused by D-galactosamine (D-GalN)/lipopolysaccharide (LPS) in rats. METHODS: Male Wistar rats were divided into 4 groups (12 rats in each group), including normal control group, GalN/LPS-treated group, and two Dicliptera chinensis (L.) Nees. polysaccharides-treated groups (150 mg/kg, 300 mg/kg, ig, respectively). The Dicliptera chinensis (L.) Nees. polysaccharides and controlled normal saline (NS) were administered once 1 d for 6 d. One hour after the latest administration, all animals except for the animals in control group were administered with D-GalN (500 mg/kg, ip), then treated with LPS 1 h later. The mortality was observed at 6 h and 12 h after modeling. The serum samples were collected at 6 h and 12 h in the survival rats by retro-orbital sampling. All samples were measured for ALT, AST, TNF-α and IL-1β. The samples collected at 12 h were also detected for NO. At 12 h, all survival rats were sacrificed and liver section was prepared for histological evaluation. RESULTS: Pretreatment with polysaccharides of Dicliptera chinensis (L.) Nees. significantly improved the histopathological changes and attenuated GalN/LPS-induced severe hepatotoxicity as evidenced by decrease in the levels of ALT and AST. The polysaccharides of Dicliptera chinensis (L.) Nees. inhibited the elevated levels of TNF-α, IL-1β and NO. CONCLUSION: Using Dicliptera chinensis (L.) Nees. polysaccharides as anti-inflammatory reagent provides a definite protective way against fulminant hepatitis caused by GalN/LPS in rat.  相似文献   

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AIM: To study the effects of Xingnao enema fluid on brain injury and IL-33/ST2 signaling pathway in rats after cardiopulmonary resuscitation, and to explore the brain protective effect and mechanism of Xingnao enema fluid. METHODS: SD rats were randomly divided into sham operation group, model group, low-dose (5 mL/kg), middle-dose (10 mL/kg) and high-dose (20 mL/kg) Xingnao enema liquid groups, and ulinastatin group, with 12 rats in each group. Except for the rats in sham operation group, the rats in other groups were used to establish the model of cardiopulmonary resuscitation and were treated with Xingnao enema fluid and ulinastatin. Seven days later, all rats were scored for neurological deficit. The rats were sacrificed, and the water content of brain tissues was calculated. Hematoxylin-eosin (HE) staining was used to detect the pathological changes of brain tissues of the rats in each group. The levels of super-oxide dismutase (SOD) and malondialdehyde (MDA) were detected in the brain tissue. The levels of S100 calcium bin-ding protein beta subunit (S100β) and neuron-specific enolase (NSE) in serum, and interleukin (IL)-1β and tumor necrosis factor (TNF)-α in brain tissue were measured by ELISA. The expression of interleukin-33 (IL-33) and growth stimulation expressed gene 2 (ST2) in brain tissue was determined by Western blot. RESULTS: Compared with sham operation group, the brain tissue of model group showed tissue disorder, focal hemorrhage, neuronal nucleus contraction, apoptosis and other pathological changes, and the neurological deficit score was increased. The water content of brain tissue, the le-vels of S100β, NSE, MDA, IL-1β, TNF-α, IL-33 and ST2 were significantly increased, and the level of SOD decreased significantly (P<0.05). Compared with model group, the pathological damage of brain tissue in low-, middle- and high-dose Xingnao encma fluid groups and ulinastatin group was reduced, and the neurological deficit score was decreased. The water content of brain tissue, levels of S100β, NSE, MDA, IL-1β, TNF-α, IL-33 and ST2 were significantly decreased, and the level of SOD was increased significantly (P<0.05). There was a dose-dependent relationship in different doses of Xingnao enema fluid groups, and no significant difference between high-dose Xingnao enema fluid group and ulinastatin group was observed (P>0.05). CONCLUSION: Xingnao enema fluid repairs brain injury in rats after cardiopulmonary resuscitation, and down-regulation of IL-33/ST2 signaling pathway may be its mechanism.  相似文献   

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AIM:To observe the dynamic changes of interleukin-4(IL-4), IL-10, IL-12 in rat serum and lung tissues during acute respiratory distress syndrome (ARDS).METHODS:The ARDS model of rats was induced by intravenous injection of oleic acid. The levels of IL-4, IL-10, IL-12 in serum and the supernatant of lung tissues were measured by enzyme linked immunosorbent assay (ELISA).RESULTS:The Levels of serum and lung IL-10, IL-12 in ARDS rats were increased in 4 h, 8 h, 16 h group compared with control group. The levels in IL-10 in serum in 16 h group and IL-10 in lung tissues of 8 h group were lower than that in 4 h group. The Levels of IL-4 in serum in 4 h, 8 h group were higher than that in control group, while IL-4 in 16 h group was lower than that in 8 h group. IL-4 of lung tissues in 4 h, 8 h, 16 h group were increased significantly, but in 16 h group were lower than that in 8 h group. The biggest changes of pulmonary coefficient and histopathology were observed at 4 h after injection of oleic acid.CONCLUSIONS:IL-4, IL-10 and IL-12 might play important roles in inflammatory reaction induced by oleic acid. The pro-and anti-inflammatory cytokines produced successively during ARDS.The relationship between unbalanced cytokines and lung injury in ARDS needs to be further studied.  相似文献   

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AIM To investigate the protective effects of gabexate mesilate (GM) on blood-brain barrier (BBB) permeability in rat model with cerebral ischemia-reperfusion (I/R). METHODS Adult male SD rats (n=180) were randomly divided into sham group, I/R group, nimodipine (NMP; 2 mg·kg-1·d-1) group and GM (5, 10 and 20 mg·kg-1·d-1) groups (n=30 in each group). The rat model of cerebral I/R was established by blocking the middle cerebral artery with thread plug for 2 h. Ten min before modeling, the drugs were given intraperitoneally. The nerve function was detected by Longa scoring method. The permeability of BBB was measured by Evans blue permeation method, and the brain water content was measured by dry-wet weight method. The activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and the content of malondialdehyde (MDA) in brain tissue were determined by biochemical analysis. The content of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6 was measured by ELISA. The mRNA expression of matrix metalloproteinase-2 (MMP-2), MMP-9 and nuclear factor-κB (NF-κB) was detected by RT-PCR. The protein levels of MMP-2, MMP-9 and NF-κB were determined by Western blot. RESULTS Compared with I/R group, the Longa score, permeability of Evans blue and brain water content of the rats in GM (10 and 20 mg·kg-1·d-1) and NMP (2 mg·kg-1·d-1) groups were decreased. The activity of SOD and GSH-Px was increased, while the content of MDA was decreased. The content of TNF-α, IL-1β and IL-6 was decreased, and the mRNA and protein expression levels of MMP-2, MMP-9 and NF-κB were significantly down-regulated. Compared with NMP (2 mg·kg-1·d-1) group, the Longa score and permeability of Evans blue were decreased in GM (20 mg·kg-1·d-1) group, the activity of SOD was increased, and the content of MDA and TNF-α was decreased. The mRNA and protein expression levels of MMP-2, MMP-9 and NF-κB were down-regulated. All of the differences were significant (P<0.05 or P<0.01). CONCLUSION GM has protective effect on BBB in the rats with cerebral I/R. Its mechanism may be related to inhibition of oxidative stress and inflammation, and down-regulation of MMP-2, MMP-9 and NF-κB expression.  相似文献   

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AIM: To explore whether IL-1β inhibits the oligodendrocyte precursor cell (OPCs) differentiation and affects axonal myelination. METHODS: One-day-old SD rats were randomly divided into control group and LPS group (48 rats in each group). The rats in LPS group were intraperitoneally injected with 1 mg/kg LPS. The rats in control group were injected with an equal volume of PBS. The rats in each group were further divided into 3 h, 24 h, 3 d, 7 d, 14 d and 28 d subgroups after injection. The expression of IL-1β and IL-1R1 in the rat corpus callosum at 3 h, 24 h, 3 d, 7 d was determined by double immunofluorescence and Western blotting. The myelin basic protein(MBP) expression in the rat corpus callosum at 14 d, 28 d after injection was also measured. In vitro, primary OPCs culture was performed and divided into control group, 30 μg/L IL-1β group, 30 μg/L IL-1β+IL-1Ra group and 30 μg/L IL-1Ra group. The expression of MBP in the OPCs induced differentiation for 3 d was observed by double immunofluorescence and Western blotting. RESULTS: The expression of IL-1β and IL-1R1 in the rat corpus callosum at 3 h, 24 h, 3 d, 7 d after LPS injection was obviously increased and the expression of MBP in the rat corpus callosum at 14 d, 28 d in LPS group was obviously decreased compared with control group in vivo. The level of MBP was significantly decreased after IL-1β treatment for 3 d in vitro. However, IL-1Ra (IL-1R inhibitor) reversed the down-regulation of MBP expression. IL-1β inhibited the expression of p-ERK, ERK over-expression reversed the down-regulation of MBP expression compared with IL-1β group. CONCLUSION: IL-1β inhibits the differentiation of OPCs, which may be involved in ERK pathways, thus leading to axonal hypomyelination in the corpus callosum of septic neonatal rats.  相似文献   

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AIM: To investigate the effect of astragaloside Ⅳ on severe acute pancreatitis (SAP)-associated acute liver injury in the rats and to explore the underlying mechanisms. METHODS: Male Sprague-Dawley (SD) rats (n=96) were randomly divided into sham-operated group, SAP model group, astragaloside Ⅳ treatment group and AG490 treatment group. SAP model was induced by retrograde injection of 5% sodium taurocholate (1 mL/kg) into the biliopancreatic duct. The rats in astragaloside Ⅳ treatment group were intraperitoneally injected with 20 mg/kg astragaloside Ⅳ, while the rats in AG490 treatment group were injected with 8.0 mg/kg AG490 2 h before sodium taurocholate injection. The rats in sham-operated group and model group received the same volume of saline. The rats were sacrificed at 12 h, 18 h and 24 h after the treatment. The levels of ascites, serum amylase, ALT and AST were detected after the blood samples were collected by the puncture through inferior vena cava. The serum levels of TNF-α, IL-6 and IL-1β were also examined by ELISA. Furthermore, HE staining was used to observe the liver pathological changes, and the protein levels of p-JAK2 and p-STAT3 in the liver were evaluated by Western blot. RESULTS: Compared with sham-operated group, the levels of ascites, serum amylase, ALT, AST, IL-6, TNF-α and IL-1β in the rats in model group were significantly increased, while they were decreased in the rats in astragaloside Ⅳ treatment group and AG490 treatment group compared with the rats in model group. Meanwhile, the phosphorylation levels of JAK2 and STAT3 was significantly increased in model group compared with sham-operated group. The rats in astragaloside Ⅳ treatment group and AG490 treatment group both had a better improvement in the liver injury and lower phosphorylation levels of JAK2 and STAT3.CONCLUSION: Astragaloside Ⅳ exerts a protective effect on pancreatitis-associated acute liver injury in the rats possibly via inhibiting JAK2/STAT3 signaling pathway.  相似文献   

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(截至2006年6月,排名前100位)序号被引文献题名被引文献作者被引文献来源被引频次1蔬菜硝酸盐累积的研究———Ⅰ.不同蔬菜硝酸盐沈明珠,翟宝杰,东惠茹,李俊国园艺学报/1982/04266和亚硝酸盐含量评价2温室土壤次生盐渍化的形成和治理途径研究童有为,陈淡飞园艺学报/1991/021323  相似文献   

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CHANG He  SONG Ying  LIU Chun-xiao 《园艺学报》2000,36(10):1729-1738
AIM To evaluate the effects of recombinant plasmids encoding interleukin-1 type II receptor (IL-1RII) and interleukin-1 receptor accessory protein (IL-1RAcP) on rat experimental autoimmune myocarditis (EAM) and the possible mechanism. METHODS The recombinant plasmids pCAGGS-IL-1RII and pCAGGS-IL-1RAcP were constructed, and pCAGGS-SP (signal peptide) served as the control plasmid. Male Lewis rats (n=29) were divided into 4 groups: control group (rats without immunization or injection, n=5), EAM+SP group (immunized rats injected with pCAGGS-SP, n=9), EAM+IL-1RII group (immunized rats injected with pCAGGS-IL-1RII, n=8) and EAM+IL-1RII+IL-1RAcP group (immunized rats injected with pCAGGS-IL-1RII and pCAGGS-IL-1RAcP, n=7). The rats were immunized to induce EAM on day 0, and injected with recombinant plasmids by hydrodynamics-based delivery on day 6. Echocardiography was performed, and the rats were killed on day 17. The ratio of heart weight to body weight (HW/BW) was evaluated, and the histopathological changes of the myocardial tissues were observed by HE staining. The mRNA expression of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and inflammatory factors in the myocardial tissues was detected by RT-qPCR. Recombinant plasmids pUC19-IL-1RII-actin and pUC19-IL-1RAcP-tub were transfected into Cos7 cells, and the culture supernatants were collected and added to lipopolysaccharide (LPS)-induced H9c2 cells. The expression of inflammatory genes were detected by RT-qPCR. Recombinant plasmids pEGFP-IL-1RII-actin and pEGFP-IL-1RAcP-tub were transfected into the Cos7 cells to identify the formation of IL-1RII/IL-1RAcP heterodimer by co-immunoprecipitation (Co-IP). RESULTS Compared with EAM+SP group, injection with plasmids effectively attenuated EAM in EAM+IL-1RII group and EAM+IL-1RII+IL-1RAcP group, as indicated by the decreases in HW/BW, left ventricular end-systolic diameter, and myocardial expression of ANP, BNP, TNF-α, IL-2, IFN-γ and TGF-β, and the increase in expression of IL-4 in the hearts. In LPS-induced H9c2 cells, compared with LPS group, the levels of TGF-β and IL-6 in the culture supernatants were significantly decreased (P<0.01), and the level of IL-10 was significantly increased (P<0.05) in LPS+IL-1RII group and LPS+IL-1RII+IL-1RAcP group. Compared with LPS+IL-1RII group, the expression of TNF-α and IL-2 was significantly decreased (P<0.05), and the expression of IL-13 was significantly increased in LPS+IL-1RII+IL-1RAcP group (P<0.01). The formation of IL-1RII/IL-1RAcP heterodimer was detected by Co-IP. CONCLUSION Plasmids encoding IL-1RII and IL-1RAcP effectively attenuate EAM, and the possible mechanism may be related to the inhibition of inflammatory factor expression and the formation of IL-1RII/IL-1RAcP heterodimer.  相似文献   

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AIM: To study the effects of Yangyu Tuji (YYTJ) on delayed healing wound of diabetic rats caused by streptozotocin (STZ). METHODS: SD male rats were randomly divided into control group (control), model group (model); and 3 different dose groups of YYTJ. 55 mg/kg STZ were given by intraperitoneal injection except for control group. After 30 days, a round skin of 1.6 cm diametre was excised on all dorsal back of rats. The healing time and healing rate were observed according to re-epithelization. The content of collagenⅠ and Ⅲ was observed by Picric acid-Sirius red staining , Matrix metalloproteinase-1, 13 (MMP-1, -13), tissue inhibitor of metalloproteinases-1 (TIMP-1) by immuno-histochemistry assay. All data were analyzed by IPP software. RESULTS: The healing time in each group treated with YYTJ was shorter than that in model group (P<0.01), and the healing rate was increased (P<0.01, P<0.05). Content of type I collagen, ratio of type Ⅰ and Ⅲ collagen of high and mid dose group were significantly higher than that in model group (P<0.01) at 3rd, 7th, 11th day. The expression of MMP-1, -13 of each groups were higher than that in model group at 7th day (P<0.01, P<0.05), and MMP-1 trend to equal with model group at 11th day. MMP-13 was significantly lower than that in model group at 11th day (P<0.01, P<0.05). TIMP-1 of each group of wound was higher than that in model group at 3rd, 7th, 11th day (P<0.01, P<0.05). The ratio of type Ⅰ and Ⅲ collagens in each group was lower than that in model group at 11th day (P<0.01). Ratio of MMP-13 and TIMP-1 of high dose group and mid dose group were higher than that in model group at 3rd and 7th day (P<0.01). The ratio of each group was lower than that in model group at 11th day (P<0.01). Meanwhile, ratio of MMP-13 and TIMP-1 of high dose group and mid dose group were lower than that of lower dose group (P<0.05). CONCLUSION: It is possible that YYTJ accelerates wound healing by increasing collagen content of type Ⅰ and Ⅲ, especially type Ⅰ, as well as improves collagen deposition by regulating the balance of MMP and TIMP.  相似文献   

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AIM:To investigate the effects of silymarin on lipopolysaccharide (LPS)-induced acute lung injury in rats and its possible molecular mechanisms. METHODS:Fifty-eight male SD rats, weighting 230-250 g, were divided into four groups randomly: normal control (n=12); acute lung injury group (n=15), receiving intravenous LPS (O55∶〖KG-*2〗B5, 5 mg/kg); silymarin alone group (50 mg/kg, n=15); intervention group (n=16, receiving silymarin 50 mg/kg and LPS 5 mg/kg). The specimens were collected 6 hours later. The following changes, including blood gas analysis, the lung wet/dry weight ratio, the pulmonary vascular permeability, histological manifestations, lung tissue myeloperoxidase activity, the levels of TNF-α, IL-1β, MCP-1 and SOD, GSH-Px as well as malonaldehyde and conjugated diene in plasma and lung tissue, were observed. RESULTS:Compared with control group, the lungs of the rats in LPS treatment group showed significant hyperemia and spotted hemorrhage. The inflammatory granulocyte infiltrating, diffused alveolar septum thickening and spotted hemorrhage were observed in pathological examinations. The lung wet/dry weight ratio and Evans blue content (per gram) increased significantly after LPS treatment. The myeloperoxidase activity in plasma and lung tissue, the levels of TNF-α, IL-1β, MCP-1 and SOD, GSH-Px as well as malonaldehyde and conjugated diene were increased significantly in LPS treatment group. However, in intervention groups, all the above-mentioned measurements were reversed significantly by silymarin treatment compared with LPS treatment group. CONCLUSION:Silymarin may decrease inflammatory reaction and oxidative stress, and further decrease lung damage induced by LPS in rats, all indicating protection of silymarin against acute lung injury.  相似文献   

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