TLR4-dependent adjuvant activity of Neisseria meningitidis lipid A

The adjuvant activity of Neisseria meningitidis serogroup B lipopoly(oligo)saccharide (LOS) from wild-type and genetically defined LOS mutants and unglycosylated meningococcal lipid A was assessed in C3H/HeN and C3H/HeJ mice. Meningococcal lipid A, a weak agonist for TLR4/MD-2 in human macrophages, was found to have adjuvant activity similar to that of wild-type and KDO(2)-lipid A LOS in C3H/HeN mice. All meningococcal LOS structures as adjuvants induced high titers of IgG1, IgG2a and IgG2b but very little IgG3 to OMP compared to no adjuvant PBS controls. In addition, induced OMP antibodies were shown to have high bactericidal activity against serogroup B meningococci. Purified LOS and lipid A structures failed to induce any adjuvant activity in C3H/HeJ mice indicating that meningococcal LOS as an adjuvant was TLR4-dependent. Unglycosylated meningococcal lipid A because of its weak agonist activity for human macrophages and retention of adjuvant activity may be a candidate for use in serogroup B meningococcal OMP and OMV vaccines and for use as an adjuvant in other vaccines.     

Phenotypic and functional maturation of dendritic cells induced by polysaccharide isolated from Paecilomyces cicadae

Paecilomyces cicadae Miquel Samson is the anamorph of Cordyceps cicadae Shing and is used in functional foods for the prevention and treatment of various diseases. In the present study, we examined the effects of P. cicadae polysaccharide (PCP) on dendritic cell (DC) maturation. Phenotypic maturation of DCs by PCP was confirmed by the elevated expressions of CD80, CD86, major histocompatibility complex (MHC)-I, and MHC-II molecules and functional maturation by increased expression of interleukin-12, interleukin-1β, and tumor necrosis factor-α, enhanced allogenic T cell stimulation, and decreased endocytosis. PCP induced the maturation of DCs from C3H/HeN and C57BL/6 mice but not from Toll-like receptor (tlr) 4?/? knockout mice and TLR4-mutated C3H/HeJ mice, which suggests that TLR4 is the membrane receptor for PCP. PCP increased the degradation of inhibitor of nuclear factor-κB (NF-κB) α/β, which enhanced the nuclear translocation of NF-κB p50/p65 and induced the phosphorylation of extracellular signal-regulated kinase, c-Jun N-terminal kinase, and p38 mitogen-activated protein kinases, which are signaling molecules downstream of TLR4. These results indicate that PCP induces DC maturation through TLR4 signaling.     

CTRP9抑制幼年哮喘小鼠气道平滑肌细胞增殖和炎性反应的研究

目的 研究C1q/肿瘤坏死因子相关蛋白9(CTRP9)对哮喘幼鼠气道平滑肌细胞(airway smooth muscle cells,ASMCs)增殖和气道炎症的作用。方法 ELISA检测正常、哮喘儿童和小鼠血清中CTRP9含量;原代培养哮喘小鼠ASMCs,经pcDNA3.1-CTRP9转染后,MTT检测ASMCs增殖,ELISA测定TNF-α和IL-6含量,Western 印记检测TLR4和NF-κB p65蛋白表达以及NF-κB p65磷酸化水平;pcDNA3.1-CTRP9转染哮喘小鼠,HE染色观察肺组织炎性细胞的浸润程度;收集小鼠支气管肺泡灌洗液(bronchoalveolar lavage fluid,BALF),光镜下检测嗜酸性粒细胞、巨噬细胞和中性粒细胞数目;检测小鼠肺部TNF-α、IL-6、TLR4和NF-κB的表达。结果 哮喘儿童和小鼠血清中CTRP9含量低于正常组;CTRP9能抑制ASMCs增殖、炎症因子分泌和TLR4/NF-κB通路活化;CTRP9也能抑制哮喘小鼠肺部炎性细胞浸润、各炎性反应细胞数目、炎症因子分泌和TLR4/NF-κB通路活化。结论 CTRP9能抑制幼年哮喘小鼠ASMCs增殖和炎性反应。     

Adjuvant effects of protopanaxadiol and protopanaxatriol saponins from ginseng roots on the immune responses to ovalbumin in mice

Protopanaxadiol saponins (Rg3, Rd, Rc, Rb1 and Rb2) and protopanaxatriol saponins (Rg1, Re and Rg2) isolated from the root of Panax ginseng C.A. Meyer were evaluated for their adjuvant effects on the immune responses to ovalbumin (OVA) in mice. BALB/c mice were subcutaneously injected twice at a 3-week interval with 10 microg of ovalbumin or 10 microg of OVA plus 50 microg of ginsenosides Rg3, Rd, Rc, Rb1, Rb2, Rg1, Re or Rg2 or Quil A (n=5). Blood samples were collected for measuring specific total-IgG, IgG1 and IgG2a, and splenocytes were harvested for determining lymphocyte proliferation as well as IFN-gamma and IL-5 production 2 weeks after the boosting. The results indicated that OVA-specific antibody responses were significantly higher in mice immunized with OVA co-administered with Rg1, Re, Rg2, Rg3 and Rb1 but not with Rd, Rc and Rb2 when compared with the control (immunized with OVA only). Significantly enhanced splenocyte proliferative responses to Con A, LPS and OVA as well as the production of both IL-5 and IFN-gamma stimulated by OVA were also detected in mice immunized with OVA co-administered with Rg1 but not with Rb1, Re and Rg3. Of the ginsenosides studied, Rg1, Re, Rg2, Rg3 and Rb1 have more potent adjuvant properties than the others, indicating that they are the major constituents contributing to the adjuvant activities of total ginseng saponins. Varieties of ginsenosides in adjuvant activity might be attributed to the varieties of molecular conformations determined by the side sugar chains attaching to their dammarane skeleton.     

白藜芦醇对脂多糖诱导小鼠腹腔巨噬细胞炎性因子生成的调控

目的探讨白藜芦醇(Res)对脂多糖(LPS)诱导小鼠腹腔巨噬细胞核因子-κB(NF-κB)活化及炎性细胞因子[肿瘤坏死因子(TNF-α)、白介素-1β(IL-1β)、白介素-6(IL-6)]基因表达的调节。方法分别用1mg/LLPS或25mmol/LRes+1mg/LLPS处理体外培养的小鼠巨噬细胞,采用电泳迁移率改变分析法(EMSA)检测细胞中NF-κB活性,逆转录-聚合酶链反应(RT-PCR)和酶联免疫吸附法(ELISA)检测细胞中TNF-α、IL-1β、IL-6mRNA和蛋白的表达。结果LPS组NF-κB活性和TNF-α、IL-1β、IL-6含量在刺激后6～12h明显高于正常对照组(P<0.001),而Res+LPS组NF-κB活性和TNF-α、IL-1β、IL-6含量均显著低于LPS组(P<0.005)。结论LPS可诱导巨噬细胞NF-κB活化,导致TNF-α、IL-1β、IL-6基因表达增强,而Res能抑制NF-κB活化而调节TNF-α、IL-1β、IL-6基因的表达。     

Stearidonic and eicosapentaenoic acids inhibit interleukin-6 expression in ob/ob mouse adipose stem cells via Toll-like receptor-2-mediated pathways

Increased adipose tissue positively correlates with circulating inflammatory cytokines such as IL-6. We previously reported that adipose stem cells from genetically obese ob/ob mice produce significantly higher levels of IL-6 compared with other cell types such as adipocytes and macrophages within adipose tissue. We also demonstrated that (n-3) PUFA have antiinflammatory effects on adipocyte IL-6 secretion. Based on these findings, we hypothesized that EPA [20:5 (n-3)] and stearidonic acid [SDA, 18:4 (n-3)] would decrease LPS (200 μg/L)-induced IL-6 secretion and IL-6 mRNA content in the adipose stem cells. SDA (100 μmol/L) and EPA (100 μmol/L) significantly reduced LPS-induced IL-6 secretion and decreased IL-6 mRNA expression. To determine the underlying intracellular mechanisms, we tested whether LPS-induced Toll-like-receptor (TLR) 4 and TLR2 expression were modulated by these fatty acids using Western-blot analysis. EPA and SDA suppressed LPS-induced TLR2 but not TLR4 protein expression in the adipose stem cells. Furthermore, SDA and EPA significantly lowered the activation and translocation of NF-κB, a TLR2 downstream signaling target, while protein expression of extracellular signal-regulated kinases-1/2 were unaffected. Collectively, our results suggest that EPA and SDA inhibit LPS-induced IL-6 secretion and IL-6 mRNA expression in the adipose stem cells by decreasing TRL2-mediated signaling pathways.     

Involvement of TLR4 in diazinon-induced neurotoxicity in mice

Our laboratory recently reported that Toll-like receptor (TLR) 4 may play a role in the neurotoxic effects in mice exposed to the environmental toxic chemical toluene. To investigate the role of TLR4 in hippocampal neurotrophin expression, C3H/HeN (TLR4 intact) and C3H/HeJ (TLR4 defective) male adult mice were administered diazinon (0, 0.05, 0.5 or 5 mg/kg) intraperitoneally once a week for three weeks. Twenty-four hours after the final diazinon injection, the hippocampus was collected from each mouse to detect mRNA expression of neurotrophins (nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF)) by the real-time RT-PCR method. There was no difference between groups in neurotrophin expression in the C3H/HeN mice. However, the expression of NGF and BDNF mRNAs was suppressed significantly in the diazinon-injected C3H/HeJ mice compared with their control group. We also found an increased tendency of proinflammatory chemokine CCL3 mRNA and a marked increase in the proapoptotic gene Bax mRNA in the diazinon-injected C3H/HeJ mice. Our findings indicate that diazinon injection affects neurotrophin expression in the hippocampus in TLR4-defective mice but not in TLR4 intact mice. These results suggest that a defective TLR4 signaling pathway in the mouse hippocampus can be easily affected by diazinon administration.     

长链非编码RNA核富含丰富的转录本1对癫痫模型海马神经元凋亡的影响和作用机制

目的 探讨长链非编码RNA(lncRNA)核富含丰富的转录本1(NEAT1)对癫痫细胞模型海马神经元凋亡的影响及作用机制,以期为NEAT1成为癫痫治疗的新靶点提供依据。方法 于2019年8月—2020年10月期间,体外培养大鼠海马神经元细胞,无镁诱导制备癫痫海马神经元模型,实验分为:对照组(正常细胞外液)、模型组(无镁细胞外液)、转染对照组(转染非特异性siRNA+无镁细胞外液)和转染组(转染NEAT1特异性siRNA+无镁细胞外液)。实时荧光定量PCR(qPCR)检测NEAT1和miR-29b-3p的表达变化,双荧光素酶报告基因实验检测NEAT1是否靶向调控miR-29b-3p,酶联免疫吸附法(ELISA)检测白细胞介素-1(IL-1)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的含量,AnnexinV-FITC/PI双染色法检测海马神经元细胞凋亡情况,蛋白免疫印迹法(Western blot)检测各组细胞中B细胞淋巴瘤/白血病-2(Bcl-2)、Bcl-2相关X蛋白(Bax)、Toll样受体4(TLR4)和核因子-κB(NF-κB)的表达水平。结果 与对照组相比,模型组海马神经元凋亡率及NEAT1、Bax、TLR4和NF-κB的表达水平升高(F＝50.980、73.668、65.635、13.203、10.292,P＜0.05),IL-1、IL-6和TNF-α的含量增多(F＝33.107、33.857、51.129,P＜0.05),miR-29b-3p和Bcl-2的表达水平降低(F＝145.023、67.655,P＜0.05);而抑制NEAT1的表达能够降低神经元凋亡,抑制Bax、TLR4和NF-κB的表达,促进miR-29b-3p和Bcl-2的表达,减少IL-1、IL-6和TNF-α的分泌。双荧光素酶报告基因实验证实NEAT1和miR-29b-3p的靶向关系。结论 lncRNA NEAT1靶向下调miR-29b-3p的表达阻断TLR4/NF-κB信号通路来抑制癫痫模型海马神经元的凋亡。     

Toll样受体7激动剂对荷瘤小鼠肾癌的抑制作用及免疫机制

目的　研究Toll样受体7激动剂Imiquimod对荷瘤小鼠肾癌的抑制作用及免疫机制。方法　用Renca肾癌细胞构建BABL/c小鼠肾癌模型,实验分为control组、imiquimod组和sorafenib组。观察3组小鼠肿瘤体积及重量、抑瘤率,qPCR法检测肿瘤组织中炎性相关因子肿瘤坏死因子α（Tumor necrosis factor-α,TNF-α）、白细胞介素1β（Interleukin-1β,IL-1β）、白细胞介素6（Interleukin-6,IL-6）、干扰素α（Interferon-α,IFN-α）、干扰素β（Interferon-β,IFN-β）、干扰素γ（Interferon-γ,IFN-γ）及Toll样受体通路相关因子Toll样受体7（Toll-like receptor 7,TLR7）、髓样分化因子88（Myeloid differentiation primary response gene 88,MyD88）、核因子κB （Nuclear factor κB,NF-κB）mRNA表达,Western blot法检测瘤组织中TLR7、MyD88、NF-κB蛋白表达。流式细胞术检测脾脏中CD4+T、CD8+T、CD4+IFN-γ和CD8+IFN-γ细胞比例。结果　与control组比较,imiquimod组和sorafenib组小鼠的肿瘤体积及瘤体重量降低（P＜0.05）;与control组相比,imiquimod组TNF-α、IL-6、IL-1β、IFN-α、IFN-β、IFN-γ及TLR7、MyD88、NF-κB mRNA水平升高（P＜0.05）,而sorafenib组各因子略有上升（P＞0.05）;与control组和sorafenib组比较,imiquimod组CD4+T、CD8+T细胞比例有不同程度的升高（P＞0.05）,CD4+IFN-γ和CD8+IFN-γ细胞比例增加（P＜0.05）。结论　Toll样受体7激动剂通过活化TLR7-MyD88-NF-κB信号刺激多种炎性细胞因子分泌,并上调CD4+T、CD8+T比例及功能,对荷瘤小鼠肾癌发挥抑制作用。     

Mycobacterium indicus pranii mediates macrophage activation through TLR2 and NOD2 in a MyD88 dependent manner

Mycobacterium indicus pranii (MIP) is a non-pathogenic strain of mycobacterium and has been used as a vaccine against tuberculosis and leprosy. Here, we investigated the role of different pattern recognition receptors in the recognition of heat-killed MIP by macrophages. Treatment of macrophages with MIP caused upregulation of pro-inflammatory cytokines (like TNFα and IL-1β) which was mediated through both TLR2 and NOD2, as revealed by our knockdown and/or knockout studies. Mechanistically, MIP-induced macrophage activation was shown to result in NF-κB activation and drastically abrogated by MyD88 deficiency, suggesting its regulation via an MyD88-dependent, NF-κB pathway. Interestingly, the IFN-inducible cytokine, CXCL10, which is known target of the TRIF-dependent TLR pathway was found to be upregulated in response to MIP but, in an MyD88-dependent manner. Collectively, these results demonstrate macrophages to recognize and respond to MIP through a TLR2, NOD2 and an MyD88-dependent pathway. However, further studies should clarify whether additional TLR-dependent or -independent pathways also exist in regulating the full spectrum of MIP action on macrophage activation.     

NF-κB对小鼠冠状病毒性肝炎致病作用

目的探讨肝脏核因子-κB(NF-κB)和血清辅助性T淋巴细胞(Th1/Th2)细胞因子方面对小鼠冠状病毒性肝炎的致病机制。方法采用4周龄雄性BALB/c小鼠,以鼠肝炎冠状病毒(MHV-A59)和大肠埃希菌作为生物致病因子,建立MHV-A59鼠肝炎模型和大肠埃希菌鼠肝炎对照模型,以正常健康小鼠为空白对照,采用免疫组化法检测小鼠肝脏NF-κB表达[吸光度(A)值],ELISA法检测小鼠血清白介素-4(IL-4)、干扰素-γ(IFN-γ)水平。结果冠状病毒模型组、大肠埃希菌对照组小鼠肝脏NF-κB表达分别为A=0.305,A=0.245;外周血Th1/Th2(IFN-γ/IL-4)比值分别为(2.17±0.16),(2.09±0.06)pg/mL,均比正常组有明显升高,差异有统计学意义(P0.05或P0.01),但冠状病毒模型组升高更明显。结论肝脏NF-κB表达增强及血清Th1/Th2细胞因子失衡可能是小鼠冠状病毒性肝炎的致病机制之一。     

Vitamin D-mediated attenuation of miR-155 in human macrophages infected with dengue virus: Implications for the cytokine response

Clinical manifestations of dengue disease rely on complex interactions between dengue virus (DENV) and host factors that drive altered immune responses, including excessive inflammation. We have recently established that vitamin D can modulate DENV-induced cytokine responses and restrict infection in human macrophages. Cytokine responses are finely regulated by several homeostatic mechanisms, including microRNAs (miRNAs) that can rapidly target specific genes involved in the control of immune signaling pathways. However, the modulation of miRNAs by vitamin D during DENV infection is still unknown. Here, using a qPCR miRNA array we profiled immune-related miRNAs induced by DENV infection in human monocyte-derived macrophages (MDM) differentiated in absence or presence of vitamin D (D₃-MDM). We found several miRNAs differentially expressed in both MDM and D₃-MDM upon DENV infection. Interestingly, from these, a set of 11 miRNAs were attenuated in D₃-MDM as compared to MDM. Gene set enrichment analysis of the predicted mRNA targets of these attenuated miRNAs suggested a predominant role of miR-155-5p in the TLR-induced cytokine responses. Indeed, validation of miR-155-5p attenuation in D₃-MDM was linked to increased expression of its target gene SOCS-1, a key component for TLR4 signaling regulation. Likewise, TLR4 activation with LPS further corroborated the same miR-155-5p/SOCS-1 negative correlation observed in D₃-MDM upon DENV exposure. Moreover, D₃-MDM differentiation induced down-regulation of surface TLR4 that was linked to less TLR4/NF-κB-derived secretion of IL-1β. These data suggest a key role of vitamin D in the control of inflammatory cytokine responses during DENV infection of human macrophages via the TLR4/NF-κB/miR-155-5p/SOCS-1 axis.     

脑梗死合并肺部感染患者TNF-α、HMGBl、TLR4-NF-κB信号通路改变研究

目的探究脑梗死合并肺部感染患者的肿瘤坏死因子-α(Tumor necrosis factor-α,TNF-α)和高迁移率族蛋白Bl(High mobility group protein Bl,HMGBl)水平及其临床价值研究。方法2018年1月-2019年2月儋州市人民医院收治的急性脑梗死患者作为研究对象,其中急性脑梗死合并肺部感染患者30例作为感染组,急性脑梗死无肺部感染患者80例作为非感染组,选择同期于此医院体检的健康者30名作为对照组。采用酶联免疫吸附法(Enzyme-linked immuno sorbent assay,ELISA)检测血清HMGB1和细胞因子IL-6、TNF-α水平,采用Western Blot法检测血清Toll样家族受体-4(Toll like receptor-4,TLR4)、核因子κB(nuclear factor kappa-B,NF-κB)、髓样分化因子(myeloiddifferentiationfactor88,MyD88)表达水平。结果感染组的血清HMGB1、TLR4、NF-κB、MyD88表达及细胞因子IL-6、TNF-α水平均高于非感染组和对照组(P<0.05);感染组患者大梗死灶、中等梗死灶、小梗死灶各指标总体水平差异具有统计学意义(P<0.05)。大梗死灶、中等梗死灶两亚组患者的血清HMGB1、TLR4、NF-κB、MyD88表达及细胞因子IL-6、TNF-α水平均高于小梗死灶亚组(P<0.05);急性脑梗死合并肺部感染患者的血清HMGB1和TNF-α水平呈正相关(r=0.523,P<0.001)。结论脑梗死合并肺部感染患者伴随TNF-α、HMGBl、TLR4-NF-κB信号通路的明显改变,且与梗死灶大小具有相关性,其机制有待进一步研究。     

Toll样受体和核转录因子-κB在子痫前期患者胎盘组织中的表达

目的：探讨子痫前期患者胎盘组织中Toll样受体4（TLR4）以及核转录因子（NF-κB）表达及意义。方法：选取50例子痫前期患者（轻度子痫前期20例,重度子痫前期30例）作为研究对象,以30例正常晚孕妇女作为正常对照,采用免疫组化及逆转录-聚合酶链反应（RT-PCR）法测定胎盘组织中TLR4及NF-κB的定位及表达。结果：轻、重度子痫前期患者胎盘组织中TLR4及NF-κB蛋白和mRNA的表达水平均明显高于正常晚孕妇女（P〈0.05）。且随着病情加重,两者表达均增强;子痫前期胎盘组织中TLR4和NF-κB的表达呈正相关（P〈0.05）。结论：TLR4介导的炎症因子释放可能是导致子痫前期发生的重要原因之一。     

The virus-induced signaling adaptor molecule enhances DNA-raised immune protection against H5N1 influenza virus infection in mice

As an adaptor molecule in the retinoic acid-inducible gene-I (RIG-I) signaling pathway, the virus-induced signaling adaptor (VISA) molecule activates NF-κB and IRF3 and thereby leads to the production of type I interferons (IFNs). To explore the potential of VISA as a genetic adjuvant for DNA vaccines, a eukaryotic expression plasmid, pVISA, was generated by cloning the VISA gene into the pVAX1vector. For comparison, the pTRIF plasmid was similarly constructed, encoding the known genetic adjuvant TRIF (TIR-domain-containing adapter-inducing interferon-β), an adapter in the Toll-like receptor (TLR) signaling pathway. Mice were immunized with the chimeric DNA vaccine pHA/NP_147-155, which encodes the HA (hemagglutinin) fused with NP (nucleoprotein) CTL epitope (NP_147-155) of H5N1 influenza virus, either alone or in combination with pVISA or pTRIF. Antigen-specific immune responses were examined in immunized mice. Our results demonstrate that co-immunization of the pHA/NP_147-155 plasmid with the VISA adjuvant augmented DNA-raised cellular immune responses and provided protection against H5N1 influenza virus challenge in mice. In addition, our data suggest that VISA acts as a stronger adjuvant for DNA immunization than TRIF. We conclude that co-inoculation with a vector expressing the adaptor molecule VISA enhanced the protective immunity against H5N1 infection induced by pHA/NP_147-155 and that VISA could be developed as a novel genetic adjuvant for DNA vaccines.     

Indole-containing fractions of Brassica rapa inhibit inducible nitric oxide synthase and pro-inflammatory cytokine expression by inactivating nuclear factor-κB

In an attempt to identify bioactive natural products with anti-inflammatory activity, we evaluated the anti-inflammatory potential of the indole-containing fraction from the roots of Brassica rapa (IBR) (Family Brassicaceae) and the underlying mechanisms. Initially, we examined the inhibitory effect of IBR on the production of pro-inflammatory mediators in vitro and then evaluated its in vivo anti-inflammatory effects. IBR was found to concentration-dependently reduce the productions of nitric oxide, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in lipopolysaccharide (LPS)-induced macrophages. Consistent with these findings, IBR suppressed the LPS-induced expressions of inducible nitric oxide synthase (iNOS) at the protein level and of iNOS, TNF-α, and IL-6 at the mRNA level. Furthermore, IBR attenuated LPS-induced DNA-binding activities of nuclear factor-κB (NF-κB), and this was accompanied by a parallel reduction in the degradation and phosphorylation of inhibitory κBα and, consequently, by a reduction in the nuclear translocation of the p65 subunit of NF-κB. In addition, treatment with IBR inhibited carrageenan-induced paw edema in rats and acetic acid-induced writing response in mice. Taken together, our data suggest that the expressional inhibitions of iNOS, TNF-α, and IL-6 caused by an attenuation of NF-κB activation are responsible for the anti-inflammatory and antinociceptive activity of IBR.     

人参皂苷Rg1通过NF-κB阻断缺氧诱导卵巢癌SKOV3细胞EMT

目的 探讨人参皂苷Rg1对卵巢癌SKOV3细胞上皮间质转化的影响及机制.方法 确定人参皂苷Rg1对SKOV3细胞生长的影响,构建缺氧诱导上皮间质转化(EMT)模型,观察细胞形态变化,检测E-cadherin,vimentin及核因子KappaB(NF-κB)蛋白的表达.结果 不同浓度的人参皂苷Rg1处理SKOV3细胞,超过40μg/mL的Rg1培养24h时对细胞生长稍有抑制,培养48h和72h时对细胞生长无明显抑制.缺氧诱导48h,SKOV3细胞呈现纺锤形、松散排列的形态,E-cadherin蛋白表达消失,vimentin蛋白表达增强.40μg/mL人参皂苷Rg1处理缺氧诱导的SKOV3细胞48h,细胞形态变化被部分逆转.E-cadherin蛋白表达恢复,vimentin蛋白表达被抑制,同时,NF-κB蛋白的表达与E-cadherin呈相反的趋势.结论 人参皂苷Rg1可能通过调控NF-κB抑制缺氧诱导卵巢癌SKOV3细胞的EMT.