ObjectiveTo observe the effect and therapeutic effect of Kaixuan Jiedu core prescription （KXJD） on skin homing of Th17 cells in the mouse model of imiquimod （IMQ） combined with restraint stress-induced psoriasis-like skin damage， and to explore its potential mechanism from the perspective of neuro-immune axis. MethodsThirty male C57BL/6J mice were randomly allocated into five groups （n=6）： Control， model （IMQ）， restraint stress model （IMQ+RS）， KXJD， and methotrexate （MTX）. The mouse model of psoriasis-like skin damage was established by 5% IMQ combined with restraint stress. At the same time of modeling， each treatment group was treated with corresponding doses of drugs， and the control， IMQ， and IMQ+RS groups were treated with the same amount of normal saline by gavage once a day for 5 days. Hematoxylin-eosin （HE） staining was used to observe the pathological changes in the skin tissue and Baker scoring was performed. Serum levels of interleukin-1β （IL-1β） and angiopoietin-2 （Ang-2） were measured by enzyme-linked immunosorbent assay （ELISA）. The levels of matrix metalloproteinase-9 （MMP-9）， tissue inhibitor of metalloproteinase-1 （TIMP-1）， C-C motif chemokine ligand 20 （CCL20）， and C-C motif chemokine receptor 6 （CCR6） in the skin tissue were determined. Immunohistochemistry （IHC） was employed to determine the protein expression of cutaneous lymphocyte-associated antigen （CLA）， integrin α_E （CD103）， cytokeratin 10 （CK10）， and nuclear factor-kappa B （NF-κB） in the skin. Immunofluorescence double staining （DIF） was adopted to detect the expression and co-localization of vascular endothelial cadherin （VE-cadherin） and platelet-endothelial cell adhesion molecule （CD31）， CCR6， CD103， substance P （SP）， calcitonin gene-related peptide （CGRP）， and protein gene product 9.5 （PGP9.5） in the skin tissue. Real-time PCR was employed to quantify the mRNA levels of IL-10， IL-17A， and IL-23. ResultsCompared with the control group， the IMQ group and IMQ+RS group showed significant inflammatory cell infiltration， abnormal proliferation of epidermal cells， keratinization and other pathological changes in the skin tissue， and a significant increase in Baker score， elevated levels of IL-1β and Ang-2 in the serum and MMP-9， CCL20 and CCR6 in the skin lesions， upregulated expression of CLA， CD103， CK10， NF-κB， IL-17A mRNA， and IL-23 mRNA in the skin lesions， and downregulated expression of TIMP-1 and IL-10 mRNA. In addition， the fluorescence intensities of VE-cadherin and CD31 co-localization， CCR6 and CD103 co-localization， SP and PGP9.5 co-localization， and CGRP and PGP9.5 co-localization were increased （P<0.05）. Compared with the IMQ group， the above indicators in the IMQ+RS group were further aggravated. Compared with the IMQ group， the above indicators in the IMQ+RS group were further aggravated. Compared with the IMQ+RS group， KXJD and MTX significantly alleviated the pathological damage of skin lesions， significantly decreased the Baker score， lowered the levels of IL-1β and Ang-2 in the serum and MMP-9， CCL20 and CCR6 in skin lesions， downregulated the expression of CLA， CD103， CK10， NF-κB， IL-17A mRNA and IL-23 mRNA in skin lesions， and upregulated the expression of TIMP-1 and IL-10 mRNA. Furthermore， KXJD and MTX reduced the fluorescence intensities of VE-cadherin and CD31 co-localization， CCR6 and CD103 co-localization， CGRP and PGP9.5 co-localization， and SP and PGP9.5 co-localization （P<0.05）. ConclusionKXJD can significantly ameliorate the psoriasis-like skin damage induced by IMQ combined with restraint stress in mice by regulating the neural-immune axis and inhibiting the skin homing of Th17 cells.

ObjectiveTo establish the mouse models of psoriasis-like lesions induced by continuous cold exposure or intermittent cold exposure combined with imiquimod （IMQ）， and to evaluate the interventional effects of Kaixuan Jiedu core prescription （KXJD） on the two models. MethodsMale C57BL/6J mice were selected and classified into two experimental batches. The first batch of 36 mice was randomized into a room temperature group， a continuous cold exposure （10 ℃/24 h） group， and an intermittent cold exposure （10 ℃/6 h） group. Each group was further divided into a normal subgroup and a model subgroup （topical application of IMQ to induce skin lesions）， with 6 mice in each subgroup， for modeling and evaluation. The second batch of 54 mice， with 6 in each group， were subjected to the same temperature grouping with an additional KXJD （30.42 g·kg^-1， continuous gavage for 5 days） group. Comprehensive evaluation of model characteristics and KXJD efficacy was conducted through Psoriasis Area and Severity Index （PASI） scoring， skin temperature measurement by infrared thermography， histopathological observation by hematoxylin-eosin （HE） staining， detection of vascular endothelial growth factor （VEGF） and platelet endothelial cell adhesion molecule 1 （CD31） by immunohistochemistry， detection of Claudin-1 and Occludin by immunofluorescence assay， determination of serum levels of tumor necrosis factor-α （TNF-α） and interleukin （IL）-10 by enzyme-linked immunosorbent assay （ELISA）， and quantification of mRNA levels of IL-17A， IL-23， IL-6， and chemokine ligand 20 （CCL20） in skin lesions by quantitative Real-time polymerase chain reaction （Real-time PCR）. ResultsModel mice in all temperature groups exhibited typical psoriasis-like skin lesions. Compared with the normal groups， the model groups showed increased PASI scores， decreased skin temperatures （P<0.05）， obvious epidermal thickening， parakeratosis， and dermal inflammatory cell infiltration， as well as elevated mRNA levels of IL-17A， IL-23， IL-6， and CCL20 （P<0.05）. Cold exposure further aggravated psoriasis. The total PASI score of the intermittent cold exposure model group was higher than that of the room temperature model group （P<0.05）. The serum IL-10 did not show a compensatory elevation， and the blood vessels presented a characteristic of elevated CD31 expression （P<0.05） without a synchronous increase in VEGF. The continuous cold exposure model group exhibited more significant dermal capillary tortuosity and dilation， with the highest mRNA levels of IL-17A， IL-23， IL-6， and CCL20 among all groups. Compared with the respective model groups， KXJD intervention alleviated skin lesions， reduced epidermal thickness and inflammatory cell infiltration， and increased skin temperature， with the temperature increase being particularly significant in the intermittent cold exposure+KXJD group （P<0.05）. Furthermore， KXJD down-regulated the expression of VEGF and CD31， restored the expression of Claudin-1 and Occludin， decreased the mRNA levels of IL-17A and IL-23 （P<0.05）， and reduced the serum TNF-α level. ConclusionThis study successfully established compound psoriasis-like mouse models induced by cold exposure combined with IMQ. It confirms that cold aggravates the severity of psoriasis by exacerbating the closure of Xuanfu （sweat pores）， microcirculation disorders， and immune imbalance. Moreover， different cold exposure patterns have distinct mechanism differences. Continuous cold exposure focuses on enhancing the inflammatory response via the IL-23/IL-17 axis and angiogenesis， simulating chronic aggravation under a long-term cold environment. Intermittent cold exposure tends to impair immune regulation and induce microvascular endothelial stress， corresponding to acute exacerbations caused by sudden temperature drops. KXJD can effectively alleviate psoriasis-like skin lesions under cold conditions by unblocking Xuanfu， regulating vasomotor function， and correcting abnormal immune-inflammatory responses.

ObjectiveTo investigate the ameliorative effects of Kaixuan Jiedu core prescription （KXJD） on skin lesions in psoriasis-like mouse models under cold environment exposure， and to analyze its influences on transient receptor potential （TRP） channels and related neuroimmune regulatory factors. MethodsThirty-six C57BL/6J mice were randomized into 6 groups， with 6 mice in each group. Two feeding conditions were set： Normal temperature and cold ［simulating a cold environment at （10±0.5） ℃， for 6 h daily］. Mice were induced to develop psoriasis-like lesions by applying imiquimod externally. The model mice were allocated into model groups and KXJD （30.42 g·kg^-1， continuous gavage for 5 days） groups. Normal mice were used as the control group. Specifically， mice were allocated into normal temperature， normal temperature model， normal temperature+KXJD， cold exposure control， cold exposure model， and cold exposure+KXJD groups. The pathological changes in skin lesions were observed by hematoxylin-eosin （HE） staining. The expression of cluster of differentiation （CD） 3⁺ T lymphocytes， CD11c⁺ dendritic cells （DCs）， phosphorylated extracellular signal-regulated kinase （p-ERK）， and substance P （SP） were detected by immunofluorescence assay. The protein level of transient receptor potential cation channel subfamily M member 8 （TRPM8） in the skin tissue was determined by Western blot. The expression of TRPM8， transient receptor potential cation channel subfamily V member 1 （TRPV1）， transient receptor potential cation channel subfamily A member 1 （TRPA1）， and transient receptor potential cation channel subfamily V member 2 （TRPV2） at the protein and mRNA levels was determined by immunohistochemistry and Real-time PCR， respectively. The levels of calcitonin gene-related peptide （CGRP） and neuropeptide Y （NPY） in the serum were analyzed by enzyme-linked immunosorbent assay （ELISA）. The enrichment analysis of differentially expressed genes （DEGs） and TRP pathway network construction were conducted based on the GEO database. The co-expression of TRPM8 and CGRP in the skin lesions was verified by immunofluorescence double labeling. ResultsBoth the normal temperature and cold exposure model groups showed typical psoriasis-like skin lesions. Compared with the normal temperature and cold exposure control groups， the model groups had excessive epidermal keratinization， thickened spinous layer， and inflammatory infiltration in the dermis， with increased pathological scores （P<0.05）， increased infiltration of CD3⁺ and CD11c⁺ cells and expression of p-ERK and SP， upregulated mRNA levels of TRPM8， TRPA1， and TRPV2， downregulated mRNA level of TRPV1 （P<0.05）， and reduced content of CGRP and increased content of NPY in the serum. Compared with the normal temperature and cold exposure model groups， KXJD reduced the pathological manifestations and pathological scores of psoriasis-like skin lesions （P<0.05）， and inhibited the infiltration of CD3⁺ and CD11c⁺ cells and the expression of p-ERK and SP. Gene enrichment analysis suggested that the DEGs of psoriasis were significantly enriched in the interleukin （IL）-17 signaling pathway and TRP channel inflammatory regulation. Compared with the normal temperature and cold exposure model groups， KXJD reversed the abnormal mRNA levels of genes related to the TRP channel subfamilies （P<0.05）， increased the CGRP level， and decreased the NPY level. Immunofluorescence double labeling further confirmed that compared with the model groups， KXJD down-regulated the co-expression of TRPM8 and CGRP in the skin lesions. ConclusionKXJD may ameliorate psoriasis-like skin lesions by downregulating the overexpressed cold-sensitive receptor TRPM8 in skin lesions and correcting the disorder of neuropeptide （such as SP and CGRP） release mediated by it， thereby inhibiting the IL-23/helper T cell 17 （Th17） core inflammatory pathway， suppressing the infiltration of inflammatory cells and the activation of the ERK signaling pathway， and regulating the Xuanfu （sweat pore）-TRPM8-neuroimmune response axis.

ObjectiveTo investigate the ameliorative effects and mechanisms of Kaixuan Jiedu core prescription （KXJD） on neuroimmunological inflammation in imiquimod （IMQ）-induced psoriasis-like mice. MethodsA total of 24 C57BL/6J mice were randomly divided into four groups （n=6）： Normal， model， KXJD， and tropomyosin receptor kinase A （TrkA） inhibitor GW441756 groups. The mice in the model， KXJD， and GW441756 groups were topically treated with 5% IMQ cream （62.5 mg·d^-1） on the back to induce psoriasis-like inflammation. The KXJD group received KXJD by gavage （30.42 g·kg^-1）， the GW441756 group received intraperitoneal injection of GW441756 （10 mg·kg^-1）， and the normal and model groups received an equal volume of normal saline by gavage， with continuous intervention for 5 days. The severity of skin lesions was evaluated using the psoriasis area and severity index （PASI）. Hematoxylin-eosin （HE） staining was used to measure epidermal thickness and observe pathological changes in the lesioned skin. Immunohistochemistry was employed to detect the expression of proliferating cell nuclear antigen （Ki67） and interleukin-17A （IL-17A） in the lesioned skin. Enzyme-linked immunosorbent assay （ELISA） was used to quantify the levels of interleukin-23 （IL-23） and calcitonin gene-related peptide （CGRP） in the lesioned tissues. Western blot was used to detect the expression of TrkA and phosphorylated TrkA （p-TrkA）. Immunofluorescence assay was performed to detect the expression of TrkA receptor， protein gene product 9.5 （PGP9.5）， cluster of differentiation 11c （CD11c）， and CGRP in the lesions. Flow cytometry was used to detect the activation of splenic dendritic cells （DCs）. ResultsCompared with the normal group， the model group exhibited typical psoriasis-like inflammation， characterized by erythema， infiltration and scaling， with histopathological findings of epidermal hyperkeratosis and acanthosis. The model group showed significantly increased expression of Ki67， IL-17A， IL-23 and p-TrkA （P<0.05， P<0.01）， increased fluorescence intensity of CD11c， and significantly decreased CGRP expression （P<0.05）. The splenic DC activation was significantly enhanced， as indicated by the increased mean fluorescence intensity （MFI） of CD86 （P<0.05）. Compared with the model group， both the KXJD and GW441756 groups showed amelioration of the psoriasis-like skin inflammation， with significantly down-regulated expression of IL-17A， IL-23 and p-TrkA （P<0.05， P<0.01）， significantly up-regulated expression of CGRP （P<0.01）， reduced CD11c⁺ DC infiltration， and restored splenic DC activation balance （down-regulated CD86 MFI and up-regulated CD80 and CD40 MFI）. Furthermore， the inhibitory effect of KXJD on Ki67 was significantly superior to that of the GW441756 group （P<0.01）. ConclusionKXJD may alleviate IMQ-induced psoriasis-like inflammation in mice by targeting and inhibiting TrkA receptor phosphorylation， regulating CGRP expression in the lesions， and ameliorating aberrant activation of dendritic cells， while also significantly inhibiting keratinocyte proliferation.

ObjectiveTo investigate the efficacy and safety of Kaixuan Jiedu compatibility and the decomposed prescriptions in the treatment of psoriasis. MethodsThirty Balb/c mice were randomly grouped as follows （n=6）： normal， model， Kaixuan Jiedu （KXJD， 15.21 g·kg^-1）， Kaixuan （KX， 3.08 g·kg^-1）， and Jiedu （JD， 12.13 g·kg^-1）. Except the normal group， the rest groups were modeled for psoriasis-like skin lesions by topical application of imiquimod， and samples were collected after 7 days of continuous intervention. Mice were photographed at the lesion site during modeling and before sampling and the psoriasis area and severity index （PASI） was calculated. Hematoxylin-eosin （HE） staining was used to observe pathological changes in the lesions and measure the epidermal thickness. Mice were photographed and observed for the tortuous dilation of dermal capillaries. The expression of vascular endothelial growth factor （VEGF）， platelet-endothelial cell adhesion molecule （CD31）， proliferating cell nuclear antigen （Ki67）， and cytokeratin 10 （CK10） in the epidermal tissue was detected by immunohistochemistry. Immunofluorescence assay was employed to determine the expression of Claudin-1 and Occludin. Real-time PCR was employed to determine the mRNA levels of interleukin-17A （IL-17A） and interleukin-23 （IL-23）. The spleen and thymus were photographed and weighed， and the spleen and thymus indices were calculated. The safety of the treatment was assessed by automatic biochemistry testing of the serum， liver， and kidney functions and by HE staining of the liver， kidney and spleen. ResultsCompared with that of the normal group， the skin of the model group showed erythema， infiltration， and typical psoriasis-like changes， tortuous dilation of dermal capillaries， hyperkeratosis in epidermal cells， acanthosis， massive lymphocytic infiltration in the dermis， impaired barrier function， increased expression of VEGF， CD31， Ki67， and CK10 （P<0.01）， reduced expression of Claudin-1 and Occludin （P<0.01） in the epidermis， and up-regulated mRNA levels of IL-17A and IL-23 （P<0.01）. In addition， the mice in the model group showed spleen enlargement， thymus atrophy， increased spleen index， and decreased thymus index （P<0.01）. Compared with the model group， KXJD and JD reduced psoriasis-like skin lesions， inhibited the tortuous dilation of dermal capillaries， reduced the expression of VEGF， CD31， Ki67， and CK10 （P<0.01）， increased the expression of claudin-1 （P<0.01）， and down-regulated the mRNA levels of inflammatory factors （P<0.01）. Moreover， the KXJD group outperformed the JD group. The JD group showed no significant difference from the model group regarding the spleen index， thymus index， and Occludin expression. The psoriasis indicators in the KX group were not significantly different from those in the model group. ConclusionKXJD and JD can reduce the symptoms of local skin lesions of psoriasis， which is manifested as different inhibition degrees of the proliferation and differentiation of keratin-forming cells， tortuous dilation of dermal capillaries， and inflammatory reactions， as well as the protection of the skin barrier. Moreover， KXJD outperformed JD. KX alone did not significantly reduce psoriasis lesions in mice. KXJD and the decomposed prescriptions are safe and effective， causing no obvious liver and kidney injuries.

ObjectiveTo investigate the efficacy and safety of Kaixuan Jiedu compatibility and the decomposed prescriptions in the treatment of psoriasis. MethodsThirty Balb/c mice were randomly grouped as follows （n=6）： normal， model， Kaixuan Jiedu （KXJD， 15.21 g·kg^-1）， Kaixuan （KX， 3.08 g·kg^-1）， and Jiedu （JD， 12.13 g·kg^-1）. Except the normal group， the rest groups were modeled for psoriasis-like skin lesions by topical application of imiquimod， and samples were collected after 7 days of continuous intervention. Mice were photographed at the lesion site during modeling and before sampling and the psoriasis area and severity index （PASI） was calculated. Hematoxylin-eosin （HE） staining was used to observe pathological changes in the lesions and measure the epidermal thickness. Mice were photographed and observed for the tortuous dilation of dermal capillaries. The expression of vascular endothelial growth factor （VEGF）， platelet-endothelial cell adhesion molecule （CD31）， proliferating cell nuclear antigen （Ki67）， and cytokeratin 10 （CK10） in the epidermal tissue was detected by immunohistochemistry. Immunofluorescence assay was employed to determine the expression of Claudin-1 and Occludin. Real-time PCR was employed to determine the mRNA levels of interleukin-17A （IL-17A） and interleukin-23 （IL-23）. The spleen and thymus were photographed and weighed， and the spleen and thymus indices were calculated. The safety of the treatment was assessed by automatic biochemistry testing of the serum， liver， and kidney functions and by HE staining of the liver， kidney and spleen. ResultsCompared with that of the normal group， the skin of the model group showed erythema， infiltration， and typical psoriasis-like changes， tortuous dilation of dermal capillaries， hyperkeratosis in epidermal cells， acanthosis， massive lymphocytic infiltration in the dermis， impaired barrier function， increased expression of VEGF， CD31， Ki67， and CK10 （P<0.01）， reduced expression of Claudin-1 and Occludin （P<0.01） in the epidermis， and up-regulated mRNA levels of IL-17A and IL-23 （P<0.01）. In addition， the mice in the model group showed spleen enlargement， thymus atrophy， increased spleen index， and decreased thymus index （P<0.01）. Compared with the model group， KXJD and JD reduced psoriasis-like skin lesions， inhibited the tortuous dilation of dermal capillaries， reduced the expression of VEGF， CD31， Ki67， and CK10 （P<0.01）， increased the expression of claudin-1 （P<0.01）， and down-regulated the mRNA levels of inflammatory factors （P<0.01）. Moreover， the KXJD group outperformed the JD group. The JD group showed no significant difference from the model group regarding the spleen index， thymus index， and Occludin expression. The psoriasis indicators in the KX group were not significantly different from those in the model group. ConclusionKXJD and JD can reduce the symptoms of local skin lesions of psoriasis， which is manifested as different inhibition degrees of the proliferation and differentiation of keratin-forming cells， tortuous dilation of dermal capillaries， and inflammatory reactions， as well as the protection of the skin barrier. Moreover， KXJD outperformed JD. KX alone did not significantly reduce psoriasis lesions in mice. KXJD and the decomposed prescriptions are safe and effective， causing no obvious liver and kidney injuries.

Objective By investigating the effects of miR-379-5p on the proliferation,invasion and metastasis of mouse breast cancer 4T1 cells,we aimed to provide new therapeutic targets for the clinical inhibition of breast cancer proliferation,invasion,and metastasis.Methods After plasmid transfection,4T1 cells were utilized to detect the expression of miR-379-5p using fluorescence quantitative PCR.While 5-ethynyl-2'doxyuridine(EdU)cell proliferation and Transwell assays were employed to detect changes in the proliferation and invasion ability of 4T1 cells in each group.The migration ability of 4T1 cells after overexpression and knockdown of miR-379-5p was examined by scratch healing assay.A transplanted tumor model of breast cancer was established in BABL/c mice,and the effects of overexpressing miR-379-5p on tumor growth and the number and size of lung metastases were observed.Results EdU result showed that knocking down miR-379-5p enhanced the proliferation ability of the cells compared with the control group cells,and miR-379-5p overexpression reduced the capacity of breast cancer cells to proliferate(P＜0.05).Transwell and wound healing assays showed that miR-379-5p knockdown enhanced,while miR-379-5p overexpression significantly inhibited,the invasion and migratory ability of breast cancer cells(P＜0.01).An in vivo tumorigenesis experiment with BABL/c mice showed that miR-379-5p overexpression significantly slowed the tumor growth rate(P＜0.05)and inhibited lung metastasis(P＜0.01).Conclusions MiR-379-5p plays a role in tumor gene suppression in breast cancer and inhibits the proliferation,invasion,and migration of mouse breast cancer 4T1 cells.

Cachexia is a common complication in patients with lung cancer. It aggravates the toxic and side effects of chemotherapy, hinders the treatment plan, weakens the responsiveness of chemotherapy, reduces the quality of life, increases complications and mortality, and seriously endangers the physical and mental health of patients with lung cancer. The causes and pathogenesis of tumor cachexia are extremely complex, which makes its treatment difficult and complex. Controlling cachexia in lung cancer patients requires many means such as anti-tumor therapy, inhibition of inflammatory response, nutritional support, physical exercise, and relief of symptoms to exert the synergistic effect of multimodal therapy against multiple mechanisms of tumor cachexia. To date, there has been a consensus within the discipline that no single therapy can control the development of cachexia. Some therapies have made some progress, but they need to be implemented in combination with multimodal therapy after fully assessing the individual characteristics of lung cancer patients. This article reviews the application of drug therapy and nutritional support in lung cancer patients, and looks forward to the research direction of cachexia control in lung cancer patients.
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Cachexia/therapy* ; Combined Modality Therapy ; Humans ; Lung Neoplasms/drug therapy* ; Neoplasms/complications* ; Nutritional Support/adverse effects* ; Quality of Life

ObjectiveTo explore the value of expanded radical resection for gallbladder cancer located respectively at body and bottom of the gallbladder and at the neck.MethodsIn this study,91 cases of gallbladder cancer were macropathologically divided into two groups, one with the lesion at the body and bottom of the gallbladder and the other at the neck, survival analysis was made accordingly. Three different kinds of resection were performed: the expanded radical resection, the standard radical resection and palliative operation.ResultsThe overall median survival rate of patients undergoing expanded radical operation was significantly longer than that of the cases doing other two procedures, that was 27. 1 ± 2. 4,10. 7 ±2. 2,4. 7 ±2.2 (months) respectively for body and bottom cancer, and 8.5 ±2. 1,6. 7 ± 1.9,3.1 ± 1.1 (months) respectively for neck cancer. For cancer at the body and bottom RO was achieved by expanded radical resection in 16/18(88％ ) cases and by standard radical resection in 7/12(58％ ) cases, while for cancer at the neck it was in 6/16(38％ ) cases, and in 3/13 (23％)cases only.ConclusionsThe median survival time is longer and RO resection rate is higher in patients with the cancer at the body and bottom than these at the neck of the gallbladder.

Objective To explore the cultivated methods of dendritic cells (DC) and the killing effect of DC stimulated by CpG ODN1826 on gastritic cancer cells MKN45 in vitro. Methods DC was induced from peripheral blood monocytes stimulated by A group ( GM- CSF + IL-4 ), B group ( GM- CSF + IL-4 + TNF- α), C group(nonCpG ODN) and D group( CpG ODN 1826). The surface markers of DC was analyzed via flow cytometry, and the abilities to stimulate proliferation of allogenic lymphocyte by DC and antitumor experiment were detected by MTT assay. Results On day 10, a majority of cells showed typical morphology of DC in D group and B group with visible branching-like and pseudopod-like structures under microscope. The results of flow cytometry showed that there are significantly high expressed co-stimulated molecules such as CD40, CD1a,CD80, CD86 and MHC- Ⅱ in D group compared to other experimental groups ( P ＜ 0.05 ), which dramatically stimulate the proliferation of allogenic lymphocytes and enhance the killing activity of DC on gastric cancer cells. Conclusion This method can acquire relatively high purified DC, and CpG ODN can significantly induce the differentiation and maturation of DC isolated from peripheral blood and enhance the killing activity of DC on MKN45 by stimulating PBMC in vitro.