Effect of Nuclear Factor-κB on Airway Remodeling in Asthmatic Rats

Summary In order to investigate the effect of nuclear factor-κB (NF-κB) on airway remodeling in asthmatic rats. 18 Wistar rats were divided into three groups: asthmatic group: pyrrolidine dithiocarbamate (PDTC) group, in which rats were injected intraperitoneally with NF-κB specific inhibitor PDTC (100 mg/kg) before ovalbumin (OVA) challenge; control group. The NF-κB activity and the expression of inhibitory protein κBα (I-κBα) in airway were detected by electrophoretic mobility shift assay (EMSA). Western blot and immunohistochemistry respectively. The infiltration of inflammatory cells, the number of Goblet cells, the area of collagen and smooth muscle in airway were measured by means of image analysis system. The results showed that with the up-regulation of airway NF-κB activity in asthmatic group, the number of goblet cells (3.08±0.86/100 μm basement membrane (BM)), the area of collagen (24.71±4.24 μm²/μm BM) and smooth muscle (13.81±2.11 μm²/μmBM) in airway were significantly increased (P<0.05) as compared with control group (0.14±0.05/100μmBM. 14.31±3.16 μm²/μm BM and 7.67±2.35 μm²/μm BM respectively) and PDTC group (0.33±0.14/100 μmBM, 18.16±2.85 μm²/μm BM and 8.95±2.16 μm²/μm BM respectively). However, there was no significant difference between PDTC group and control group (P>0.05). It was concluded that the activity of NF-κB is increased in airway of asthmatic rats. Inhibition of NF-κB, activation can attenuate constructional changes in asthma airway, suggesting NF-κB may contribute to asthmatic airway remodeling. XU Shuyun, female, born in 1970, M. D. Ph. D. This project was supported by a grant from Foundation for University Key Teacher by the Ministry of Education (2000 year).     

Increased expression of receptor activator of nuclear factor-κB ligand in osteoblasts from adolescent idiopathic scoliosis patients with low bone mineral density

Persistent generalized low bone mineral density (BMD) has been reported in patients with adolescent idiopathic scoliosis (AIS).However,the exact mechanisms and causes of the low BMD in AIS patients are largely unknown.The purpose of this study was to examine the relationship between the receptor activator of NF-κB ligand (RANKL)/osteoprotegerin (OPG) levels in osteoblasts (OBs) from AIS patients with low BMD and with comparison made between the patients and controls.Twenty AIS patients and eight age-matched controls were included in the present study.The BMD of lumbar spine and proximal femur was measured in all subjects.OBs from the cancellous bone of each subject was harvested and primarily cultured.The mRNA and protein expression of RANKL and OPG in OBs was detected by RT-PCR and Western blotting.The results showed BMD was lower in AIS patients than in controls.A significantly higher mRNA and protein expression of RANKL was observed in OBs from AIS patients,while no significant difference was found in the expression of OPG between AIS patients and controls.As a result,RANKL/OPG ratio in patients with AIS was remarkably higher than controls.Our study preliminarily demonstrated expression of RANKL was higher in OBs from AIS patients with low BMD as compared with controls,suggesting the unbalanced RANKL/OPG ratio caused by an over-expression of RANKL in OBs may be responsible for the low BMD in AIS patients.     

Effects of Triptolide on the Expression and Activity of NF-κB in Synovium of Collagen-induced Arthritis Rats

Summary： The expression and activity of NF-kB in the synovium of collagen-induced arthritis （CIA） rats was detected in order to investigate the possible therapeutic effects of triptolide on rheumatoid arthritis （RA）. The experimental Wistar rat model of CIA was set up by intradermal injection of emulsion of bovine collagen 11 and the successful rate of setting-up models was evaluated by arthritis index （AI）. Rats were grouped randomly into three groups： normal, model and treatment group. The expression of TNF-α and IL-6 in synovial fluid was detected by ELISA, and the expression and activity of NF kB in synovium by immunohistochemistry method and by electrophoretic mobility shift assay （EMSA） respectively. As compared with normal group, the expression of TNF a and IL-6 in synovia （P〈0. 05）, and the expression and activity of NF-kB （P〈0.05） in synovium were increased in model group. There was statistical difference in above-mentioned indexes between model group and treatment group. Triptolide may play a protective role in IRA via downregulating the expression and activity of NF-kB in synovium.     

Expression of Nuclear Factor-κB in Mouse Uterus during Peri-implantation

To investigate the expression of the subunit p65 of NF-κB and inhibitor kappa B alpha (IκBα) in mouse uterus during peri-implantation, thereby investigating whether transient activation of nuclear factor-κB (NF-κB) takes place during embryo implantation in mice. Immunohistochemical technique was used to examine the expression and localization of p65 in endometrium or deciduas, and Western blot analysis was employed to detect the levels of IκBα protein in mouse endometrium or deciduas. P65 protein was detected in stromal cells, epithelial cells of endometrium as well as in myometrium. Staining was predominately seen in the cytoplasm of the cells. Staining intensity for p65 was stronger in the epithelial compartment than the stromal compartment and myometrium. Staining intensity increased slightly during pregnancy, and it reached a high level on pregnancy day 5 and day 8. In contrast to p65, the level of IκBα protein was lowest on pregnancy day 5 in all groups. Our results suggested that NF-κB may regulate embryo implantation by its transient activation in mice.     

Ursolic Acid Inhibits T-Cell Activation through Modulating Nuclear Factor-κB Signaling

<正>Objective:To investigate the effects of ursolic acid(UA) on T-cell proliferation and activation,as well as to examine its effect on nuclear factor-κB(NF-κB) signaling pathway in T cells.Methods:T-cells isolated from BALB/c mice were incubated with UA at concentrations ranging from 5-30μmol/L in the presence of phorbol 12-myristate 13-acetate(PMA) or PMA plus ionomycin.The proliferation of T cells was measured by the MTT assay.The expressions of CD69,CD25,and CD71 on T-cell surface were analyzed using flow cytometry. The level of interleukin-2(IL-2) in the culture supernatant of activated T cells was quantified by enzyme-linked immunosorbent assay(ELISA).The level of phosphorylated IκB-α(p-lκB-α) in total protein and p65,a subunit of NF-κB,nuclear translocation were measured by Western blot analysis.Results:UA in a dose-dependent manner significantly decreased the proliferation and inhibited the surface expressions of CD69,CD25,and CD71 in murine T lymphocytes upon in vitro activation(P0.01).Significant reduction of IL-2 production was found in activated T cells treated with UA(P0.01).The PMA-induced increase in p-lκB-αprotein was inhibited,and nuclear translocation of p65 from the cytoplasm was blocked by UA.Conclusion:UA is a potent inhibitor for T cell activation and proliferation;these effects are associated with the inhibition of NF-κB signaling pathway.     

Activation of NF-κB in bronchial epithelial cells from children with asthma

Objectives To determine whether nuclear factor-κB (NF-κB) is activated in epithelial cells from children with asthma and to understand the role of NF-κB in airway inflammation in asthma. Methods Bronchial mucosa specimens were obtained from 9 children with asthma and 6 control subjects. NF-κB expression in epithelial cells were detected by immunohistochemical examination, and NF-κB-DNA binding was measured by electrophoretic mobility shift assay (EMSA). Results Nuclear expression of NF-κB in epithelial cells was observed in the 9 asthmatic children. NF-κB-DNA binding was found in 4 asthmatic children (EMSA was performed in 6 asthmatic children). In contrast, both nuclear expression and NF-κB-DNA binding were absent in the 6 control subjects. Conclusion These results indicated that NF-κB is activated in epithelial cells from asthmatic children and the NF-κB activation may be the basis for the increased expression of many inflammatory genes and for airway inflammation in asthma.     

Inhibitory Effects of Parthenolide on the Activity of NF-κB in Multiple Myeloma via Targeting TRAF6

This study examined the mechanism of the inhibitory effect of parthenolide(PTL) on the activity of NF-κB in multiple myeloma(MM). Human multiple myeloma cell line RPMI 8226 cells were treated with or without different concentrations of PTL for various time periods, and then MTT assay was used to detect cell proliferation. Cell cycle and apoptosis were flow cytometrically detected. The level of protein ubiquitination was determined by using immunoprecipitation. Western blotting was employed to measure the level of total protein ubiquitination, the expression of IκB-α in cell plasma and the content of p65 in nucleus. The content of p65 in nucleus before and after PTL treatment was also examined with immunofluorescence. Exposure of RPMI 8226 cells to PTL attenuated the level of ubiquitinated Nemo, increased the expression of IκB-α and reduced the level of p65 in nucleus, finally leading to the decrease of the activity of NF-κB. PTL inhibited cell proliferation, induced apoptosis and blocked cell cycle. Furthermore, the levels of ubiquitinated tumor necrosis factor receptor-associated factor 6(TRAF6) and total proteins were decreased after PTL treatment. By using Autodock software package, we predicted that PTL could bind to TRAF6 directly and tightly. Taken together, our findings suggest that PTL inhibits the activation of NF-κB signaling pathway via directly binding with TRAF6, thereby suppressing MM cell proliferation and inducing apoptosis.     

Smilax China L. Rhizome Extract Inhibits Nuclear Factor-κB and Induces Apoptosis in Ovarian Cancer Cells

Objective: To study the antitumor effects and associated mechanisms of extract of the Smilax china L. rhizome (SCR) on ovarian cancer cells. Methods: Ovarian cancer cells A2780 were treated with different concentrations of SCR extract (SCRE), and compared with controls. Effects on cell growth were evaluated by cell counting kit-8 (CCK-8) assay; proliferation effects by EdU incorporation assay; cell cycle by propidium iodide staining; apoptosis by annexin V-fluorescein isothiocyanate/propidium iodide; cellular distribution of nuclear factor-κB (NF-κB) by immunofluorescence; protein levels of NF-κB, caspase-3, poly-adenosine diphosphate (ADP)-ribose polymerase (PARP), Bcl-2-associated X protein (Bax), cellular inhibitor of apoptosis (cIAP)-1, anti-X-linked inhibitor of apoptosis protein (XIAP), B-cell lymphoma-extra large (Bcl-XL), B-cell lymphoma-2 (Bcl-2) and AKT by Western blotting; and effects of SCRE combined with cisplatin or adriamycin on A2780 cells by CCK-8 assay. Results: SCRE suppressed A2780 cell proliferation in a dose-dependent manner (P<0.05, P<0.01), arrested cells in G2/M phase and induced apoptosis by activating caspase-3, PARP and Bax. SCRE treatment also correlated with inhibition of NF-κB and downregulation of Bcl-2, Bcl-XL, cIAP-1, XIAP and AKT. SCRE can promote chemosensitivity to cisplatin and adriamycin in A2780 cells (P<0.01). Conclusion: SCR effectively inhibits NF-κB, induces apoptosis and reduces chemoresistance to cisplatin and adriamycin in ovarian cancer cells, which might be its molecular basis for treating ovarian cancer.     

Implication of Receptor Activator of NF-κB Ligand in Wnt/β-Catenin Pathway Promoting Osteoblast-like Cell Differentiation

Recent studies showed that activation of Wnt/β-catenin pathway promoted the differentiation of osteoblast-like cells in the arterial calcification, but its mechanism remains unknown. In this study, the hypothesis that Wnt/β-catenin pathway promotes the differentiation of osteoblast-like cells by upregulating the expression of receptor activator of NF-κB ligand (RANKL) was examined. LiCl was used to activate the Wnt/β-catenin pathway. The differentiation of osteoblast-like cells was observed by Von Kossa staining, calcium content assay, alkaline phosphatase (ALP) activity assay, and detection of osteocalcin expression. Real-time PCR was performed to detect the expression of RANKL and osteoprotegerin (OPG, the decoy receptor of RANKL) during the osteoblast-like cell differentiation. Different concentrations of OPG were added to the culture media respectively to inhibit the function of RANKL, and the change in the differentiation of osteoblast-like cells was evaluated. The results showed that when the Wnt/β-catenin pathway was activated by LiCl, the expression of RANKL was significantly in-creased, which coincided with the differentiation of osteoblast-like cells (P<0.05), and the OPG treatment could partly attenuate the promoting effect of Wnt/β-catenin pathway on the differentiation of osteoblast-like cells (P<0.05), but it failed to completely abolish such effect. It was concluded that activation of Wnt/β-catenin pathway promotes the differentiation of osteoblast-like cells by both RANKL-dependent and RANKL-independent mechanisms.     

Effects of Huogu I Formula (活骨I方) on correlated factors of bone regeneration in chickens with steroid-induced necrosis of femoral head

Objective:To study the mechanism of HuoguⅠFormula（活骨Ⅰ方） in treating osteonecrosis of femoral head.Methods:Forty-eight healthy female Leghorn chickens were randomly divided into control group,model group and HuoguⅠgroup,and each group consisted of 16 chickens.At the meantime of model establishment,chickens of the HuoguⅠgroup were administrated with decoction,while the model and control group with distilled water by gavage.At the 8th and 16th week after medication,blood samples were obtained for blood lipid detection while both sides of femoral head were harvested for the rest of examinations.Specifically, expressions of bone morphogenetic protein-2（BMP2）,transforming growth factor betal（TGFβ₁）,Smad4 and Smad7 were evaluated by immunohistochemistry,while expression of osteoprotegerin/receptor activator of nuclear factor kappaB ligand（OPG/RANKL） mRNA was detected by in situ hybridization.Results:Compared with the control group,serum levels of total cholesterol（TC）,triglyceride（TG） and low-density lipoprotein cholesterol （LDL-C） in the model group rose significantly.Positive cell counting of BMP2,TGFβ₁,Smad4 and OPG in femoral head of the model group dropped prominently.Positive cell counting of Smad7 and RANKL increased dramatically. In contrast with the model group,levels of TC,TG and LDL-C in Huogu I group reduced significantly.Positive cell counting of BMP2,TGFβ₁,Smad4 and OPG in femoral head of the Huogu I group increased prominently. Indices of Smad7 and RANKL both decreased significantly.Especially at the 8th week,these variations were more significant.Conclusion:HuoguⅠFormula is effective in promoting repair of necrotic femoral head by regulating the expressions of BMP2,TGFβ₁,Smads and OPG/RANKL of osteoclast in femoral head.     

Effects of andrographolide on the activation of mitogen activated protein kinases and nuclear factor-κB in mouse peritoneal macrophage-derived foam cells

Objective:To observe the effect of andrographolide on the activation of mitogen-activated protein kinases(MAPKs) and expression of nuclear factor-κB(NF-k B) in macrophage foam cells.Methods:The mouse peritoneal macrophages were cultured in the media in the presence of oxidized low-density lipoprotein (ox-LDL),ox-LDL+andrographolide,or neither(control).The phosphorylation of MAPK molecules(p38MAPK, JNK,ERK1/2) and the expressions of NK-κB p65 were examined by Western blot.Results:As compared with cells in the control group,the expressions of phospho-p38 and NF-κB p65 were increased in the cells cultured with either ox-LDL or ox-LDL+andrographolide(P<0.01),but attenuated significantly in the presence of ox-LDL+ andrographolide when compared with ox-LDL(P<0.05).The phospho-JNK increased in the presence of either ox-LDL or ox-LDL+andrographolide when compared with control cells(P<0.01),but no significant difference existed between ox-LDL and ox-LDL+andrographolide(P>0.05).The expression of phospho-ERK1/2 was increased in the presence of ox-LDL compared with the control cells(P<0.01),but no significant differences existed between the cells cultured in the presence of ox-LDL+andrographolide and the control medium(P>0.05). Conclusions:Andrographolide could inhibit the activation of ERK1/2,p38MAPK and NK-k B induced by ox-LDL in macrophage foam cells,which might be one of its mechanisms in preventing atherosclerosis.     

Effect of Electroacupuncture Stimulation on mRNA Expression of Angiotensinogen,Angiotensin Ⅱ Type 1 Receptor,Endothelin-1,and Endothelin A Receptor in Spontaneously Hypertensive Rat Aorta

Objective: To observe the effect of electroacupuncture(EA) stimulation on the expressions of angiotensinogen(AGT), angiotensin Ⅱ type 1 receptor(AT1R), endothelin-1(ET1), and endothelin A receptor(ETAR) m RNA in spontaneously hypertensive rat(SHR) aorta. Methods: Eighteen male SHRs were randomly divided into three groups, an SHR group, an SHR Baihui(DU 20) and Zusanli(ST 36) acupoint(SHR-AP) group, and an SHR non-acupoint(SHR-NAP) group, with 6 rats in each group. Six Wistar rats were used as a control. Rats in the SHR-AP group were stimulated by DU 20 and ST 36 acupoints, both of which were connected with EA. EA was handled one time every Monday, Wednesday and Friday, for total 24 times(8 weeks). SHRNAP rats were acupointed at a 15°angle flat into 0.5 cm to two points, which were 1 and 2 cm from rail tip separately. EA parameters were the same as the SHR-AP rats. SHR control rats and Wistar rats were fixed without EA. Real-time quantitative polymerase chain reaction(PCR) was used to measure AGT, AT1 R, ET1, and ETAR m RNA expression in rat aorta. Results: EA stimulation significantly reduced rat aorta vascular AGT, ET1, ETAR and AT1 R m RNA expressions in the SHR-AP and SHR-NAP groups(P0.01). Among these four genes, AT1 R m RNA expression was significantly lower in the SHR-AP than in the SHR-NAP group(P0.01). Conclusion: EA could reduce the AT1 R m RNA expression in SHR-AP rat aorta, indicating a potential mechanism for the hypotensive effects of EA.     

Effect of Wenhua Juanbi Recipe (温化蠲痹方) on Expression of Receptor Activator of Nuclear Factor Kappa B Ligand, Osteoprotegerin, and Tumor Necrosis Factor Receptor Superfamily Member 14 in Rats with Collagen-Induced Arthritis

Objective: To study the effect of Wenhua Juanbi Recipe(温化蠲痹方, WJR) on expression of receptor activator of nuclear factor kappa B ligand(RANKL), osteoprotegerin(OPG), and tumor necrosis factor receptor superfamily member 14(TNFRSF14, also known as LIGHT) in rats with collagen-induced arthritis(CIA). Methods: CIA rats were generated by subcutaneous injection of bovine collagen type-Ⅱ at the tail base. Sixty CIA rats were randomly assigned(10 animals/group) to: model, methotrexate(MTX)-treated(0.78 mg/kg body weight), and WJR-treated(22.9 g/kg) groups. Healthy normal rats(n=10) were used as the normal control. Treatments or saline were administered once daily by oral gavage. Rats were sacrificed at day 28 post-treatment and knee synovium and peripheral blood serum were collected. Toe swelling degree and expression of RANKL, OPG, and LIGHT were determined by Western blot and immunohistochemistry. Results: Compared with the normal group, toe swelling degree was significantly increased in the model group(P0.01). After treatment, toe swelling degree decreased significantly in the WJR and MTX groups compared with the model group(P0.01). Compared with the normal group, expression of RANKL and LIGHT were significantly increased and OPG significantly decreased in peripheral blood and synovium of the model group(P0.01). Conversely, RANKL and LIGHT expression were significantly reduced and OPG increased in the WJR and MTX groups compared with the model group(P0.01). No statistically significant difference existed between WJR and MTX groups. Conclusion: WJR likely acts by reducing RANKL expression and increasing OPG expression, thus inhibiting RANKL/RANK interaction and reducing LIGHT expression, thereby inhibiting osteoclast formation/activation to block bone erosion.     

Role of β2-adrenoceptor-β-arrestin2-nuclear factor-κB signal transduction pathway and intervention effects of oxymatrine in ulcerative colitis

Objective:To investigate the β2-adrenoceptor(β2AR)-β-arrestin2-nuclear factor-κB(NF-κB) signal transduction pathway and the intervention effects of oxymatrine in a rat model of ulcerative colitis.Methods: Forty SD rats were randomly divided into four groups,which included the normal control group,the model group, the mesalazine group and the oxymatrine treatment group,with 10 rats per group.Experimental colitis induced with trinitrobenzene sulfonic acid(TNBS) was established in each group except the normal control group.The rats in the oxymatrine treatment group were treated with intramuscular injection of oxymatrine 63 mg/(kg·d) for 15 days and the rats in the mesalazine group were treated with mesalazine solution 0.5 g/(kg·d) by gastric lavage for 15 days. The rats in the normal control group and model group were treated with 3 mL water by gastric lavage for 15 days. Diarrhea and bloody stool were carefully observed.Histological changes in colonic tissue were examined on day 7 in 2 rats per group that were randomly selected.The expression of β2AR,β-arrestin2 and NF-κB p65 in colon tissue and spleen lymphocytes were detected with immunohistochemistry and Western immunoblotting techniques on day 16 after fasting for 24 h.Six rats died of lavage with 2 each in the normal control,the model group and the mesalazine group;and were not included in the analysis.Results:The rats in the model group suffered from looser stool and bloody purulent stool after modeling.But in the oxymatrine and mesalazine groups,looser stool and bloody purulent stool reduced after treatment.And the colonic wall in the model group was thickened and the colon length shortened.The colon mucosa was congested in multiple areas with edema,erosion,superficial or linear ulcer and scar formation,while the intestinal mucosa injury reduced in the mesalazine and oxymatrine groups(P<0.01).In colonic mucosa and in spleen lymphocytes,compared with the normal control group,the expression of NF-κBp65 were significantly increased(P<0.01) in the model group while the expressions ofβ2AR andβ-arrestin2 were significantly decreased(P<0.01).Compared with the model group,the expression of NF-κBp65 was significantly decreased in the mesalazine group(P<0.01) and oxymatrine treatment group(P<0.01) while the expressions of β2AR and β-arrestin2 were significantly increased(P<0.01).There were no statistically significant differences in the expression of β2AR,β-arrestin2 and NF-κBp65 between the mesalazine group and oxymatrine group(P>0.05).Conclusions:The β2AR-β-arrestin2-NF-κB signal transduction pathway participated in the pathologic course of ulcerative colitis.Oxymatrine attenuated ulcerative colitis through regulating the β2AR-β-arrestin2-NF-κB signal transduction pathway.     

Fuzheng Huayu Formula (扶正化瘀方) Prevents Rat Renal Interstitial Fibrosis Induced by HgCl2 via Antioxidative Stress and Down-regulation of Nuclear Factor-Kappa B Activity

Objective: To investigate the mechanism of action of Fuzheng Huayu Formula (扶正化瘀方, FZHY) against renal interstitial fibrosis (RIF) relating to oxidative injury and nuclear factor-kappa B (NF-κB) activity. Methods: Thirty-two Sprague-Dawley rats were randomly divided into 3 groups: normal group, model group and FZHY treatment group. The RIF model was induced by oral administration of HgCl2 at a dose of 8 mg/kg body weight once a day for 9 weeks. Meanwhile, rats in FZHY treatment group orally took FZHY at a dose of 4.0 g/kg rat weight for 9 weeks. The content of hydroxyproline (Hyp) and collagen deposition in kidney were observed. The activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), the content of glutathione (GSH) and malondialdehyde (MDA) of kidney were tested. The expressions of inhibitor-κappa B (IκB), phospho-IκB (p-IκB), tumor necrosis factor-α (TNF-α), matrix metalloproteinase-2 (MMP-2) and α-smooth muscle actin (α-SMA) were analyzed by Western blot. α-SMA expression was also observed by immunofluorescent staining. MMP-2 activity was measured by gelatin zymography. NF-κB activation was determined by electrophoretic mobility shift assay. Results: Renal interstitial fibrosis was induced by HgCl2, demonstrated by remarkably increased Hyp contents and excessive collagen deposition in kidney (P<0.01). FZHY significantly inhibited renal interstitial collagen deposition and reduced Hyp content of the HgCl2-treated rats (P<0.01). GSH content decreased obviously, and MDA content increased significantly in HgCl2-treated rats compared with that of normal rats (P<0.01). FZHY significantly increased GSH content and decreased MDA content in the model rats (P<0.01). The expression α-SMA was increased in model rats compared with that of normal rats, FZHY significantly decreased its expression (P<0.01). The expressions of p-IκB and TNF-α and MMP-2, MMP-2 activity, and NF-κB activation were increased in model group compared with that in normal group (P<0.01), FZHY significantly decreased NF-κB activation, MMP-2 activity and p-IκB and TNF-α expressions (P<0.01). Conclusions: FZHY could protect kidney from oxidative injury intoxicated by HgCl2, and antagonized oxidative stress-stimulated NF-κB activity through inhibition of IκB phosphorylation in the interstitial fibrotic kidney, these effects importantly contributed to FZHY action mechanism against renal interstitial fibrosis.     

Effect of gypenosides-containing serum on the NF-κB pathway in photoaging HaCaT cell

目的 探讨绞股蓝总皂苷含药血清对光老化人永生化皮肤角质形成细胞株(HaCaT)细胞分泌肿瘤坏死因子α(TNF-α)及调节核因子-κB (NF -κB)表达的干预作用.方法 采用中波紫外线(UVB)照射的方法建立光老化HaCaT细胞模型,并给予含不同浓度绞股蓝总皂苷的大鼠血清进行干预,12 h后采用ELISA、Western blot方法检测各组细胞分泌TNF-α含量及NF-κB蛋白的表达水平.结果 与正常对照组比较,紫外线(UV)模型组细胞培养上清液中TNF-α含量及细胞NF-κB表达水平显著上调.与UV模型组比较,低、中、高剂量绞股蓝总皂苷含药血清组细胞培养上清液中TNF-α含量及细胞NF -κB蛋白表达水平显著下调.结论 抑制NF -κB信号通路可能是绞股蓝总皂苷含药血清苷抑制皮肤光老化的作用机制之一.