目的探究蛋白激酶B(Akt)/核转录因子(NF-κB)信号通路、白介素-37(IL-37)对儿童重症肺炎(SP预后的预测价值。方法选取2022年3月至2024年7月郑州大学第一附属医院收治的230例重症肺炎患儿作为研究组,另选同期115例轻症肺炎患儿作为对照...目的探究蛋白激酶B(Akt)/核转录因子(NF-κB)信号通路、白介素-37(IL-37)对儿童重症肺炎(SP预后的预测价值。方法选取2022年3月至2024年7月郑州大学第一附属医院收治的230例重症肺炎患儿作为研究组,另选同期115例轻症肺炎患儿作为对照组。比较研究组和对照组患儿的血清Akt mRNA、NF-κB mRNA、IL-37水平,并比较不同临床特征SP患儿和不同28 d预后SP患儿的血清Akt mRNA、NF-κB mRNA、IL-37水平。应用Spearman分析血清Akt mRNA、NF-κB mRNA、IL-37水平与重症肺炎患儿临床特征、预后的相关性,应用受试者工作特征(ROC)曲线分析血清Akt mRNA、NF-κB mRNA、IL-37水平对重症肺炎患儿预后的预测价值。结果研究组患儿的血清Akt m RNA、NF-κB m RNA、IL-37水平分别为1.09±0.27、1.06±0.25、(98.67±27.56)pg/mL,明显高于对照组的0.82±0.21、0.79±0.23、(65.19±18.91)pg/mL,差异均有统计学意义(P<0.05);伴有肺不张、胸腔积液、肺实变、肺外并发症的SP患儿的血清Akt mRNA、NF-κB m RNA、IL-37水平明显高于无肺不张、无胸腔积液、无肺实变、无肺外并发症的SP患儿,差异均有统计学意义(P<0.05);SP患儿治疗28 d后评估预后,其中71例预后不良,159例预后良好;研究组预后不良患儿血清Akt m RNA、NF-κB m RNA、IL-37水平分别为1.35±0.32、1.31±0.30、(122.68±37.19)pg/mL,明显高于预后良好患儿的0.97±0.20、0.95±0.19、(87.95±20.86)pg/mL,差异有统计学意义(P<0.05);Spearman分析结果显示,血清Akt mRNA、NF-κB m RNA、IL-37水平与SP患儿肺不张、胸腔积液、肺实变、肺外并发症、预后不良均呈正相关(P<0.05);ROC分析结果显示,血清Akt mRNA、NF-κB m RNA、IL-37水平预测SP患儿预后不良的曲线下面积(AUC)分别为0.760、0.761、0.792,三者联合预测预后不良的AUC为0.894,明显大于各指标单独预测的AUC(P<0.05)。结论SP患儿血清Akt mRNA、NF-κB m RNA、IL-37水平明显升高,且与临床特征、预后不良密切相关,三者联合可为临床预测SP患儿预后提供可靠临床依据。展开更多
Background:The aim was to elucidate the function of IL-37 in middle east respiratory syndrome coronavirus(MERS-CoV)infection,thereby providing a novel therapeutic strategy for managing the clinical treatment of inflam...Background:The aim was to elucidate the function of IL-37 in middle east respiratory syndrome coronavirus(MERS-CoV)infection,thereby providing a novel therapeutic strategy for managing the clinical treatment of inflammatory response caused by respiratory virus infection.Methods:We investigated the development of MERS by infecting hDPP4 mice with hCoV-EMC(107 TCID50[50%tissue culture infectious dose])intranasally.We infected A549 cells with MERS-CoV,which concurrently interfered with IL-37,detecting the viral titer,viral load,and cytokine expression at certain points postinfection.Meanwhile,we administered IL-37(12.5μg/kg)intravenously to hDPP4 mice 2 h after MERS-CoV-2 infection and collected the serum and lungs 5 days after infection to investigate the efficacy of IL-37 in MERS-CoV infection.Results:The viral titer of MERS-CoV-infected A549 cells interfering with IL-37 was significantly reduced by 4.7-fold,and the viral load of MERS-CoV-infected hDPP4 mice was decreased by 59-fold in lung tissue.Furthermore,the administration of IL-37 suppressed inflammatory cytokine and chemokine(monocyte chemoattractant protein 1,interferon-γ,and IL-17A)expression and ameliorated the infiltration of inflammatory cells in hDPP4 mice.Conclusion:IL-37 exhibits protective properties in severe pneumonia induced by MERS-CoV infection.This effect is achieved through attenuation of lung viral load,suppression of inflammatory cytokine secretion,reduction in inflammatory cell infiltration,and mitigation of pulmonary injury.展开更多
BACKGROUND Excessive endoplasmic reticulum(ER)stress in intestinal epithelial cells can lead to damage to the intestinal mucosal barrier,activate the signal transducer and activator of transcription 3(STAT3)/nuclear f...BACKGROUND Excessive endoplasmic reticulum(ER)stress in intestinal epithelial cells can lead to damage to the intestinal mucosal barrier,activate the signal transducer and activator of transcription 3(STAT3)/nuclear factor kappa B(NF-κB)signaling pathway,and exacerbate the inflammatory response,thus participating in the pathogenesis of ulcerative colitis(UC).Mesalazine is a commonly used drug in the clinical treatment of UC.However,further studies are needed to determine whether mesalazine regulates the ER stress of intestinal epithelial cells,downregulates the STAT3/NF-κB pathway to play a role in the treatment of UC.AIM To study the therapeutic effects of mesalazine on spontaneous colitis in interleukin-10(IL-10)-/-mice.METHODS The 24-week-old IL-10-/-mice with spontaneous colitis were divided into the model group and the 5-amino salicylic acid group.Littermates of wild-type mice of the same age group served as the control.There were eight mice in each group,four males and four females.The severity of symptoms of spontaneous colitis in IL-10-/-mice was assessed using disease activity index scores.On day 15,the mice were sacrificed.The colon length was measured,and the histopathological changes and ultrastructure of colonic epithelial cells were detected.The protein expressions of STAT3,p-STAT3,NF-κB,IκB,p-IκB,and glucoseregulated protein 78 were identified using Western blotting.The STAT3 and NF-κB mRNA expressions were identified using real-time polymerase chain reaction.The glucose-regulated protein 78 and C/EBP homologous protein expressions in colon sections were detected using immunofluorescence.RESULTS Mesalazine reduced the symptoms of spontaneous colitis in IL-10 knockout mice and the histopathological damage of colonic tissues,and alleviated the ER stress in epithelial cells of colitis mice.Western blotting and quantitative real-time polymerase chain reaction results showed that the STAT3/NF-κB pathway in the colon tissue of model mice was activated,suggesting that this pathway was involved in the pathogenesis of UC and might become a potential therapeutic target.Mesalazine could down-regulate the protein expressions of p-STAT3,NF-κB and p-IκB,and down-regulate the mRNA expression of STAT3 and NF-κB.CONCLUSION Mesalazine may play a protective role in UC by reducing ER stress by regulating the STAT3/NF-κB signaling pathway.展开更多
In order to study the effects of Saussurea laniceps polysaccharides(SLPs)on the expression of inflammatory factors and antimicrobial peptide LL-37 in UVB-induced keratinocytes,SLPs were extracted by the ethanol therma...In order to study the effects of Saussurea laniceps polysaccharides(SLPs)on the expression of inflammatory factors and antimicrobial peptide LL-37 in UVB-induced keratinocytes,SLPs were extracted by the ethanol thermal reflux method,and SLPs at different concentrations were used to examine the inhibitory effect of COX-2(a key mediator of inflammatory pathway).A cell model of UVB irradiation-induced inflammation was established to determine the influence of SLPs on prostaglandin E2(PGE-2),TNF-αand IL-1βinflammatory factors,as well as the relationships of SLPs with LL-37 expression.An enzyme-linked immunosorbent assay(ELISA)and western blot analysis were used to detect the production of inflammatory factors and LL-37 antimicrobial peptide.The results showed that the inhibition rate of COX-2 was 82.41%at 1000μg/mL,and the expression of PGE-2,TNF-αand IL-1βinflammatory factors in HaCaT cells was significantly downregulated at 100μg/mL(P<0.01).In addition,SLPs at 50μg/mL and 100μg/mL concentrations enhanced the expression of LL-37 antimicrobial peptide(P<0.01),thereby down-regulating the expression of TNF-αand IL-1βinflammatory factors,then reducing skin inflammation.Conclusion:SLP can significantly inhibit the inflammatory response induced by UVB,and can further slow down the damage caused by inflammation to the skin by regulating LL-37 antimicrobial peptides,which has the potential to prevent skin inflammatory damage caused by UVB irradiation.展开更多
Background:VPS37A(VPS37A subunit of ESCRT-I),a component of the ESCRT-I(endosomal sorting complex required for transport I)complex,mediates vesicular trafficking through sorting endocytic ubiquitinated cargos into mul...Background:VPS37A(VPS37A subunit of ESCRT-I),a component of the ESCRT-I(endosomal sorting complex required for transport I)complex,mediates vesicular trafficking through sorting endocytic ubiquitinated cargos into multivesicular bodies(MVBs).Although accumulating evidence indicates that VPS37A deficiency occurs in numerous malignancies and exerts tumor-suppressive effects during cancer progression,its functional significance in colorectal cancer(CRC)pathogenesis remains poorly characterized.Therefore,this study aims to further investigate the functional and molecular mechanisms by which VPS37A downregulation contributes to malignant biological phenotypes in CRC,with a specific focus on how its dysregulation affects cell death pathways.Methods:Multi-omics analysis of TCGA,GEO,and CPTAC cohorts identified VPS37A as a downregulated tumor suppressor gene in CRC.The prognostic relevance of VPS37A was validated in two clinical cohorts(Cohorts 1 and 2)using immunohistochemistry.Functional assays in VPS37A-overexpressing CRC cells and xenografts assessed proliferation,cell cycle progression,and stress-induced cell death.RNA sequencing,nuclear factor kappa-B(NF-κB)luciferase reporter assays,and lysosomal inhibition experiments elucidated the mechanisms underlying tumor necrosis factor receptor 1(TNFR1)degradation.Results:VPS37A is significantly downregulated in advanced-stage CRC and independently predicts poor survival.Functionally,VPS37A overexpression suppresses proliferation and induces G2/M arrest in vitro,while reducing xenograft growth.Under metabolic stress(glucose deprivation/galactose adaptation),VPS37A triggers cell death via apoptosis,necroptosis,and ferroptosis.Mechanistically,VPS37A redirects TNFR1 to lysosomal degradation,suppressing NF-κB nuclear translocation and transcriptional activity.Conclusion:VPS37A deficiency drives CRC progression by sustaining TNFR1/NF-κB signaling under metabolic stress.Restoring VPS37A activity promotes TNFR1 degradation,offering a therapeutic strategy to counteract NF-κB-mediated treatment resistance in CRC.展开更多
Background: Interleukin-37 b(IL-37 b), a vital negative regulator of the innate immune system, has been reported to be a tumor inhibitor in different type of cancers. However, little is known about the relationship be...Background: Interleukin-37 b(IL-37 b), a vital negative regulator of the innate immune system, has been reported to be a tumor inhibitor in different type of cancers. However, little is known about the relationship between IL-37 b and hepatocellular carcinoma(HCC). The present study aimed to investigate the potential roles of IL-37 b in HCC progression. Methods: Subjects( n = 237) were recruited, and serum IL-37 b was measured using ELISA. The tumorsuppressive capacity and underlying mechanisms of IL-37 b in HCC were investigated in vitro and in vivo. Results: Compared to healthy controls, serum IL-37 b levels were elevated in chronic hepatitis B(CHB) patients but decreased significantly in HBV-HCC patients, especially for those with portal venous tumor thrombus. Low level serum IL-37 b in HBV-HCC patients correlated with high HCC stage and poor overall survival and disease-free survival. In vitro and in vivo, recombinant human IL-37 b inhibited proliferation and metastasis in HCC cells. Furthermore, IL-37 b inhibited epithelial mesenchymal transition in HCC cells in vitro by downregulating IL-6, pSTAT3(Y705), N-cadherin, and vimentin expression and by upregulating E-cadherin expression. These effects were partially reversed by transfection of adenovirus encoding human IL-6. Conclusions: IL-37 b inhibits HCC growth, metastasis and epithelial mesenchymal transition by regulating IL-6/STAT3 signaling. Serum IL-37 b may be a biomarker for HBV-HCC and its staging.展开更多
白细胞介素-1(IL-1)家族成员IL-1F7(IL-1 family 7)最近被命名为IL-37,它共有五种不同的亚型(IL-37a-e)。研究表明,IL-37b(IL-1F7b)可以与IL-18受体的α链结合,但并不影响IL-18的生理功能;IL-37b与IL-18结合蛋白(IL-18BP)结合后,可以增...白细胞介素-1(IL-1)家族成员IL-1F7(IL-1 family 7)最近被命名为IL-37,它共有五种不同的亚型(IL-37a-e)。研究表明,IL-37b(IL-1F7b)可以与IL-18受体的α链结合,但并不影响IL-18的生理功能;IL-37b与IL-18结合蛋白(IL-18BP)结合后,可以增强IL-18BP对IL-18的抑制作用。IL-37b的主要作用是抑制炎症反应,它在多种炎症相关性疾病中起重要作用。展开更多
文摘目的探究蛋白激酶B(Akt)/核转录因子(NF-κB)信号通路、白介素-37(IL-37)对儿童重症肺炎(SP预后的预测价值。方法选取2022年3月至2024年7月郑州大学第一附属医院收治的230例重症肺炎患儿作为研究组,另选同期115例轻症肺炎患儿作为对照组。比较研究组和对照组患儿的血清Akt mRNA、NF-κB mRNA、IL-37水平,并比较不同临床特征SP患儿和不同28 d预后SP患儿的血清Akt mRNA、NF-κB mRNA、IL-37水平。应用Spearman分析血清Akt mRNA、NF-κB mRNA、IL-37水平与重症肺炎患儿临床特征、预后的相关性,应用受试者工作特征(ROC)曲线分析血清Akt mRNA、NF-κB mRNA、IL-37水平对重症肺炎患儿预后的预测价值。结果研究组患儿的血清Akt m RNA、NF-κB m RNA、IL-37水平分别为1.09±0.27、1.06±0.25、(98.67±27.56)pg/mL,明显高于对照组的0.82±0.21、0.79±0.23、(65.19±18.91)pg/mL,差异均有统计学意义(P<0.05);伴有肺不张、胸腔积液、肺实变、肺外并发症的SP患儿的血清Akt mRNA、NF-κB m RNA、IL-37水平明显高于无肺不张、无胸腔积液、无肺实变、无肺外并发症的SP患儿,差异均有统计学意义(P<0.05);SP患儿治疗28 d后评估预后,其中71例预后不良,159例预后良好;研究组预后不良患儿血清Akt m RNA、NF-κB m RNA、IL-37水平分别为1.35±0.32、1.31±0.30、(122.68±37.19)pg/mL,明显高于预后良好患儿的0.97±0.20、0.95±0.19、(87.95±20.86)pg/mL,差异有统计学意义(P<0.05);Spearman分析结果显示,血清Akt mRNA、NF-κB m RNA、IL-37水平与SP患儿肺不张、胸腔积液、肺实变、肺外并发症、预后不良均呈正相关(P<0.05);ROC分析结果显示,血清Akt mRNA、NF-κB m RNA、IL-37水平预测SP患儿预后不良的曲线下面积(AUC)分别为0.760、0.761、0.792,三者联合预测预后不良的AUC为0.894,明显大于各指标单独预测的AUC(P<0.05)。结论SP患儿血清Akt mRNA、NF-κB m RNA、IL-37水平明显升高,且与临床特征、预后不良密切相关,三者联合可为临床预测SP患儿预后提供可靠临床依据。
基金the National Natural Science Foundation of China,Grant/Award Number:32000358the CAMS initiative for Innovative Medicine of China,Grant/Award Number:2021-I2M-1-035Young Elite Scientists Sponsorship Program by CAST(YESS),Grant/Award Number:2020QNRC001。
文摘Background:The aim was to elucidate the function of IL-37 in middle east respiratory syndrome coronavirus(MERS-CoV)infection,thereby providing a novel therapeutic strategy for managing the clinical treatment of inflammatory response caused by respiratory virus infection.Methods:We investigated the development of MERS by infecting hDPP4 mice with hCoV-EMC(107 TCID50[50%tissue culture infectious dose])intranasally.We infected A549 cells with MERS-CoV,which concurrently interfered with IL-37,detecting the viral titer,viral load,and cytokine expression at certain points postinfection.Meanwhile,we administered IL-37(12.5μg/kg)intravenously to hDPP4 mice 2 h after MERS-CoV-2 infection and collected the serum and lungs 5 days after infection to investigate the efficacy of IL-37 in MERS-CoV infection.Results:The viral titer of MERS-CoV-infected A549 cells interfering with IL-37 was significantly reduced by 4.7-fold,and the viral load of MERS-CoV-infected hDPP4 mice was decreased by 59-fold in lung tissue.Furthermore,the administration of IL-37 suppressed inflammatory cytokine and chemokine(monocyte chemoattractant protein 1,interferon-γ,and IL-17A)expression and ameliorated the infiltration of inflammatory cells in hDPP4 mice.Conclusion:IL-37 exhibits protective properties in severe pneumonia induced by MERS-CoV infection.This effect is achieved through attenuation of lung viral load,suppression of inflammatory cytokine secretion,reduction in inflammatory cell infiltration,and mitigation of pulmonary injury.
基金Supported by Xi’an Science and Technology Plan Project,No.23YXYJ0162Shaanxi Province Traditional Chinese Medicine Research and Innovation Talent Plan Project,No.TZKN-CXRC-16+2 种基金Project of Shaanxi Administration of Traditional Chinese Medicine,No.SZYKJCYC-2025-JC-010Shaanxi Province Key Research and Development Plan Project-Social Development Field,No.S2025-YF-YBSF-0391the Science and Technology Innovation Cultivation Program of Longhua Hospital affiliated to Shanghai University of Chinese Medicine,No.YD202220。
文摘BACKGROUND Excessive endoplasmic reticulum(ER)stress in intestinal epithelial cells can lead to damage to the intestinal mucosal barrier,activate the signal transducer and activator of transcription 3(STAT3)/nuclear factor kappa B(NF-κB)signaling pathway,and exacerbate the inflammatory response,thus participating in the pathogenesis of ulcerative colitis(UC).Mesalazine is a commonly used drug in the clinical treatment of UC.However,further studies are needed to determine whether mesalazine regulates the ER stress of intestinal epithelial cells,downregulates the STAT3/NF-κB pathway to play a role in the treatment of UC.AIM To study the therapeutic effects of mesalazine on spontaneous colitis in interleukin-10(IL-10)-/-mice.METHODS The 24-week-old IL-10-/-mice with spontaneous colitis were divided into the model group and the 5-amino salicylic acid group.Littermates of wild-type mice of the same age group served as the control.There were eight mice in each group,four males and four females.The severity of symptoms of spontaneous colitis in IL-10-/-mice was assessed using disease activity index scores.On day 15,the mice were sacrificed.The colon length was measured,and the histopathological changes and ultrastructure of colonic epithelial cells were detected.The protein expressions of STAT3,p-STAT3,NF-κB,IκB,p-IκB,and glucoseregulated protein 78 were identified using Western blotting.The STAT3 and NF-κB mRNA expressions were identified using real-time polymerase chain reaction.The glucose-regulated protein 78 and C/EBP homologous protein expressions in colon sections were detected using immunofluorescence.RESULTS Mesalazine reduced the symptoms of spontaneous colitis in IL-10 knockout mice and the histopathological damage of colonic tissues,and alleviated the ER stress in epithelial cells of colitis mice.Western blotting and quantitative real-time polymerase chain reaction results showed that the STAT3/NF-κB pathway in the colon tissue of model mice was activated,suggesting that this pathway was involved in the pathogenesis of UC and might become a potential therapeutic target.Mesalazine could down-regulate the protein expressions of p-STAT3,NF-κB and p-IκB,and down-regulate the mRNA expression of STAT3 and NF-κB.CONCLUSION Mesalazine may play a protective role in UC by reducing ER stress by regulating the STAT3/NF-κB signaling pathway.
文摘In order to study the effects of Saussurea laniceps polysaccharides(SLPs)on the expression of inflammatory factors and antimicrobial peptide LL-37 in UVB-induced keratinocytes,SLPs were extracted by the ethanol thermal reflux method,and SLPs at different concentrations were used to examine the inhibitory effect of COX-2(a key mediator of inflammatory pathway).A cell model of UVB irradiation-induced inflammation was established to determine the influence of SLPs on prostaglandin E2(PGE-2),TNF-αand IL-1βinflammatory factors,as well as the relationships of SLPs with LL-37 expression.An enzyme-linked immunosorbent assay(ELISA)and western blot analysis were used to detect the production of inflammatory factors and LL-37 antimicrobial peptide.The results showed that the inhibition rate of COX-2 was 82.41%at 1000μg/mL,and the expression of PGE-2,TNF-αand IL-1βinflammatory factors in HaCaT cells was significantly downregulated at 100μg/mL(P<0.01).In addition,SLPs at 50μg/mL and 100μg/mL concentrations enhanced the expression of LL-37 antimicrobial peptide(P<0.01),thereby down-regulating the expression of TNF-αand IL-1βinflammatory factors,then reducing skin inflammation.Conclusion:SLP can significantly inhibit the inflammatory response induced by UVB,and can further slow down the damage caused by inflammation to the skin by regulating LL-37 antimicrobial peptides,which has the potential to prevent skin inflammatory damage caused by UVB irradiation.
基金funded by the National Natural Science Foundation of China(81902815,81802786)the Natural Science Foundation of Shandong Province(ZR2023MH011,ZR2019BH044,ZR2018BH025).
文摘Background:VPS37A(VPS37A subunit of ESCRT-I),a component of the ESCRT-I(endosomal sorting complex required for transport I)complex,mediates vesicular trafficking through sorting endocytic ubiquitinated cargos into multivesicular bodies(MVBs).Although accumulating evidence indicates that VPS37A deficiency occurs in numerous malignancies and exerts tumor-suppressive effects during cancer progression,its functional significance in colorectal cancer(CRC)pathogenesis remains poorly characterized.Therefore,this study aims to further investigate the functional and molecular mechanisms by which VPS37A downregulation contributes to malignant biological phenotypes in CRC,with a specific focus on how its dysregulation affects cell death pathways.Methods:Multi-omics analysis of TCGA,GEO,and CPTAC cohorts identified VPS37A as a downregulated tumor suppressor gene in CRC.The prognostic relevance of VPS37A was validated in two clinical cohorts(Cohorts 1 and 2)using immunohistochemistry.Functional assays in VPS37A-overexpressing CRC cells and xenografts assessed proliferation,cell cycle progression,and stress-induced cell death.RNA sequencing,nuclear factor kappa-B(NF-κB)luciferase reporter assays,and lysosomal inhibition experiments elucidated the mechanisms underlying tumor necrosis factor receptor 1(TNFR1)degradation.Results:VPS37A is significantly downregulated in advanced-stage CRC and independently predicts poor survival.Functionally,VPS37A overexpression suppresses proliferation and induces G2/M arrest in vitro,while reducing xenograft growth.Under metabolic stress(glucose deprivation/galactose adaptation),VPS37A triggers cell death via apoptosis,necroptosis,and ferroptosis.Mechanistically,VPS37A redirects TNFR1 to lysosomal degradation,suppressing NF-κB nuclear translocation and transcriptional activity.Conclusion:VPS37A deficiency drives CRC progression by sustaining TNFR1/NF-κB signaling under metabolic stress.Restoring VPS37A activity promotes TNFR1 degradation,offering a therapeutic strategy to counteract NF-κB-mediated treatment resistance in CRC.
基金supported by grants from the Scientific and Technological Research Program of Chongqing Municipal Education Commission(KJ1400220)the Basic Science and Frontier Technology Research Program of Chongqing Science and Technology Commission(cstc2017jcyjAX0224)
文摘Background: Interleukin-37 b(IL-37 b), a vital negative regulator of the innate immune system, has been reported to be a tumor inhibitor in different type of cancers. However, little is known about the relationship between IL-37 b and hepatocellular carcinoma(HCC). The present study aimed to investigate the potential roles of IL-37 b in HCC progression. Methods: Subjects( n = 237) were recruited, and serum IL-37 b was measured using ELISA. The tumorsuppressive capacity and underlying mechanisms of IL-37 b in HCC were investigated in vitro and in vivo. Results: Compared to healthy controls, serum IL-37 b levels were elevated in chronic hepatitis B(CHB) patients but decreased significantly in HBV-HCC patients, especially for those with portal venous tumor thrombus. Low level serum IL-37 b in HBV-HCC patients correlated with high HCC stage and poor overall survival and disease-free survival. In vitro and in vivo, recombinant human IL-37 b inhibited proliferation and metastasis in HCC cells. Furthermore, IL-37 b inhibited epithelial mesenchymal transition in HCC cells in vitro by downregulating IL-6, pSTAT3(Y705), N-cadherin, and vimentin expression and by upregulating E-cadherin expression. These effects were partially reversed by transfection of adenovirus encoding human IL-6. Conclusions: IL-37 b inhibits HCC growth, metastasis and epithelial mesenchymal transition by regulating IL-6/STAT3 signaling. Serum IL-37 b may be a biomarker for HBV-HCC and its staging.
文摘白细胞介素-1(IL-1)家族成员IL-1F7(IL-1 family 7)最近被命名为IL-37,它共有五种不同的亚型(IL-37a-e)。研究表明,IL-37b(IL-1F7b)可以与IL-18受体的α链结合,但并不影响IL-18的生理功能;IL-37b与IL-18结合蛋白(IL-18BP)结合后,可以增强IL-18BP对IL-18的抑制作用。IL-37b的主要作用是抑制炎症反应,它在多种炎症相关性疾病中起重要作用。
