scholarly journals Effect of Zhuang Medicine Feilongzhangxue on the Expression of HMGB1-TLR4 / RANKL-NF-?B Signaling Pathway Related Factors in Osteoclasts

2021 ◽  
Vol 5 (3) ◽  
Author(s):  
Qinghuai Zhang ◽  
Zhiyong Cao ◽  
Lan Huang ◽  
Yimin Zhang ◽  
Zhao Tian ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Inhibitory Effect ◽  
Control Group ◽  
Test Results ◽  
Regulatory Effect ◽  
Rt Pcr ◽  
Immunofluorescence Test ◽  
Related Factors ◽  
Blank Group ◽  
Protein Expressions

Objective: To study the regulatory effect of feilongzhangxue on the levels of HMGB1-TLR4 / RANKL-NF-?B signaling pathway related factors HMGB1, RANKL, rank, TRAF-6 and NF-?Bp65 in osteoclasts, so as to explore the mechanism of feilongzhangxue intervention in RA; Methods: The osteoclasts with good activity were randomly divided into blank group, methotrexate control group and Zhuang medicine feilongzhang blood containing serum treatment group, which were divided into OC + blank group, OC + methotrexate control group, OC + Zhuang medicine feilongzhang blood containing serum group; The expression of HMGB1, RANKL, rank, TRAF-6 and NF-?Bp65 mRNA was detected by RT-PCR; The protein expressions of HMGB1, RANKL, RANK, TRAF-6 and NF-?Bp65 were detected by immunofluorescence. Results: PCR results showed that: Compared with the blank group, feilongzhangxue could effectively inhibit the expression levels of HMGB1, RANKL, rank, TRAF-6 and NF-? B p65 mRNA in OC cells, and the inhibitory effect was stronger than methotrexate. Immunofluorescence test results showed that: Compared with the blank group and methotrexate group, feilongzhangxue could effectively inhibit the protein expression of HMGB1, RANKL, rank, TRAF-6 and NF - ? B p65 in OC cells. Conclusion: The effect of Zhuang medicine feilongzhangxue on hmgb1-tlr4 / rankl-nf - ? B signaling pathway of osteoclasts is through the regulation of related factors HMGB1, RANKL, rank, TRAF-6 and NF-?Bp65, which may be the key mechanism of Zhuang medicine feilongzhangxue on rheumatoid arthritis.

Mesoporous TiO2 Nanaoparticles Inhibits Malignant Pancreatic Cancer Cells Through STAT Pathway

2021 ◽  
Vol 13 (9) ◽  
pp. 1716-1723
Author(s):  
Jie Li ◽  
Chao Xu ◽  
Yueyue Lu ◽  
Yan Zhang ◽  
Xiaoping Tan
Keyword(s):  
Pancreatic Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Inhibitory Effect ◽  
Positive Control ◽  
Control Group ◽  
Blank Group ◽  
Pancreatic Cancer Cells ◽  
Experimental Group ◽  
Stat Pathway

Nanoparticles are known to have recognition ability for targeted delivery, and are thus widely used in the treatments of diseases. Mesoporous nano-titanium dioxide (TiO2) nanoparticles have characteristics of nanomaterials and their porous structure with high surface area strengthens their drug-loading capacity and targeting ability. This study aimed to investigate the effect of mesoporous nano-TiO2 on pancreatic cancer cells and STAT pathway activity. Initially, we prepared mesoporous TiO2 nanoparticles that were characterized. Pancreatic cancer cells were co-cultured with mesoporous nano-TiO2 nanoparticles at different concentrations (0.1 μg/mL, 0.5 μg/mL, 1 μg/mL, 5 μg/mL, and 10 μg/mL) or 10 μg/mL nano-TiO2 (positive control group) or cells cultured alone (blank group). Cell viability was determined at several specific time points (24 h, 48 h, and 72 h). Transwell assay and scratching assay were conducted to determine the number of migrated and invaded cells. STAT3 and JAK2 expressions were examined by RT-qPCR and Western blot analysis. The prepared mesoporous nano-TiO2 exhibited sharp diffraction peaks with enhanced intensity and diffraction rings. STAT pathway was activated in pancreas cancer cells, which had more fluorescent cells than normal cells. The presence of mesoporous nano-TiO2 nanoparticles suppressed cancer cell viability and their inhibition rate increased with increased of nano-TiO2 concentration. The concentration of 10 μg/mL exhibited greatest inhibitory effect and 10 μg/mL mesoporous nano-TiO2 thus was chosen for experimental group. The width of the scratch in the experimental group (19.97±0.82 mm) was higher than in the blank group and positive control group (P < 0.05); 10 μg/mL mesoporous nano-TiO2 significantly decreased the number of invaded cells (71.97±17.84) and number of cell clones (156.91±31.03) (P < 0.05). The expression levels of STAT3 (0.41±0.06 μg/μL) and JAK2 (0.39±0.04 ug/ul) were diminished by treatment with mesoporous nano-TiO2. Mesoporous nano-TiO2 inhibits pancreatic cancer cell growth and STAT expression, as its inhibitory effect depends on its concentration. These findings might provide a novel insight into nanoparticle-based treatment for pancreatic cancer.

scholarly journals Effect of Curcumol on the Fenestrae of Liver Sinusoidal Endothelial Cells Based on NF-κB Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Yang Zheng ◽  
Jiahui Wang ◽  
Jiaru Wang ◽  
Haiyuan Xie ◽  
Tiejian Zhao
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Signaling Pathway ◽  
Intervention Group ◽  
Positive Control ◽  
Positive Control Group ◽  
Control Group ◽  
Rt Pcr ◽  
Liver Sinusoidal Endothelial Cells ◽  
Scanning Electron

Objective. To study the effect of curcumol on liver sinusoidal endothelial cells (LSECs) and to analyze the mechanism of antihepatic fibrosis. Methods. The effects of drug intervention on cell proliferation rates were detected by MTT assay. The expression of NF-κB was detected by RT-PCR and WB. The NF-κB expression and entry into the nucleus were detected by immunofluorescence; scanning electron microscopy was used to observe the changes of LSECs fenestrae. Results. MTT results showed that the interference of cell proliferation in each group was small. RT-PCR showed that the expression of NF-κB in the curcumol intervention group was significantly lower than that in the positive control group (P<0.05). The WB detection found that, in the curcumol intervention group, the expression of pNF-κB in the NF-κB signaling pathway was significantly lower than that in the positive control group (P<0.05). Scanning electron microscopy showed that the LSEC fenestrae were significantly improved compared with the positive control group. Conclusion. Curcumol may be one of the mechanisms of antihepatic fibrosis by inhibiting the activity of the NF-κB signaling pathway and increasing the fenestrae of LSECs.

scholarly journals Puerarin Suppress Apoptosis of Human Osteoblasts via ERK Signaling Pathway

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Ling-juan Liu ◽  
Li-qun Liu ◽  
Tao Bo ◽  
Shi-jun Li ◽  
Zhen Zhu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Chinese Herb ◽  
Inhibitory Effect ◽  
Erk Signaling ◽  
Control Group ◽  
Human Osteoblasts ◽  
Antiapoptotic Effect ◽  
Protein Levels ◽  
Bax Protein ◽  
Radix Puerariae

Puerarin, the main isoflavone glycoside extracted from Radix Puerariae, is an isoflavone traditional Chinese herb. Previous studies have demonstrated that puerarin could regulate osteoblast proliferation and differentiation to promote bone formation. However, the effect of puerarin on the process of human osteoblasts (hOBs) apoptosis is still unclear. In this study, we detected the function of puerarin on serum-free-induced cell apoptosis using ELISA and TUNEL arrays and then found that the mortality of hOBs was significantly decreased after exposure to 10−10–10−6 M puerarin and reached the maximal antiapoptotic effect at the concentration of 10−8 M. In addition, compared with the control group, puerarin notably increased the Bcl-2 protein levels while it decreased the Bax protein levels in the hOBs in a dose-dependent way. 10−7 M puerarin decreased the Bax/Bcl-2 ratio with a maximal decrease to 0.08. Moreover, puerarin activated ERK signaling pathways in hOBs, and the antiapoptotic effect induced by puerarin was abolished by incubation of ERK inhibitor PD98059. Similarly, the estrogen receptor antagonist ICI182780 also suppressed the inhibitory effect of puerarin on hOBs apoptosis. In conclusion, puerarin could prevent hOBs apoptosis via ERK signaling pathway, which might be effective in providing protection against bone loss and bone remolding associated with osteoporosis.

scholarly journals Intermittent Stretching and Osteogenic Differentiation of Bone Marrow Derived Mesenchymal Stem Cells via the p38MAPK-Osterix Signaling Pathway

2015 ◽  
Vol 36 (3) ◽  
pp. 1015-1025 ◽  
Author(s):  
Wen-lin Xiao ◽  
Dai-zun Zhang ◽  
Cun-hui Fan ◽  
Bao-jun Yu
Keyword(s):  
Western Blot ◽  
Osteogenic Differentiation ◽  
Signaling Pathway ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Mechanical Strain ◽  
Control Group ◽  
Rt Pcr ◽  
Rnai Technology ◽  
P38mapk Signaling

Aims: The relationship between the p38MAPK signaling pathway and osterix in osteogenic differentiation of BMMSCs subjected to intermittent stretching was investigated. Methods: BMMSCs derived from C57BL/6J mice were divided into the following groups: 1) control, 2) stretch, and 3) SB203580+stretch (SB203580 is a p38MAPK signal pathway inhibitor). BMMSCs were exposed to an intermittent mechanical strain of 0.8% (8000μ strain) at 0.5 Hz, twice a day for 30 min each application. BMMSCs were harvested on days 1, 3, and 5 post-treatment. The expression of ALP, COL I, OCN, and osterix mRNA was assessed utilizing RT-PCR while the expression of P-p38MAPK and osterix protein was assessed by Western blot analysis. The osterix gene in mouse BMMSCs was knocked down using RNAi technology and its protein expression was also assessed by Western blot. RT-PCR was used to detect ALP, COL I, and OCN mRNA expression. Results: Intermittent stretching was found to promote expression of ALP, COL I, OCN, and osterix mRNA. Silencing the osterix gene was found to reduce levels of ALP, COL I, and OCN mRNA. Western blot analysis demonstrated that the levels of osterix and P-p38MAPK proteins in the stretch group were significantly higher than in the control group (P<0.05). There was less expression of ALP, COL I, OCN, and osterix mRNA in the SB203580+stretch group than in the control and stretch groups. Conclusions: Data demonstrate that intermittent stretching promotes osteogenic differentiation of BMMSCs, and the p38MAPK-osterix pathway has an important role in the control of osteogenesis-related gene expression.

scholarly journals IL-38 restrains inflammatory response of collagen-induced arthritis in rats via SIRT1/HIF-1α signaling pathway

2020 ◽  
Vol 40 (5) ◽  
Author(s):  
Bing Pei ◽  
Keyan Chen ◽  
Shenglai Zhou ◽  
Dongyu Min ◽  
Weiguo Xiao
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathway ◽  
Joint Damage ◽  
Inhibitory Effect ◽  
Angiogenic Factor ◽  
Inflammatory Factors ◽  
Control Group ◽  
Collagen Induced Arthritis ◽  
Related Proteins

Abstract Objective: To observe the restraining effect of IL-38 on inflammatory response in collagen-induced arthritis rats (CIA), and to explore the regulatory mechanism of SIRT1/HIF-1α signaling pathway. Methods: 40 SD rats were randomly divided into Control group, CIA group, CLL group and CLH group, with 10 rats in each group; CIA rat model was established. The effects of IL-38 on arthritis index, inflammatory response, osteogenic factor and angiogenic factor were observed by methods including HE staining, ELISA, immunohistochemical and immunofluorescence. Human synoviocytes were cultured in vitro, and SIRT1 inhibitors were added to detect the expression for relating factors of SIRT1/HIF-1α signaling pathway by Western blot. Results: IL-38 could alleviate CIA joint damage and restrain inflammatory response, could up-regulate the expression of OPG in CIA rats and could down-regulate the expression of RANKL and RANK. IL-38 could restrain the expression of VEGF, VEGFR1, VEGFR2 and HIF. Moreover, we found that IL-38 could up-regulate the SIRT1 expression and down-regulate the HIF-1α, TLR4 and NF-KB p65 expression in CLL and CLH groups. From the treatment of synoviocytes to simulate the CIA model and the treatment of SIRT1 inhibitors, we demonstrated that the inhibitory effect of IL-38 on inflammatory factors and regulation of SIRT1/HIF-1α signaling pathway-related proteins were inhibited. Conclusion: IL-38 can restrain the inflammatory response of CIA rats, can promote the expression of osteogenic factors, can inhibit neovascularization, and can alleviate joint damage in rats. The mechanism may be related to the regulation of SIRT1/HIF-1α signaling pathway.

scholarly journals MiR-571 affects the development and progression of liver fibrosis by regulating the Notch3 pathway

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shuo Cong ◽  
Yongmei Liu ◽  
Yi Li ◽  
Yu Chen ◽  
Rui Chen ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Western Blot ◽  
Signaling Pathway ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Rt Pcr ◽  
Related Factors ◽  
Promote Cell Proliferation ◽  
And Migration ◽  
Set Up

AbstractExploring the expression of miR-571 in patients with liver fibrosis and its role in the progression of liver fibrosis. A total of 74 patients with liver fibrosis in our institution from September to December 2018 were collected for study, and the expression of miR-571, Notch3 and Jagged1 in patients with different progressions of liver fibrosis was determined by RT-PCR and Western blot analysis. Set up Notch3 up group and Notch3 down regulated group, RT-PCR and Western blot were used to determine the effect of Notch signaling on the expression of fibrogenic factors. CCK-8, cell scratch assays, Transwell assays, flow cytometry were used to determine the effect of miR-571 on LX-2 proliferation, migration, apoptosis in human stem stellate cells, and RT-PCR, Western blot assays were performed to determine the effect of miR-571 on the Notch3 signaling pathway and the expression of profibrogenic factors. miR-571, Notch3 and Jagged1 are up-regulated in patients with liver fibrosis and is associated with the progression of liver fibrosis. Notch3 signaling pathway can promote the expression of fibroblast in human hepatic stellate cells; miR-571 can inhibit the apoptosis of human hepatic stellate cells, promote cell proliferation and migration; up regulation of miR-571 can promote the expression of Notch3 and Jagged1, and up-regulation of miR-571 also promoted the expression of related fibroblasts. MiR-571 can promote the activation of human stem cell stellate cells and the expression of fibroblast related factors through Notch3 signaling pathway.

scholarly journals A Network Pharmacology-Based Approach to Investigating the Mechanisms of Fushen Granule Effects on Intestinal Barrier Injury in Chronic Renal Failure

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Miaoru Han ◽  
Hangxing Yu ◽  
Kang Yang ◽  
Panying Liu ◽  
Haifeng Yan ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Signaling Pathway ◽  
Intestinal Barrier ◽  
Enrichment Analysis ◽  
Control Group ◽  
T84 Cells ◽  
Protein Expressions ◽  
Group Protein ◽  
Cox 2

Purpose. Fushen Granule (FSG) is a Chinese medicine prepared by doctors for treating patients with chronic renal failure, which is usually accompanied by gastrointestinal dysfunction. Here, we explore the protective effect of FSG on intestinal barrier injury in chronic renal failure through bioinformatic analysis and experimental verification. Methods. In this study, information on the components and targets of FSG related to CRF is collected to construct and visualize protein-protein interaction networks and drug-compound-target networks using network pharmacological methods. DAVID is used to conduct gene ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Then, it is validated by in vitro experiments. In this study, the human intestinal epithelial (T84) cells are used and divided into four groups: control group, model group, FSG low-dose group, and FSG high-dose group. After the experiment, the activity of T84 cells is detected by a MTT assay, and the expressions of tight junction protein ZO-1, claudin-1, nuclear factor erythroid 2-related factor (Nrf2), heme oxygenase-1 (HO-1), malondialdehyde (MDA), and cyclooxygenase-2 (COX-2) are examined by immunofluorescence and/or western blotting. Results. Eighty-six potential chronic renal failure-related targets are identified by FSG; among them, nine core genes are screened. Furthermore, GO enrichment analysis shows that the cancer-related signaling pathway, the PI3K-Akt signaling pathway, the HIF1 signaling pathway, and the TNF signaling pathway may play key roles in the treatment of CRF by FSG. The MTT method showed that FSG is not cytotoxic to uremic toxin-induced injured T84 cells. The results of immunofluorescence and WB indicate that compared with the control group, protein expressions level of ZO-1, claudin-1, and Nrf2 in T84 cells is decreased and protein expressions level of HO-1, MDA, and COX-2 is increased after urinary toxin treatment. Instead, compared with the model group, protein expressions level of ZO-1, claudin-1, and Nrf2 in T84 cells is increased and protein expressions level of HO-1, MDA, and COX-2 is decreased after FSG treatment. Conclusion. FSG had a protective effect on urinary toxin-induced intestinal epithelial barrier injury in chronic renal failure, and its mechanism may be related to the upregulation of Nrf2/HO-1 signal transduction and the inhibition of tissue oxidative stress and inflammatory responses. Screening CRF targets and identifying the corresponding FSG components by network pharmacological methods is a practical strategy to explain the mechanism of FSG in improving gastrointestinal dysfunction in CRF.

The Involvement of the Fcεri Signaling Pathway in the Pathogenesis of Lacrimal Gland Benign Lymphoepithelial Lesions

2021 ◽  
Author(s):  
Jing Li ◽  
Rui Liu ◽  
Mei Sun ◽  
Jinjin Wang ◽  
Nan Wang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Western Blotting ◽  
Lacrimal Gland ◽  
Immunohistochemical Staining ◽  
Proteome Analysis ◽  
Control Group ◽  
Rt Pcr ◽  
Expression Levels ◽  
Benign Lymphoepithelial Lesion ◽  
Medical University

Abstract Objective: Benign lymphoepithelial lesion of lacrimal gland (LGBLEL) is a common orbital inflammatory disease with unknown pathogenesis. T his paper analyzed the role of the FcepsilonRI (FcεRI) signaling pathway in the pathogenesis of LGBLEL.Methods: Transcriptome sequencing and proteome sequencing were performed on LGBLEL and orbital CH diag nosed by histopathology in Beijing Tongren Hospital, Capital Medical University, between July 2010 and October 2013. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were used to jointly analyze the differentially expressed ge nes and proteins related to FcεRI signaling pathway. Four LGBLEL and three orbital CH diagnosed by histopathology in Beijing Tongren Hospital, Capital Medical University, between October 2018 and August 2019 were randomly selected as the experimental group and the control group, respectively. RT PCR, immunohistochemical staining, and western blotting were used to verify the genes and proteins related to the FcεRI signaling pathway.Results: Combined transcriptome and proteome analysis showed that the FcεRI signaling pathway was up regulated in LGBLEL (P=0.0040), and that the important proteins such as SYK, p38, JNK, PI3K, and ERK were highly expressed in LGBLEL tissues. RT PCR results showed that the mRNA expression levels of SYK, p38, JNK, PI3K, and ERK wer e significantly increased in the LGBLEL group (P=0.0066, P=0.0002, P=0.0003, P<0.0001, P<0.0001, respectively). Immunohistochemical staining results showed that the protein expression levels of SYK, p38, JNK, PI3K, and ERK in LGBLEL tissues were significan tly higher than in orbital CH. Western Blotting showed that the protein contents of p SYK, p p38, p JNK, p PI3K, and p ERK were significantly higher than in orbital CH (P=0.0169, P=0.0074, P=0.0046, P=0.0157, P=0.0156, respectively). Conclusion: The genes and proteins related to the FcεRI signaling pathway are up regulated in LGBLEL, indicating that the FcεRI signaling pathway participates in the pathogenesis of LGBLEL.

scholarly journals Effects of Polygonatum sibiricum Polysaccharides (PSP) on Human Esophageal Squamous Cell Carcinoma (ESCC) via NF-κB Signaling Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Weizheng Zhou ◽  
Jiang Hong ◽  
Ji Zhu ◽  
Xiaowei Wang
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Squamous Cell ◽  
Migration And Invasion ◽  
Control Group ◽  
Dependent Manner ◽  
Rt Pcr ◽  
Expression Levels

Objective. To explore the effects of different concentrations of Polygonatum sibiricum polysaccharides (PSP) on human esophageal squamous cell carcinoma (ESCC) cell line Eca109 and explore the new approach for the treatment of ESCC. Methods. Eca109 cells were divided into 5 groups, including one control group and 4 experimental groups where the concentrations of PSP used were 50, 100, 200, and 400 μg/mL. The proliferation rate of Eca109 cells in each group was measured with the CCK8 assay, and the apoptosis rate in each group was analyzed by flow cytometry; the in vitro scratch assay was used to determine the migration ability of Eca109 cells after PSP treatment; the expression levels of IL-1, IL-6, IL-10, TNF-α, and TGF-β were measured by RT-PCR, and the expression levels of TLR4 and proteins that are related to NF-κB signaling pathways were determined by Western blot. Results. PSP significantly inhibited the proliferation of Eca109 cells (p<0.05) on a time- and dose-dependent manner; the apoptosis rates of Eca109 cells in experimental groups were significantly increased after 48 h of culture (p<0.05); PSP significantly reduced the migration and invasion ability of Eca109 cells (p<0.05); RT-PCR results showed that the expression of IL-10 in Eca109 cells increased significantly after treatment with PSP (p<0.05), while the expression of IL-1, IL-6, TNF-α, and TGF-β decreased significantly (p<0.05). Compared with the control group, the expression level of TLR4, NF-κB/p50, and NF-κB/p65 protein in each experimental group was significantly lower than that in the control group (p<0.05). Conclusions. PSP significantly inhibited the proliferation, invasion, and migration of Eca109 cells and promoted cell apoptosis. These observed effects were probably due to the PSP’s inhibition on the NF-κB signaling pathway in Eca109 cells via the regulation of the TLR4 expression.

scholarly journals Apatinib Inhibits the Invasion and Metastasis of Liver Cancer Cells by Downregulating MMP-Related Proteins via Regulation of the NF-κB Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Xiaoxiao He ◽  
Zaozao Huang ◽  
Ping Liu ◽  
Qiuting Li ◽  
Mengmeng Wang ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Inhibitory Effect ◽  
Control Group ◽  
Invasion And Metastasis ◽  
Expression Levels ◽  
Liver Cancer Cells

Objective. We aimed to investigate whether apatinib has an inhibitory effect on the invasion and metastasis of liver cancer in vitro. Methods. The anti-invasion and antimetastasis effects of apatinib in HepG2, Hep3B,Huh7 and SMMC-7721 liver cancer cell lines were tested by the wound-healing and transwell invasion assays. Real-time PCR and Western blot were used to detect the influence of apatinib on the gene expression of MMPs, TIMPs, and constituents of the NF-κB signaling pathway in Hep3B and HepG2 liver cell lines. Results. Apatinib has a significant inhibitory effect on the metastasis and invasion of liver cancer cells. The expression levels of MMP-1, MMP-2, MMP-3, MMP-7, MMP-9, MMP-10, MMP-11, and MMP-16 were downregulated, while the expression levels of TIMP-3 and TIMP-4 were upregulated by apatinib treatment at both the mRNA and protein levels. The phosphorylation of IκBα and NF-κB p65 was significantly reduced compared with that in the control group. Conclusions. Apatinib inhibits the invasion and metastasis of human liver cancer cells by downregulating the expression of MMP-related genes. This may be achieved by inhibiting the activation of the NF-κB signaling pathway.

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