Food & Function
·
2024
·
IF 5.1
Yajie Ma,Fan Zhang,Yujun Xie,Luyao An,Bo-Li Zhang,Bo-Yang Yu,Renshi Li
Asparagi Radix is a healthy food type with medicinal and edible homology, which is now widely used for improving pulmonary inflammation in clinical. However, the lung-protective effect and the active constituents of Asparagi Radix have yet to be elucidated. Herein, the potential pulmonary protective effect of oligosaccharides was investigated. We firstly identified eighteen oligosaccharides with different degrees of polymerization from Asparagi Radix using HPLC-QTOF MS. Oligosaccharides were found to be simultaneously determined in 20 batches of Asparagi Radix collected from various regions in China by HILIC-ELSD, and oligosaccharides stably exist in this herb. In the present study, we found that AROS significantly reduced NO production, and effectively down-regulated the mRNA expression of IL-6, IL-1β and TNF-α in RAW 264.7 cells, thereby reducing the inflammatory response induced by LPS. AROS also inhibited LPS-stimulated intracellular ROS production. A murine model of lipopolysaccharide (LPS)-induced acute lung injury was used to evaluate the in vivo anti-inflammatory and lung protective efficacy of AROS. AROS could ameliorate the damage of the pulmonary cellular architecture pathological injury and lung edema. AROS significantly decreased the levels of cytokines IL-6, TNF-α and IL-1β, as well as the levels of MPO and MDA, and superoxide dismutase consumption in vivo. This effect of oligosaccharides could explain the traditional usage of Asparagus cochinchinensis as a tonic medicine for respiratory problems and oligosaccharides from Asparagi Radix used as a natural ingredient could play an important role in protecting from lung injury.
研究领域:
药理学
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免疫学
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肺科学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
Natural Product Communications
·
2024
·
IF 1.5
Chunyang Mao,Yan Du,Kun Niu,Fan Yang,Changcai Bai,Bo Zhou,Yang Niu
Objective: The Traditional Chinese Medicine Qingzao Jiufei Tang decoction (QZJFD) is effective for the treatment of idiopathic pulmonary fibrosis (IPF). In this study, we explored the anti-pulmonary fibrosis effect of QZJFD and the underlying mechanism. Methods: The effects of QZJFD at low, medium, and high doses were investigated in a rat model of lung fibrosis induced by tracheal injection of bleomycin; pirfenidone was included as a positive control. Serum levels of interleukin-6 (IL-6), tumor necrosis factors (TNF-α), and IL-1β in rats were detected by enzyme-linked immunosorbent assay (ELISA). Expression of α-smooth muscle actin (α-SMA), TGF-β1, p-Jun N-terminal kinase (p-JNK), JNK, p-P38 mitogen-activated protein kinase (MAPK), P38 MAPK, collagen I, and fibronectin-1 (FN1) in lung tissues was detected by immunofluorescence labeling and western blot analysis. Results: QZJFD contained 209 main components and 575 corresponding targets. In total, 3875 disease action targets were related to IPF, with 308 common targets shared by drugs and diseases. The key targets included albumin (ALB), recombinant protein, TNF, IL-6, and tumor protein p53. In total, 3061 items were identified in the gene ontology enrichment analysis (P < .05) and 197 signaling pathways in the Kyoto encyclopedia of genes and genomes (P < .05), including MAPK, calcium, advanced glycosylation end products - receptors, TNF, and IL-17. Molecular docking simulation showed that the 2 predominant compounds of QZJFD, naringenin, and kaempferol, bound with high affinity to ALB. Serum levels of IL-6, TNF-α, and IL-1β and the expression levels of α-SMA, TGF-β1, p-JNK, p-P38 MAPK, collagen I, and FN1 in lung tissues were significantly increased in the model rats (P < .001). After treatment with pirfenidone and QZJFD at the medium and high doses, serum levels of IL-6, TNF-α, and IL-1β and expression levels of α-SMA, p-JNK, p-P38 MAPK, collagen I, and FN1 in lung tissues of rats were significantly lower than those in the model group (P < .05). Conclusions: QZJFD may exert antifibrotic and anti-inflammatory effects that improve the status of IPF by regulating the MAPK signaling pathway.
研究领域:
中医
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药理学
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呼吸病学
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分子生物学
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DOI
高影响因子
COLLOIDS AND SURFACES B-BIOINTERFACES
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2025
·
IF 5.6
Yuan Fan,Yuxiang Liu,Liujiao Wang,Huashan Xu,Lele Yu,Yue Lang,Huafei Li,Fuxue Chen,Shini Feng
Protein hydrolysis-targeted chimeras (PROTACs) are heterobifunctional molecules designed for the selective degradation of target proteins. MS4078, a novel PROTAC, shows promise for treating ALK-positive non-small cell lung cancer (NSCLC), yet its clinical efficacy is hindered by suboptimal tumor targeting and off-target toxicities. To enhance its therapeutic profile, we developed human heavy chain ferritin (HFN) as a targeted delivery system, leading to the creation of HFN@MS4078 nanocages. Prepared via passive loading, HFN@MS4078 achieved a drug loading capacity of 178 molecules per nanocage with a HFN recovery rate of 70.1 %. The nanocages exhibited a rapid release profile under lysosomal conditions (pH 5.0), with approximately 80 % drug release after 60 h, while maintaining over 80 % stability at physiological pH 7.4. In vitro, HFN@MS4078 was actively internalized into lysosomes via TfR1 receptor binding, resulting in a 2.7–2.8 times reduction in IC 50 values compared to free MS4078. Furthermore, HFN@MS4078 significantly decreased the expression levels of ALK, p-ALK, p-AKT, and p-ERK in NCI-H2228 and NCI-H3122 cell lines. In vivo, HFN@MS4078 substantially reduced tumor volume and prolonged survival while exhibiting negligible systemic toxicity. These results suggest that HFN@MS4078 represents a promising strategy for targeted therapy in ALK-positive NSCLC, enhancing therapeutic efficacy while minimizing systemic toxicity.
研究领域:
肿瘤学
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药学
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纳米技术
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分子生物学
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药物递送
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生物医学工程
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产品关联
DOI
PubMed
高影响因子
ACS Nano
·
2023
·
IF 17.1
Anwei Zhou,Kerong Chen,Ya Gao,Xinyuan Zhou,Zihan Tian,Weiwei Chen,Yurui Xu,Zhuo Chen,Xinghai Ning
Cytokine storm is a common complication of COVID-19 pneumonia and has been proven to contribute to high mortality rates. However, current treatment approaches exhibit limited potential to balance immune response and overproduction of inflammatory cytokines, leading to poor therapeutic outcomes. Herein, a smart bioengineered neutrophil, Extinguisher, composed of live neutrophils encapsulating the liposome formulation of NF-κB suppressor MLN4924 and STING inhibitor H-151 (Lip@MH), is developed for alleviating the hyperinflammatory cytokine storm. Extinguisher inherits motility and chemotaxis characteristics of neutrophils, allowing for the specific delivery and sustained release of Lip@MH within inflamed tissues. Subsequently, Lip@MH effectively transports anti-inflammatory agents into macrophages and synergistically inhibits inflammatory pathways of NF-κB and STING, leading to decreased production of cytokines. In vivo studies demonstrate that Extinguisher not only selectively accumulates at the site of pneumonia caused by Pseudomonas aeruginosa-induced acute lung injury but inhibits the production of inflammatory factors through regulating NF-κB/STING signaling pathways, thereby effectively calming cytokine storm. Importantly, Extinguisher significantly improves therapeutic benefits and survival in mice with acute pneumonia. Therefore, Extinguisher represents an appropriate combination of cell therapy and immunoregulation for cytokine storm intervention and may bring insights into the treatment of COVID-19 pneumonia.
研究领域:
免疫学
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生物技术
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药学
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分子生物学
✓ 已验证
DOI
PubMed
高影响因子
COPD-Journal of Chronic Obstructive Pulmonary Disease
·
2023
·
IF 2.2
Chuanxin Yang,Libing Deng,Fang Bao,Hui Jiang,Long Zhang
Chronic obstructive pulmonary disease (COPD) is a difficult-to-cure disease that mainly affects the respiratory system. Inhaled anesthetic drug such as sevoflurane plays a controversial role in COPD by different concentration, but the underlying epigenetic mechanism remains unclear. Here, we prepared lipopolysaccharide (LPS)-induced COPD rat model, and isolated Alveolar type II (ATII) cells. We mainly focused DNA methylation on the promoter of COPD-related genes including Sftpa1, Napsa, Ca2, Sfta2, Lamp3, Wif1, Pgc, and Etv5. We observed COPD rat treated by sevoflurane with low (0.5%) and high (2%) concentrations displayed an opposite DNA methylation pattern. These six genes' promoter were all hypomethylated by 0.5% sevoflurane whereas hypermethylated by 2% sevoflurane, accompanied with the opposite transcriptional activity. We further verified that the DNMT1 binding ability contributed to DNA methylation these six genes' promoter. Moreover, we also captured DNMT1 and identified REC8 meiotic recombination protein (REC8) as the specific binding protein only existed in ATII cells treated with 0.5% sevoflurane rather than 2% and control. The binding ability of REC8 on these target genes' promoter showed highly positive correlation with DNMT1. In summary, we uncovered a potential epigenetic role of sevoflurane with low concentration in ATII cells of COPD that may help us deeply understand the pathogenesis and treatment mechanism of inhaled anesthesia drugs in COPD via a dose-dependent manner.
研究领域:
肺病学
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分子生物学
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表观遗传学
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药理学
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DOI
高影响因子
BMC Veterinary Research
·
2022
·Vol. 18
·期 1
·1-14
·
IF 2.792
Hao Fei,Xie Xing,Feng Zhixin,Chen Rong,Wei Yanna,Liu Jin,Xiong Qiyan,Shao Guoqing,Lin Johnson
Background Mycoplasma hyopneumoniae (M. hyopneumoniae) is the etiological agent of enzootic pneumonia, a highly infectious swine respiratory disease that distributed worldwide. The pathogenesis and virulence factors of M. hyopneumoniae are not fully clarified. As an important virulence factor of bacteria, nicotinamide adenine dinucleotide (NADH) oxidase (NOX) participates in host-pathogen interaction, however, the function of NOX involved in the pathogenesis of M. hyopneumoniae is not clear.Results In this study, significant differences in NOX transcription expression levels among different strains of M. hyopneumoniae differed in virulence were identified, suggesting that NOX may be correlated with M. hyopneumoniae virulence. The nox gene of M. hyopneumoniae was cloned and expressed in Escherichia coli, and polyclonal antibodies against recombinant NOX (rNOX) were prepared. We confirmed the enzymatic activity of rNOX based on its capacity to oxidize NADH to NAD+. Flow cytometry analysis demonstrated the surface localization of NOX, and subcellular localization analysis further demonstrated that NOX exists in both the cytoplasm and cell membrane. rNOX was depicted to mediate adhesion to immortalized porcine bronchial epithelial cells (hTERT-PBECs). Pre-neutralizing M. hyopneumoniae with anti-rNOX antibody resulted in a more than 55% reduction in the adhesion rate of high- and low-virulence M. hyopneumoniae strains to hTERT-PBECs. Moreover, a significant difference appeared in the decline in CCU50 titer between virulent (168) and virulence-attenuated (168L) strains. NOX not only recognized and interacted with host fibronectin but also induced cellular oxidative stress and apoptosis in hTERT-PBECs. The release of lactate dehydrogenase by NOX in hTERT-PBECs was positively correlated with the virulence of M. hyopneumoniae strains.Conclusion sNOX is considered to be a potential virulence factor of M. hyopneumoniae and may play a significant role in mediating its pathogenesis.
研究领域:
微生物学
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兽医学
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分子生物学
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病理学
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产品关联
DOI
PubMed
高影响因子
BIOMEDICINE & PHARMACOTHERAPY
·
2022
·
IF 7.419
Huan-huan Zhang,Xiao-jie Zhou,Yu-sen Zhong,Li-ting Ji,Wen-ying Yu,Jie Fang,Hua-zhong Ying,Chang-yu Li
Naringin is one of the natural flavonoids extracted from many Chinese medicines. It ameliorates endothelial dysfunctions in atherosclerosis, diabetes, and cardiovascular diseases through free radical scavenging and antioxidant activities. The aim of the present study was to investigate the protective effects of naringin against pulmonary endothelial permeability in addition to airway inflammation in lipopolysaccharide/cigarette smoke (LPS/CS)-induced chronic obstructive pulmonary disease (COPD) mice.The COPD mice were exposed to LPS twice through intranasal inhalation and then to cigarette smoke daily for 6 weeks. The mice were orally administrated with naringin at doses of 40 or 80 mg/kg one hour before cigarette smoke exposure since the first day of the experiment. Naringin significantly alleviated pulmonary histopathological injury, and suppressed inflammatory cell infiltration and cytokine release in bronchoalveolar lavage fluid. Naringin decreased fluorescence intensity of Evans Blue in the lung tissues, and elevated the expression levels of tight junctional proteins. Meanwhile, naringin decreased neutrophil/lymphocyte/platelet counts and MDA content in blood, and upregulated Aquaporin1 (AQP1) in the lung tissues. However, the effect of naringin on airway inflammation and pulmonary endothelial permeability was inhibited in LPS/CS-treatment AQP1 deficiency mice. These results indicated that naringin attenuated LPS/CS-induced airway inflammatory and pulmonary hyperpermeability via upregulating AQP1 expression.
研究领域:
药理学
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肺科学
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免疫学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ONCOLOGY REPORTS
·
2025
·Vol. 53
·期 5
·1-14
·
IF 3.9
Ying Hu,Xin Liu,Ziheng Yuan,Jianping He,Run Ma,Yuming Wang,Genfa Yi
Globally, lung adenocarcinoma (LUAD) remains the leading cause of cancer‑related mortality, highlighting the urgent need for innovative therapeutic approaches. Necroptosis has been recognized as a crucial mechanism for inhibiting cancer progression. Research has revealed a significant association between microRNA (miRNA)‑mediated necroptosis and tumor progression. The present study aimed to elucidate the role and underlying mechanisms of miR‑10b‑5p in regulating necroptosis in the context of LUAD. In an investigation of LUAD, miRNA sequencing was conducted on both LUAD and adjacent non‑tumor tissues, followed by the integration of external database information to identify specific target miRNAs. The expression of miR‑10b‑5p was verified in LUAD tissues and corresponding adjacent non‑cancerous tissues using immunohistochemistry. In vitro experiments, utilizing LUAD cell lines engineered to modulate miR‑10b‑5p levels, assessed its effects on cellular activities and necroptosis. The inhibition of PKP3 by miR‑10b‑5p was determined using a dual luciferase reporter system. Furthermore, alterations in miR‑10b‑5p levels were found to affect PKP3 expression and inhibit the RIPK3/MLKL signaling pathway, as evidenced by western blot analysis in LUAD cell lines. The effect of PKP3 knockdown on cell activity and necroptosis in LUAD cell lines with low miR‑10b‑5p expression levels was assessed using cell function assays. Finally, a nude mouse xenograft model was used to investigate the effect of miR‑10b‑5p on LUAD growth in vivo and its specific mechanism of action. It has been revealed that miR‑10b‑5p levels are significantly elevated in LUAD specimens. Further investigations demonstrated that an increase in miR‑10b‑5p enhances the proliferation of LUAD cells and suppresses the progression of necroptosis, as evidenced by in vitro experiments. Through dual luciferase reporter assays, PKP3 was confirmed as a direct target negatively regulated by miR‑10b‑5p, leading to reduced expression levels. Western blot analysis indicated that miR‑10b‑5p inhibits the RIPK3/MLKL pathway activation through downregulation of PKP3, which leads to increased cell proliferation and decreased necroptosis. However, knockdown of PKP3 reversed the inhibitory effect of miR‑10b‑5p inhibitors on cellular activity and inhibited necrosis by suppressing the RIPK3/MLKL signalling pathway. In addition, animal model studies demonstrated that inhibition of miR‑10b‑5p activated the RIPK3/MLKL pathway by promoting PKP3 expression and significantly reduced LUAD growth by promoting necroptosis. In conclusion, our studies have revealed that the miR‑10b‑5p functions as a tumorigenic factor, enhancing various cellular activities in LUAD cells and suppressing necroptosis by specifically targeting PKP3, thereby inhibiting activation of the RIPK3/MLKL pathway. Importantly, interventions using inhibitors that specifically target miR‑10b‑5p have shown significant success in impeding the progression of LUAD by promoting necroptosis in both cellular and animal models. Thus, targeting miR‑10b‑5p holds considerable potential as a therapeutic strategy for LUAD.
研究领域:
肿瘤学
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分子生物学
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医学遗传学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
BIOCHEMICAL PHARMACOLOGY
·
2025
·
IF 5.6
Jiani Zhan,Yijia Chen,Yuying Liu,Yunqiu Chen,Zhiyao Li,Xuewen Li,Zhenning He,Fangzhou Meng,Xiaoyang Qian,Lili Yang,Qing Yang
Ferroptosis is a type of cell death marked by iron-dependent lipid peroxide accumulation. Indoleamine 2,3-dioxygenase 1 (IDO1), a key enzyme in the catabolism of tryptophan through kynurenine pathway, participates in the development of multiple tumor types. However, the role of IDO1 in tumor ferroptosis is unclear. In this study, we identified IDO1 as a key regulator of ferroptosis in lung cancer. With Erastin-treated lung cancer cells, we found that IDO1 inhibited ferroptosis, reduced the generation of lipid peroxide and ROS. Mechanistically, IDO1 promoted the expression of nuclear factor erythroid 2-related factor 2 (NRF2) through activating aryl hydrocarbon receptor (AhR) pathway. IDO1 up-regulated the expression of solute carrier family 7 member 11 (SLC7A11) and the activity of pentose phosphate pathway (PPP) via AhR-NRF2 axis, promoted the production of reduced nicotinamide adenine dinucleotide phosphate (NADPH) and glutathione (GSH), thereby inhibiting ferroptosis. Moreover, combined treatment with IDO1 inhibitor and Erastin inhibited tumor growth, down-regulated SLC7A11 expression and PPP activity, promoted tumor ferroptosis in lung cancer-bearing mice. In conclusion, this study revealed the function of IDO1 in lung cancer ferroptosis and provided a new strategy for lung cancer therapy.
研究领域:
肿瘤学
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分子生物学
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
FASEB JOURNAL
·
2025
·Vol. 39
·期 5
·e70420
·
IF 4.2
Min Zhu,Xiaofang Fan,Nan Zhang,Hui Wang,Jianshe Ma,Xianghong Yin,Junyan Cai,Linjing Cong,Ran Chen,Junming Fan,Xiaoxia Kong,Bin Geng,Yongsheng Gong,Congkuo Du
Endothelial pyroptosis, a pro-inflammatory programmed cell death, promotes endothelial inflammation and is a pivotal process in the initial stage of acute lung injury (ALI). Hydrogen sulfide (H 2 S), a gasotransmitter primarily dependent on cystathionine γ-lyase (CSE) in the cardiovascular and respiratory systems, plays a protective role during ALI. Nonetheless, the modulatory role and precise molecular mechanism of endothelial endogenous CSE/H 2 S in the pathogenesis of ALI remain elusive. Herein, we prepared an ALI mouse model using intratracheal administration of LPS (5 mg/kg), and lung injury was assessed by evaluating pulmonary edema, inflammatory response, and endothelial pyroptosis. In this model, H 2 S production from pulmonary tissues declined in a time-dependent manner, accompanied by a compensatory elevation of CSE protein levels. Treatment with the H 2 S donor (NaHS) attenuated pulmonary edema, inflammatory cell infiltration, endothelial pyroptosis, and reduced serum levels of tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6). Meanwhile, the inducible deletion of CSE in endothelial cells exacerbated these changes. The blocking effect of CSE/H 2 S on endothelial pyroptosis (evidenced by caspase-11 activation and GSDMD-NT formation) was also confirmed in cultured pulmonary microvascular endothelial cells (PMECs). Mechanistically, H 2 S-mediated regulation of sirtuin-1 (SIRT1) expression and activation (via sulfhydration) contributed to the modulatory process. Collectively, we uncovered that endothelial endogenous CSE/H 2 S alleviates endothelial pyroptosis by activating SIRT1, thereby preventing LPS-induced acute lung injury. Graphical In the LPS-induced ALI model, caspase-1-independent pyroptosis was activated. The expression of activated caspase-11 and GSDMD-NT was increased, accompanied by pulmonary edema and inflammatory infiltration. Endothelial CSE/H 2 S deficiency aggravated endothelial pyroptosis and acute lung injury. Mechanistically, endothelial endogenous CSE/H 2 S mediated the expression and activation of sirtuin-1 (SIRT1) via sulfhydration, one of the post-translational modifications. Activated SIRT1 inhibited the activation of caspase-11 and GSDMD-NT to inhibit endothelial pyroptosis, thereby alleviating acute lung injury.
研究领域:
医学
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分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
RESPIRATORY RESEARCH
·
2025
·Vol. 26
·期 1
·1-17
·
IF 5
Ren Shencheng,Zhu Junkan,Shan Guangyao,Liang Jiaqi,Bian Yunyi,Lin Han,Shi Haochun,Pan Binyang,Zhao Guangyin,Yang Huiqin,Huang Xiaolong,Zhan Cheng,Ge Di,Bi Guoshu
Background Lung cancer remains the leading cause of cancer-related mortality globally, with lung adenocarcinoma (LUAD) being the most prevalent subtype. Despite extensive research efforts, the role of transcription factors in LUAD progression remains largely uncharacterized. In this study, we focused on ZNF266, a transcription factor whose impacts on LUAD have not been investigated. Methods Using high-throughput sequencing data, we observed a significant downregulation of ZNF266 expression in LUAD tissues. To validate this finding, we conducted a retrospective analysis of nearly three thousand LUAD patients’ data from public databases and our institution. Functional studies were performed using cell lines, organoids, and xenograft models to assess the role of ZNF266 in LUAD progression. RNA sequencing, chromatin immunoprecipitation, DNA pull-down assays, and dual-luciferase reporter assays were employed to elucidate the underlying mechanism. Additionally, adeno-associated virus (AAV)-mediated overexpression of ZNF266 was used to evaluate its therapeutic potential. Results Patients with low ZNF266 expression had poorer prognosis compared to those with high expression. ZNF266 inhibits the malignant phenotypes of LUAD, including proliferation, migration, and invasion. Mechanistically, ZNF266 binds to the promoter region of CA9, suppressing its transcription. This leads to a reduction in intracellular pH and subsequent inhibition of the mTOR signaling pathway, which is crucial for cancer cell growth and survival. Furthermore, AAV-mediated overexpression of ZNF266 significantly inhibited tumor growth in patient-derived xenograft models. Conclusions Our study demonstrated that ZNF266 inhibits LUAD progression in a pH-dependent manner via modulating CA9 expression, uncovering its therapeutic significance for LUAD treatment.
研究领域:
肿瘤学
·
分子生物学
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医学遗传学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
TROPICAL JOURNAL OF PHARMACEUTICAL RESEARCH
·
2018
·Vol. 17
·期 7
·1379-1384
·
IF 0.444
Jianfeng Quan,Yanli Zhao
Purpose: To investigate the anti-tumor effects of nedaplatin (NDP) and CpG oligodeoxynucleotide (CpG-ODN) combination therapy in a mouse-modeled lung cancer.Methods: To evaluate the anti-tumor effects of NDP and CpG-ODN combination therapy, a lung cancer xenograft mouse model was established by subcutaneous injection of LA-795 cells. BALB/c mice were divided into four groups as follows: NDP, CpG-, NDP + CpG-ODN and untreated control group. The sections of lung cancer tissue were stained with hematoxylin and eosin (H&E) and morphologically examined. Spleen, body weight, and spleen index were measured. Flow cytometry was used to determine the proportions of CD3+, CD8+, CD4+ and CD4+/CD8+ in mice blood cells. Serum levels of interferon-γ (IFN-γ) and interleukin-12 (IL-12) were measured by enzyme-linked immunosorbent assay (ELISA).Results: NDP + CpG-ODN therapy significantly reduced tumor volume and prolonged the survival time of tumor-bearing mice. NDP + CpG-ODN induced a change in cancer cell morphology, including large areas of necrosis which correlated with a reduction in tumor size. NDP + CpG-ODN significantly increased spleen weight/index and dramatically enhanced immune cell activation. This was evident in the increase serum levels of IFN-γ and IL-12.Conclusion: NDP and CpG-ODN combination therapy inhibits the growth of lung cancer and prolongs the survival time of tumor-bearing mice. This may result from the activation of immune cells and increased expression of IFN-γ and IL-12.Keywords: CpG ODN, NDP, Lung cancer, Combination therapy
研究领域:
肿瘤学
·
免疫学
✓ 已验证
DOI
高影响因子
危险品化学品经营许可证（带存储）