[Study on the association between urinary organic arsenic and 8-hydroxydeoxyguanine in workers exposed to arsenic].

OBJECTIVE: To evaluate the association between metabolism of arsenic and DNA oxidative damage in workers in a arsenic mill. METHODS: Urinary organic arsenic and 8-hydroxydeoxyguanine were detected in 37 workers highly exposed to arsenic and 16 administrative and logistic staff with mild exposure in a arsenic mill in Yunnan province, and also 28 local people who did not have the exposure in the near past time. The correlation between metabolism of arsenic and DNA oxidative damage was evaluated. RESULTS: The urinary organic arsenic concentration was respectively (0.48 +/- 0.37) mg/L and (0.08 +/- 0.05) mg/L for men with high and low exposure, and was respectively 0.11 mg/L and (0.30 +/- 0.24) mg/ L for women with high and low exposure, while it was lower than 0.02 mg/L in the controls. Urinary 8-hydroxydeoxyguanine concentration was (18.07 +/- 11.68) micromol/mol creatinine, (11.79 +/- 8.25) micromol/mol creatinine, (10.07 +/- 3.04) micromol/mol creatinine for the males with high and low exposure and of controls, respectively, (P < 0.05), and it was 84.35 micromol/mol creatinine, (21.27 +/- 5.89) micromol/mol creatinine, (14.43 +/- 2.58) micromol/mol creatinine for females with high and low exposure and of controls, respectively. The female workers exposed to arsenic had higher urinary 8-hydroxydeoxyguanine levels than males did (P < 0.05). The increased tendencies of urinary 8-hydroxydeoxyguanine levels with the organic arsenic concentration were found in workers (r(s) = 0.279, P = 0.019). CONCLUSION: Occupational individuals exposed to arsenic have obvious DNA oxidative damage, which is more severe in females. The difference of metabolism of arsenic may play a key role.

[The mechanisms and effects of lutein on inducing the cell differentiation of human esophagus cancer EC9706].

OBJECTIVE: The purpose of the study was to explore the effects and molecular mechanisms of lutein on the differentiation of esophagus cancer EC9706 cell. METHODS: EC9706 cells were seeded in 1640 medium before the addition of test compounds. The respective test compound was added in fresh medium and the control cell received the vehicle (DMSO) or Fluorouracil. The proliferation and cell cycle of EC9706 were determined by MTT assay and flow cytometry, respectively. The change in cytomorphology was investigated by using HE staining. Proliferation and differentiation cells were checked and observed by methyl green-pyronine staining. The protein expression of cyclin D1 was detected by immunohistochemistry. RESULTS: Compared with the DMSO control group, the proliferation of the EC9706 cells treated with lutein (100 microg/mL and 150 microg/mL) could markedly be decreased and the cell cycle was blocked at G0/G1 phage which caused significant changes in the cytomorphology of EC9706 cell line, and the cell malignant degree tended to drop down, the protein expression of cyclin D1 was also down-regulated significantly. CONCLUSION: Lutein can inhibit the proliferation of EC9706 cell, and promote the cancer cell differentiation. cyclin D1 may be involved in cell proliferation and differentiation events in esophageal cancer EC9706 cell, which is regulated by lutein.

[Experiment research on the location of DNA lesion in the nucleic acid sequence].

OBJECTIVE: To research on establishing a method that can detect the DNA lesion at the level of nucleic acid. METHODS: The TK6 cell was cultured and treated, the genomic DNA was extracted, and the strand cleavage was induced by the endonuclease Hinf I. Then the genomic DNA was amplified by randomized terminal linker-dependent PCR (RDPCR), and hybridized by Southern hybridization with the single-stranded probes of the exon 2 of k-ras gene. The PCR products were sequenced. RESULTS: The clear hybridized band from the products of RDPCR was seen at the expectant position cut by Hinf I. The sequencing analysis showed that the position of DNA lesion linked by the linker was just the restriction site of Hinf I. CONCLUSION: It can be used to detect the DNA lesion at the level of nucleic acid sequence with the combination of sequence and RDPCR technologies.

[Real-time PCR used to detect p53 gene damage in workers exposed to arsenic].

OBJECTIVE: To evaluate the relationship between the metabolism of arsenic and the damage of exon 5 and 8 of p53 gene from workers in a arsenic mill, and with real-time PCR technique, to establish the method probing the gene-specific DNA damage in people. METHODS: By real-time PCR, the damages of exon 5 and 8 of p53 gene were probed in 37 workers exposed highly to, 16 manager and logistic employees exposed less to an arsenic mill in Yunnan province, and also 25 local people who did not contact with any white arsenic in near past time. At the same time, the urinary total and organic arsenic of workers were detected. The correlation between metabolism of arsenic and damage of p53 gene was evaluated. RESULTS: Total urinary arsenic concentrations were (1.18 +/- 0.76) mg/L and (0.32 +/- 0.28) mg/L for high and low exposed male workers, and 0.23 mg/L, (0.53 +/- 0. 30) mg/L for high and low exposed females. Organic urinary arsenic concentrations were (0.48 +/- 0.37) mg/L and (0.08 +/- 0.05) mg/L for high and low exposed males, and 0.11 mg/L, (0.30 +/- 0.24) mg/L for high and low exposed females. The total and organic urinary arsenic of high exposed group was higher than that of control male (P < 0.05), all in control group were lower than 0.02 mg/L for reference. The Ct relative value of exon 5 of p53 gene in high exposed group was higher than that in control male (P < 0.05), and the increased tendency of Ct relative value of exon 5 of p53 gene was found in workers with organic arsenic concentration going up (r(s) = 0.355, P = 0.011). The Ct relative value of exon 8 of p53 gene in low exposed group was higher than that in control male (P < 0.05), but the difference between high exposed and low exposed or reference's was not obvious (P > 0.05). CONCLUSION: The damages in exon 5 and 8 of p53 gene in workers exposed to arsenic may be induced. The metabolism of arsenic may be very important in the damage of exon 5. It is feasible for real-time PCR technique used to detect gene-specific DNA damage in people.

[Effects and mechanism of lutein on apoptosis of esophageal carcinoma EC9706 cells].

OBJECTIVE: To study the effects of lutein on apoptosis and its mechanism. METHOD: The cells of human esophageal carcinoma EC9706 were grown in RPMI medium containing 10% bovine serum and were treated with lutein at 100 microg x mL(-1) concentration. Flow cytometry was employed to investigate the effects of lutein on cell apoptosis of EC9706 cells. Histochemistry was performed to determine apoptosis-related protein expresion. RESULT: Flow cytometry analyses revealed that lutein increased EC9706 cell apoptosis ratio when treated with lutein 100 microg x mL(-1) at 96 h. Lutein decreased the expression of Bcl-2 protein and increased the expression of Bax protein in EC9706 cells. CONCLUSION: Lutein could inhibit mitosis and stimulate apoptosis of EC9706 cells. The apoptotic effect may result from the down-regulation of expression of Bcl-2 and up-regulation expression of Bax.

[Study on rat's DNA damage of p53 induced by chlorinated acetic acids of drinking water disinfection by-products].

OBJECTIVE: To study on the DNA damage of p53 induced by dichloroacetic acid(DCA) and trichloroacetic acid( TCA), approve their genotoxicity and discuss molecular mechanism of their carcinogenic action. METHODS: Administered SD rats with DCA or TCA by i.p. injection, extracted DNA from rat's liver, and then used RDPCR to detect DNA damage of exon 70f p53 gene. RESULTS: Two hybridization bands were detected in treated group induced by DCA. It was indicated that DCA can result in DNA damage of exon 7 of p53 gene of rat's liver tissue, and there were two broken sites. It was not detected damage of exon 7 of p53 gene of rat induced by TCA. CONCLUSION: There may be the relationship between DCA carcinogenic action and the damage of p53. The result that the damage of p53 of target tissue detected by RDPCR was consistent well with rat carcinogenic test.

[Study of rat's p53 gene damage and organ specificity induced by benzidine].

OBJECTIVE: Studying the main target organs and the genetic toxicity mechanism of benzidine. METHODS: SD rats were given benzidine i.p. injection. DNA was extracted from rat's liver, kidney, lung and bladders. Then ss probes RDPCR was used to detect the damaged DNA of exon 7 of p53 gene. RESULTS: Hybridization bands were found in liver, bladder and lung tissues after ss probes RDPCR, while no hybridization bands were found in kidney tissues. CONCLUSION: The result indicates that benzidine can cause the DNA lesions of exon 7 of p53 gene and its major target organs are liver, bladder and lung. The toxicity mechanism of benzidine is probably related to p53 gene damage.

[Blood leptin, orexins and NPY levels and their relations in obese children].

OBJECTIVE: To investigate the concentration levels of leptin, orexins and neuropeptide Y (NPY) in the blood of obese children, and to analysed the relationship between these substances. METHODS: RIA methods were used to measure the concentrations of leptin, orexinA, orexinB, and NPY in the blood of 98 obese children [BMI: male (29.24 +/- 1.87) kg/mZ, female (28.12 +/- 2.30) kg/m2] and in 104 normal children [BMI: male (20.49 +/- 1.95) kg/m2, female (19.59 +/- 1.51) kg/m2] as the control group. RESULTS: The leptin concentrations in obese children [male (26.00 +/- 14.66) ng/mL; female (33.59 +/- 14.63) ng/mL] were higher than those in the control group [male (6.65 +/- 44.49) ng/mL; female [10.48 +/- 5.52) ng/mL P < 0.013]. The concentrations of plasma orexinA in obes children [male (3.23 +/- 1.86) pg/mL; female (3.38 +/- 1.80) pg/mL] were lower than those in the control group [male (4.52 +/- 1.52) pg/mL; female (4.71 +/- 1.53) pg/mL P < 0.05]; Negative correlations between leptin and NPY were noted in the obesity group (r = -0.302) and the control group (r = -0.310, P < 0.01), while the slopes in the two groups were different (control group -2.969; obese group -0.809). A positive correlation between NPY and orexinA was noted (r = 0.207, P < 0.05). The fluctuation range of orexinA in obese children was markedly narrowed when compared with that in the control group. CONCLUSION: The concentration level of peripheral orexinA and leptin in the obese and non-obese children change inversely. The obesity in children correlates with the concentrations of orexinA, leptin, NPY as well as with their interactions.

Mutation analysis of HOXD13 gene in a Chinese pedigree with synpolydactyly.

OBJECTIVE: To study the clinical features and to identify homeobox D13 (HOXD13) gene mutation of the affected individuals in a Chinese synpolydactyly (SPD) kindred. METHODS: Clinical data and peripheral blood samples of SPD family members were obtained through field investigation. For every member of this pedigreeìthe fragment containing mutational hot spots of HOXD13 was amplified by PCR for mutation screening. To examine whether there is any other mutation within coding sequence of HOXD13, exon 1 and exon 2 of HOXD13 were also amplified by PCR. All the amplified fragments were electrophoresed on 2% agarose gels and then the mutant fragments were electrophoresed on 5% polyacrylamide gels to be separated. Purified PCR products of normal and selected mutant alleles were directly sequenced. RESULTS: Comparing the HOXD13 coding sequence of the affected individuals with HOXD13 sequence in the GenBank and with that of the unaffected, an inserted segment coding 8 alanine residues within HOXD13 was found segregating with the disorder. This mutation is also termed polyalanine expansion. The 8-alanine expansion can be interpreted as a reduplication of normal alanines 5-12. CONCLUSION: The results suggest that synpolydactyly in this kindred may be caused by polyalanine expansion in HOXD13.

[Detecting the DNA damage of N-ras gene induced by potassium dichromate].

OBJECTIVE: Applying RDPCR to detect the DNA damage of N-ras gene induced by Potassium dichromate METHODS: Preparing single-stranded probes of exon 1 of N-ras gene in human. The genomic DNA was treated with Potassium dichromate, then amplified by RDPCR and detected by Southern hybridization with the probe. RESULTS: The clear hybridized bands can be seen in the position which is induced by Potassium dichromate on the dose of 100 micromol/L, but can't be detected on the dose over 1000 mol/L. CONCLUSION: It indicates that Potassium dichromate can cause the DNA damage of N-ras gene, which should be the key point of its carcinogenesis mechanisms.

[Application with single-stranded probes in randomized terminal linker-dependent PCR].

OBJECTIVE: Preparing single-stranded (ss) probes in place of double-stranded (ds) probes to improve the hybridization efficiency and specificity of randomized terminal linker-dependent PCR (RDPCR). METHODS: Using asymmetric PCR and single-primer PCR to prepare ss probes of extron 7 of p53 gene in rat, then comparing the results hybridized with ss probes and ds probes. RESULTS: Preparation of ss probes by asymmetric PCR and single-primer PCR gets success. Hybridization results showed that the ss probes could get better signals and less noise than ds probes. CONCLUSION: In comparison with ds probes, the application of ss probes can increase the hybridization sensitivity and specificity of RDPCR.

[Establishment and characterization of the lung cancer A549 cell stains with down-regulated expressed HOGG1 genes].

OBJECTIVE: To establish lung cancer A549 cell strains with down-regulated expressed HOGG1 genes and study its biological characteristics. METHODS: The eukaryotic expression vectors with genes of hammerhead ribozyme targeting human 8-oxoguanine DNA glycosylase 1 (HOGG1) mRNA were transfected into A549 cells by liposmes, and then were screened by G418 till stable cell strains were constructed. The positive recombinants were identified by RT-PCR to amplify NEO genes. The efficacy of inhibition was tested by RT-PCR. Furthermore, morphology, survival curves, cell cycle, cloning efficiency grow in the soft agar and the activity of superoxide dismutase (SOD) were investigated. RESULTS: The HOGG1-down-regulated expressed A549 cell strains were obtained after G418 selection and NEO genes identification. The mRNA expression level of HOGG1 genes in the down-regulated expressed cells named A549-R were decreased 61.5% than in the untransfected cells A549 (P < 0.05). There was no significant difference between A549-R cells and A549 cells in morphology, the population doubling time and cell cycle. The numbers of clones in the soft agar of A549-R cells was decreased nearly to 50% than of A549 cells (P < 0.05), but the activity of SOD was increased obviously (P < 0.05). CONCLUSION: The lung cancer A549 cell strains with down-regulated expressed HOGG1 genes by silencing and incision of ribozyme were successfully established. Its biological characteristics have no significant changes in most of indexes.

[Establishing a method to detect the DNA damage of N-ras gene].

OBJECTIVE: Applying RDPCR to detect the DNA damage of N-ras gene in human. METHODS: Single-primer PCR was used to prepare single strand (ss) probes of extron 1 of N-ras gene in human. The genomic DNA was digested completely by restriction endonuclease, then amplified by RDPCR and detected by Southern hybridization with the probe. RESULTS: The ss probes were successfully prepared by single-primer PCR. The hybridized bands were clearly seen in the expected migration positions. CONCLUSION: The result shows that the method to detect the damaged position of N-ras gene has been established, which would be helpful to further studies on chemical carcinogenesis and on the prevention of tumor.

Randomized terminal linker-dependent PCR: a versatile and sensitive method for detection of DNA damage.

OBJECTIVE: To design and develop a novel, sensitive and versatile method for in vivo foot printing and studies of DNA damage, such as DNA adducts and strand breaks. METHODS: Starting with mammalian genomic DNA, single-stranded products were made by repeated primer extension, these products were ligated to a double-stranded linker having a randomized 3' overhang, and used for PCR. DNA breaks in p53 gene produced by restriction endonuclease AfaI were detected by using this new method followed by Southern hybridization with DIG-labeled probe. RESULTS: This randomized terminal linker-dependent PCR (RDPCR) method could generate band signals many-fold stronger than conventional ligation-mediated PCR (LMPCR), and it was more rapid, convenient and accurate than the terminal transferase-dependent PCR (TDPCR). CONCLUSION: DNA strand breakage can be detected sensitively in the gene level by RDPCR. Any lesion that blocks primer extension should be detectable.

[Epidemiological analysis of syndactyly in Chinese perinatals].

OBJECTIVE: To study the epidemiological features of syndactyly (SD) in Chinese perinatals. METHODS: Data were collected through Chinese Birth Defects Monitoring Network, a hospital-based congenital malformation registry system. From 1987 through 2001 (except 1994, 1995), all live or still births with 28 weeks of gestation or more born in participating hospitals were assessed within 7 days after delivery. RESULTS: Totally 2311 perinatals with SD were identified among 7 478 746 births, and 57.2% of them were in association with other anomalies. The overall prevalence rate of SD was 3.09/10 000, the rate of isolated SD and associated SD was 1.32/10 000, and 1.77/10 000 respectively. The prevalence rates in urban and rural areas, in male and female births were 3.22/10 000 and 2.79/10 000, 3.42/10 000 and 2.59/10 000 respectively. An increasing trend was found during that period. The perinatal fatality rate of SD was 20.7%, that of isolated form was 5.7%, while that of associated form was 31.9%. The proportion of SD occurring in right side was the same as that in left side, and the proportion of SD in upper limbs equaled to that in lower limbs. CONCLUSIONS: The prevalence rate of SD in Chinese perinatals was similar to that reported in foreign literatures. Associated form of SD was more frequently seen. The prevalence of SD in urban areas was higher than in rural areas. Male excess was identified in both isolated and associated forms of SD. No selective predominance was observed either by affected side or by affected limbs.

Study on Preparation of Triptolide-glycyrrhetic Acid Compound Microemulsion and Its Physicochemical Properties and in vitro Release Characteristics / 中国药房

OBJECTIVE： To establish content determination method of Triptolide-glycyrrhetic acid compound microemulsion， optimize the formula and investigate its physicochemical properties and release rate in vitro. METHODS： The content of Triptolide- glycyrrhetic acid compound microemulsion was determined by UPLC. The determination was performed on ACQUITY UPLC BEH C18 column with mobile phase consisted of 0.1％ formic acid aqueous solution-acetonitrile （gradient elution） at the flow rate of 0.4 mL/min. The column temperature was 40 ℃. The detection wavelength was set at 218 nm， and sample size was 5 μL. Pseudo-ternary phase diagrams were drawn by water titration method. Using oil phase， surfactants and co-surfactants as index， the formula was optimized， and in intro release characteristics was investigated by in vitro release test. RESULTS： The linear range of triptolide and glycyrrhetinic acid were 1-40 μg/mL（r＝0.999 7） and 10-400 μg/mL（r＝0.999 8）， respectively. The limits of quantitation were 0.5 and 0.8 μg/mL； the limits of detection were 0.1 and 0.2 μg/mL. RSDs of precision， stability and reproducibility tests were all less than 2％. Average recoveries were 100.32％-101.15％ （RSD＝0.36％， n＝6）， 99.78％-101.42％ （RSD＝0.59％，n＝6）. The optimal formula included that medium chain triglyceride as oil phase， polyethylene glycol hydroxy stearate as surfactants， ethanol as co-surfactants， water as water phase， the proportion of them was 8 ∶  28 ∶ 14 ∶ 50. The obtained microemulsion was O/W type， being transparent and clear， with average diameter， average polydispersity index and average viscosity of （62.38±3.44） nm， 0.096±0.001 and （26.84±1.10） mPa·S. Within 24 h， cumulative release rates of triptolide and glycyrrhetinic acid in obtained microemulsion were 99.8％ and 99.7％ （in PBS pH 2.0）， 99.3％ and 99.4％ （in PBS pH 7.4）， 98.9％ and 98.4％ （in PBS pH 9.0）， respectively. Triptolide and glycyrrhetinic acid released faster in the single microemulsion than in the compound microemulsion. CONCLUSIONS： Established content determination method is simple and stable. The optimized formula is stable and feasible. Obtained iriptolide-glycyrrhetinic acid compound microemulsion show better sustained-release effect than sigle microemulsion.

Discovery of new antibiotics using genome data mining / 药学学报

With the worldwide spread of multi-drug resistant (MDR) bacteria, bacterial resistance has become a major issue affecting human health. Although traditional methods for obtaining antibiotics by screening bacterial strains have found the most available antibiotics for us, this method has resulted in fewer and fewer antibiotics in the past few decades and is increasingly difficult to find the new structure of the compound entity. At present, there are few drugs that can fight super-resistant bacteria in the clinic or even research. therefore, the development and application of new technologies to address the issue of bacterial resistance is imminent. Since the first bacterial genome was sequenced more than 20 years ago, a large number of bacterial genomic sequence information can provide clues for the discovery of new antibiotics. In this review, we briefly outline the available data sources and highlight the use of genomic mining and metagenomics in discovery of new antibiotics.

Mechanical properties and cytocompatibility of a new-type nano-bionic anti-adhesion hernia mesh / 中国组织工程研究

BACKGROUND:A new-type nano-bionic anti-adhesion hernia mesh was developed in our previous research.OBJECTIVE:To investigate the mechanical properties and cytocompatibility of the new-type nano-bionic anti-adhesion hernia mesh.METHODS:The tensile strength of the compound hernia mesh was detected using a textile detector.Mouse fibroblasts (L929) were cultured with the compound hernia mesh,and cell structures on the mesh surface were observed under electron microscope at 1,3,5 days after culture.In addition,L929 cells were co-cultured with compound hernia mesh,polypropylene patch,and polyester patch,respectively.Cells cultured alone were used as negative controls.After 1,3,5 days of culture,MTS array was used to detect cell proliferation and evaluate cytotoxicity;after 3 days of culture,western blot was used to detect the content of type Ⅰ and Ⅲ collagens.RESULTS AND CONCLUSION:The average tensile strength of the compound hernia mesh was 31.2 N The number of fibroblasts on the nanofibrous layer of the compound hernia mesh increased as long as cultured.The cells spread along the nanofibers and pseudopodia extended from the cells formed polygon and fusiform structures,with a good cross-linking with the mesh.A complete cell layer covered all pores of the nanofibers at 5 days.The cytotoxicity of the nanofibrous layer of the compound hernia mesh was graded 0,and the cytotoxicity was graded 1 of polypropylene and polyester patches.All the three kinds of patches fulfilled the implantation requirements,and the compound hernia mesh had better biological properties.No significant differences were found among groups in the contents of type Ⅰ and Ⅲ collagens at 3 days of culture.To conclude,the new-type nano-bionic anti-adhesion hernia mesh has good mechanical properties and cytocompatibility.

Effect of ABCB13435C>T Genetic Polymorphism on Plasma Concentration and Adverse Reactions of High-dose Methotrexate in Acute Lymphoblastic Leukemia Children / 中国药师

Objective: To investigate the association between the genetic polymorphism of ABCB1 C3435T and plasma concentration and adverse reactions of high-dose methotrexate(HD-MTX) chemotherapy in children with acute lymphoblastic leukemia(ALL).Methods: A total of 70 peripheral blood samples were obtained from the children with acute lymphoblastic leukemia for extracting genome DNA.The genetic polymorphism of ABCB1 C3435T locus was examined by using PCR technology and direct sequencing;enzyme-amplified immunoassay (EMIT) was employed to determine the plasma concentration of MTX in 48 h;the clinical data of patients were collected during the HD-MTX chemotherapy, the adverse reactions were statistically analyzed.The association between ABCB1 C3435T genotypes and MTX plasma concentration and adverse reactions were investigated.Results: Genetic polymorphism existed at the SNP of ABCB1 C3435T.At the SNP of ABCB1 C3435T, the percentage of CC, CT and TT genotype in the children with ALL was 31.43%, 47.14% and 21.43%, respectively.The order of C/D ratio of MTX from low to high was CC, CT and TT genotypes, there was a significant association between the gene polymorphism and the C/D ratio of MTX (P<0.05);the order of incidence of oral mucosa damage from low to high was CC, CT and TT genotypes, there was a significant association between the gene polymorphism and oral mucosa damage (P<0.05);the order of incidence of hepatotoxicity from low to high were CC, CT and TT genotypes, the gene polymorphism and hepatotoxicity had a significant association (P<0.05).Conclusion: ABCB1 C3435T genetic polymorphism and C/D ratio of MTX, gastrointestinal side effects and hepatotoxicity after HD-MTX chemotherapy in the children with ALL exhibit significant association.

Effect of Matrix Metallopeptidase 13 on the Function of Mouse Bone Marrow-derived Dendritic Cells / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Dendritic cells are professional antigen-presenting cells found in an immature state in epithelia and interstitial space, where they capture antigens such as pathogens or damaged tissue. Matrix metallopeptidase 13 (MMP-13), a member of the collagenase subfamily, is involved in many different cellular processes and is expressed in murine bone marrow-derived dendritic cells (DCs). The function of MMP-13 in DCs is not well understood. Here, we investigated the effect of MMP-13 on DC maturation, apoptosis, and phagocytosis.</p><p><b>METHODS</b>Bone marrow-derived dendritic cells were obtained from C57BL/6 mice. One short-interfering RNA specific for MMP-13 was used to transfect DCs. MMP-13-silenced DCs and control DCs were prepared, and apoptosis was measured using real-time polymerase chain reaction and Western blotting. MMP-13-silenced DCs and control DCs were analyzed for surface expression of CD80 and CD86 and phagocytosis capability using flow cytometry.</p><p><b>RESULTS</b>Compared to the control DCs, MMP-13-silenced DCs increased expression of anti-apoptosis-related genes, BAG1 (control group vs. MMP-13-silenced group: 4.08 ± 0.60 vs. 6.11 ± 0.87, P = 0.008), BCL-2 (control group vs. MMP-13-silenced group: 7.54 ± 0.76 vs. 9.54 ± 1.29, P = 0.036), and TP73 (control group vs. MMP-13-silenced group: 4.33 ± 0.29 vs. 5.60 ± 0.32, P = 0.001) and decreased apoptosis-related genes, CASP1 (control group vs. MMP-13-silenced group: 3.79 ± 0.67 vs. 2.54 ± 0.39, P = 0.019), LTBR (control group vs. MMP-13-silenced group: 9.23 ± 1.25 vs. 6.24 ± 1.15, P = 0.012), and CASP4 (control group vs. MMP-13-silenced group: 2.07 ± 0.56 vs. 0.35 ± 0.35, P = 0.002). Protein levels confirmed the same expression pattern. MMP-13-silenced groups decreased expression of CD86 on DCs; however, there was no statistical difference in CD80 surface expression. Furthermore, MMP-13-silenced groups exhibited weaker phagocytosis capability.</p><p><b>CONCLUSION</b>These results indicate that MMP-13 inhibition dampens DC maturation, apoptosis, and phagocytosis.</p>