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AIM:To explore the effect of pidotimod on the renal function in IgA nephropathy (IgAN) rat model, and to further study whether this effect is related to the inhibition of inflammatory response. METHODS:The SD rats (n=36) were randomly divided into control group, IgAN model group, IgAN with prednisone treatment group and IgAN with pidotimod treatment group, with 9 rats in each group. The IgAN model was induced by consecutive oral administration of bovine gamma globulin (BGG) for 8 weeks followed by injection of BGG through tail vein for 3 d. After the IgAN model was established, the drug was continuously used for 4 weeks. At the end of the treatment, the urine protein, serum creatinine and blood urea nitrogen were examined by an automated analyzer. IgA deposition in the renal tissues was observed by immunofluorescence staining. The mRNA expression levels of renal fibrosis markers transforming growth factor-β1 (TGF-β1) and fibronectin 1 in the renal tissues were detected by RT-qPCR. The mRNA and protein levels of pro-inflammatory cytokines interleukin-1β (IL-1β) and IL-6 in the renal tissues were determined by RT-qPCR and Western blot, respectively. RESULTS:No significant difference of the body weight was observed in different groups. Compared with control group, the content of urine protein, serum creatinine and blood urea nitrogen were significantly increased (P<0.01), whereas those were reversed by pidotimod treatment. The results of immunofluorescence staining showed that pidotimod inhibited IgA deposition in the IgAN rats. Pitomod treatment inhibited the mRNA expression levels of renal fibrosis markers TGF-β1 and fibronectin 1, and the mRNA and protein levels of pro-inflammatory cytokines IL-1β and IL-6 in the renal tissues of IgAN rats. CONCLUSION:Pidotimod alleviates IgAN progression in rats by inhibition of inflammatory response. 相似文献
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Rosa María Ramírez Yolanda Almanza Rafael González Santos García Norma Heredia 《Veterinary research communications》2009,33(4):379-386
Avian colisepticemia frequently occurs after respiratory tract damage, the primary site for infection allows bacteria to encounter
an exposed basement membrane, where laminin and fibronectin are important components. We investigated the ability of an isolate
of avian pathogenic Escherichia coli to bind fibronectin and laminin. Using Far-western dot blot analysis, we demonstrated the ability of this microorganism to
bind basement membrane proteins fibronectin and laminin. Results from an ELISA-based approach indicate that the binding to
these membrane proteins was bacterial-dose dependent. Furthermore, two specific E. coli polypeptides, of 32 kDa and 130 kDa, reacted with laminin and fibronectin, respectively. Further evaluation of these potential
bacterial adhesins may provide insights into the pathogenesis of colibacillosis. 相似文献
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AIM: To observe the expression of transforming growth factor β1 (TGF-β1), MAPK1/3 and fibronectin (FN) in the development of renal tubulointerstitial disease. METHODS: Wistar male rats were randomly divided into normal control group, diabetic group of 1week, 2 weeks, 4 weeks and 8 weeks. Diabetic model was induced by peritoneal injection of streptozotocin. Immunohistochemistry was employed to detect the expression of TGF-β1, MAPK1/3 and FN in the kidney. TGF-β1 protein in the renal cortex was checked by Western blot. BG, Scr and UP were analysed by biochemical methods, and the morphological changes in renal tubulointerstitium were also examined under microscopy on sections stained with HE and PAS. RESULTS: The expression of MAPK1/3 and FN was observed, but not the expression of TGF-β1 in normal renal tissue. Positive staining of TGF-β1 was observed in the renal tubulo-interstitium in 1-week diabetic group and thereafter it increased in the course of diabetes. A continuous increase in the expression of MAPK1/3 and FN was also observed in two - week diabetic rats. Chronologically the expression of TGF-β1,MAPK1/3 and FN and the ratio of KW/BW were positively correlative with each other in diabetic animals except one -week diabetic rats. There was also a positive correlation between MAPK1/3 and FN in l -week diabetic rats. CONCLUSION: Our data suggest that TGF-β1 appears in the renal tubulointerstitium in early period of diabetes and then its signal is mediated by MAPK1/3 cascades to accelerate production of FN ,and in turn leads to renal hypertrophy and tubulointerstitial fibrosis. 相似文献
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AN Fang-yu YAN Chun-lu LIU Yong-qi WANG Ji-long ZHAO Lei XIA Peng-fei LOU Ya-li WANG Guo-wen ZHAO Chong-bo DENG Jie 《园艺学报》2020,36(1):157-163
AIM: To observe the effect of Youguiwan (YGW) on the expression of heat shock protein 90α (Hsp90α) in articular cartilage tissues of knee osteoarthritis (KOA) rats, and to further reveal its mechanism. METHODS: SD rats (n=60) were randomly divided into 6 groups:sham control (SC) group, model (M) group, glucosamine sulfate (GS) group, and high-, middle-and low-dose YGW (YGW-H, YGW-M and YGW-L) groups. The modified Hulth method was used to make KOA models for 6 weeks. The rats were gavaged with corresponding drugs for 8 weeks. HE staining was used and Makin score was evaluated. The expression of Hsp90α, fibronectin (Fn) and collagen type Ⅱ (COL-II) was determined by immunohistochemistry. The expression of interleukin-1β (IL-1β), matrix metalloproteinase (MMP)-3 and MMP-13 was analyzed by RT-qPCR. The protein expression of Hsp90α and COL-II was determined by Western blot. RESULTS: As compared with SC group, the Makin score was obviously raised in M group, the expression levels of Hsp90α, IL-1β, MMP-3 and MMP-13 were evidently increased, the expression levels of COL-II and Fn were evidently decreased (P < 0.01), articular cartilage was seriously damaged, and the chondrocytes were disarranged. As compared with M group, the Makin score and the expression of Hsp90α were obviously decreased in YGW-H group, the protein expression of Fn was evidently increased in YGW-H group, the protein expression of COL-II was evidently increased in YGW-H and YGW-M groups, the mRNA expressions of IL-1β, MMP-3 and MMP-13 were evidently decreased in YGW-H, YGW-M and YGW-L groups (P < 0.05 or P < 0.01), cartilage structure tended to be normal, the chondrocytes distribution was uneven, and articular cartilage surface was not smooth. CONCLUSION: Youguiwan is effective for treatment of KOA. Youguiwan protects against articular cartilage degeneration by down-regulating the expression of Hsp90α and up-regulating the expression of Fn, and reducing the secretion of inflammatory factors and the degradation of extracellular matrix. 相似文献
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PAN Zhi-yu DA Jing-jing DONG Rong WU Jing PI Ming-jing YU Jia-li SUN Yi NIE Ying-jie ZHA Yan 《园艺学报》2017,33(9):1662-1668
AIM: To observe the expression of Snail1 and insulin-like growth factor-1 (IGF-1) in NRK-52E cells induced by high glucose, and to investigate the relationship of Snail1 and IGF-1 in the mechanism of epithelial to mesenchymal transition (EMT) in diabetic kidney disease (DKD).METHODS: The NRK-52E cells were treated with Snail1 siRNA and IGF-1 siRNA after cultured with high glucose medium for 72 h, and divided into control group, high glucose group, non-targeting (NT) siRNA group, Snail1 RNAi group and IGF-1 RNAi group. The cells were harvested at 48 h and 72 h. Real-time PCR was used to detect the mRNA expression of Snail1, IGF-1, E-cadherin and fibronectin (FN), and the protein levels were determined by immunofluorescence staining.RESULTS: Compared with control group, the expression of E-cadherin at mRNA and protein levels declined after stimulation with high glucose (P<0.01), while that of FN was elevated (P<0.01). Meanwhile, the mRNA and protein levels of Snail1 and IGF-1 were markedly increased (P<0.01).The expression of E-cadherin at mRNA and protein levels was improved in Snail1 RNAi group as compared with high glucose group(P<0.01), while that of FN, IGF-1 and Snail1 was significantly down-regulated (P<0.01). The same changes were observed in IGF-1 RNAi group (P<0.01). The protein expression of each factor in NT group had no significant change as compared with high glucose group (P>0.05). Pearson correlation analysis showed a close positive relationship between the expression of Snail1 and IGF-1 protein (r=0.852, P<0.01).CONCLUSION: Snail1 may facilitate DKD development by regulating IGF-1 in the process of EMT. 相似文献
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AIM：To investigate the role of caveolae in high glucose (HG)-induced extracellular matrix (ECM) production in rat mesangial cells (MCs). METHODS：Synchronized rat MCs were divided into normal glucose group, HG group, HG+methyl-β-cyclodextrin (β-MCD) group and HG+β-MCD+cholesterol (Chol) group. Western blotting was used to detect the protein expression of caveolin-1 (Cav-1), phosphorylated caveolin-1 (p-Cav-1-Y14) and collagen type 1 (Col I). The mRNA expression of Cav-1 was determined by real-time PCR. ELISA was used to measure the level of fibronectin (FN) in the supernatant. RESULTS：High glucose significantly increased the expression of FN and Col I. In HG 12, 24 and 48 h groups, the mRNA and protein levels of Cav-1 were not significantly different from those in HG 0 h group, whereas the level of p-Cav-1-Y14 was significantly increased. β-MCD significantly attenuated HG-induced elevation of p-Cav-1-Y14 and FN production, but had no effect on HG-induced Col I expression. All these responses to β-MCD were abolished by Chol. CONCLUSION：High glucose significantly increases the production of Col I and FN in rat MCs. FN production induced by high glucose is mediated by p-Cav-1-Y14. 相似文献
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鸡血浆纤维连接蛋白的提纯及酶联免疫吸附检测方法的建立 总被引：4，自引：0，他引：4
利用纤维连接蛋白（FN）与明胶特异结合的特点，用明胶亲和层析结合电泳裁胶的方法提纯鸡血浆FN并制备了兔抗鸡FN抗血清。纯化的FN经凝胶电泳鉴定为一条蛋白带与人FN在同一位置上，亚单位分子量约230KDa；经免疫鉴定，提纯鸡血浆FN与兔抗人FN抗体有交叉反应性。用兔抗鸡FN抗体包被捕捉抗原，建立了检测鸡血浆FN的双抗体酶联免疫吸附法（ELISA），此法具有操作简单、特异性强、灵敏度高的特点，适用于鸡血浆FN的检测。鸡血浆FN的提及其检测方法的建立，为FN的兽医领域的进一步研究和应用奠定了基础。 相似文献
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AIM: To observe the effect of mineral trioxide aggregate (MTA) combined with fibronectin as pulp capping agents. METHODS: The 48 pulps of 4 cats were exposed mechanically and then capped directly with MTA, MTA combined with fibronectin, calcium hydroxide, fibronectin and starch as control. After 12 weeks observation, the experimental teeth were extracted and observed with scanning electronic microscope. RESULTS: In calcium hydroxide group and MTA group, specimens showed irregular dentin bridge structures along the pulp-MTA interface. In MTA combined with fibronectin group, continuous and complete dentin bridge structures were found along the pulp-MTA interface, the crystalline-like structures were in direct contact with the dentin wall of pulp chamber, the exposed pulp sites were closed by the dentin bridge. In fibronectin and starch group, no reparative dentin was observed. CONCLUSION: The present experiment indicated that MTA combined with fibronectin was an effective pulp-capping material and may have potential for clinical application. 相似文献
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For many pathogens, adherence and/or invasion involve association with host extracellular matrix molecules, such as fibronectin (Fn). Pasteurella multocida was found to bind significantly to Fn and collagen type IX but not to laminin and collagen types IV and X. The binding of P. multocida to Fn was dose-dependent and was inhibited by heparin (Hep). Removal of polysaccharide capsule enhanced the binding capacity of the bacterium to Fn and inhibition by Hep. Protease treatment of bacteria decreased binding, implicating surface protein(s) as adhesive components. Investigation of the binding domain(s) of P. multocida on the Fn molecule revealed preferential binding to the N-terminal Hep-binding domain of Fn but not to the carboxyl-terminal Hep-binding domain. Furthermore, Fn, and anti-Fn antibodies inhibited P. multocida adherence to Madin-Darby bovine kidney cells, suggesting the involvement of Fn in the bacterium adherence to host cells. Ligand blotting, batch affinity purification and MALDI-TOF mass spectrometry implicated several proteins as putative adhesins of P. multocida in the Fn-mediated adherence. Taken together, the data suggest that P. multocida-Fn interaction may play a role in the bacterium adherence to host cells, and this may be mediated by bacterial surface proteins with preferential affinity for the Hep-1 binding domain of Fn. 相似文献
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