LIVIVO - Search results -

Search results

Result 1 - 10 of total 36185

Search options

Article ; Online: Andrographolide inhibits Burkitt's lymphoma by binding JUN and CASP3 proteins.

Zeng, Junquan / Zheng, Yongliang / Dong, Si / Ding, Ting / Zhang, Shouhua / Li, Kuangfan / Liu, Haiyun / Fang, Quangang / Yuan, Sheng / Wei, Yujing / Li, Jing / Liu, Tingting

Cancer chemotherapy and pharmacology

2023 Volume 93, Issue 4, Page(s) 381–391

Abstract: ... a increased in the expression of JUN (c-Jun) and CASP3 (Caspase 3) proteins in Burkitt's lymphoma cells ... by inhibiting JUN and CASP3 proteins. ...

Abstract	Background: Burkitt's lymphoma, one of the most common subtypes of pediatric malignant lymphoma, is notorious for its swift onset, aggressive proliferation, pronounced invasiveness, and marked malignancy. The therapeutic landscape for Burkitt's lymphoma currently falls short of providing universally effective and tolerable solutions. Andrographolide, a primary active component of Andrographis paniculata, is renowned for its properties of heat-clearing, detoxification, inflammation reduction, and pain relief. It is predominantly used in treating bacterial and viral infections of the upper respiratory tract, as well as dysentery. Various reports highlight the antitumor effects of andrographolide. Yet, its specific impact and the underlying mechanism of action on Burkitt's lymphoma remain an uncharted area of research. Method: We employed network pharmacology to pinpoint the targets of andrographolide's action on Burkitt's lymphoma and the associated pathways. We then evaluated the impact of andrographolide on Burkitt's lymphoma using both in vitro and in vivo patient-derived xenograft (PDX) models. Concurrently, we confirmed the molecular targets of andrographolide in Burkitt's lymphoma through immunofluorescence assays. Result: Utilizing network pharmacology, we identified 15 relevant targets, 60 interrelationships between these targets, and numerous associated signaling pathways for andrographolide's action on Burkitt's lymphoma. In vitro efficacy tests using High-throughput Drug Sensitivity Testing and in vivo PDX model evaluations revealed that andrographolide effectively curtailed the growth of Burkitt's lymphoma. Moreover, we observed a increased in the expression of JUN (c-Jun) and CASP3 (Caspase 3) proteins in Burkitt's lymphoma cells treated with andrographolide. Conclusion: Andrographolide inhibits the growth of Burkitt's lymphoma by inhibiting JUN and CASP3 proteins.
MeSH term(s)	Humans ; Child ; Burkitt Lymphoma/drug therapy ; Burkitt Lymphoma/metabolism ; Burkitt Lymphoma/pathology ; Caspase 3 ; Diterpenes
Chemical Substances	Caspase 3 (EC 3.4.22.-) ; andrographolide (410105JHGR) ; CASP3 protein, human (EC 3.4.22.-) ; Diterpenes
Language	English
Publishing date	2023-12-26
Publishing country	Germany
Document type	Journal Article
ZDB-ID	6820-2
ISSN	1432-0843 ; 0344-5704 ; 0943-9404
ISSN (online)	1432-0843
ISSN	0344-5704 ; 0943-9404
DOI	10.1007/s00280-023-04626-4
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1420: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Corrigendum to "Hemoporfin-mediated photodynamic therapy for the treatment of port-wine stain: A multicenter, retrospective study" [Photodiagnosis Photodyn Ther. 2023 Jun;42:103545].

Zhang, Xiaofeng / Yuan, Chen / Xiao, Xuemin / Yin, Rui / Lei, Hongzhao / Li, Yan / Zheng, Shumao / Wen, Sijian / Li, Dongsheng / Wang, Xuejun / Lu, Zhong / Zhang, Yunfeng / Zeng, Weihui / He, Sijin / Li, Yuzhen / Jian, Dan / Yang, Jun / Zhong, Hua / Han, Dawei /

Chen, Xiaoying / Zhou, Junfeng / Cai, Yantao / Peng, Xi / Li, Zhiming / Liu, Xueying / Lin, Tong / Zhang, Ruzhi / Li, Guang / Zhuang, Yin / Liu, Ling / Yan, Yan / Wang, Baoxi

Photodiagnosis and photodynamic therapy

2023 Volume 45, Page(s) 103931

Language	English
Publishing date	2023-12-26
Publishing country	Netherlands
Document type	Published Erratum
ZDB-ID	2149918-4
ISSN	1873-1597 ; 1572-1000
ISSN (online)	1873-1597
ISSN	1572-1000
DOI	10.1016/j.pdpdt.2023.103931
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: LANA regulates miR-155/GATA3 signaling axis by enhancing c-Jun/c-Fos interaction to promote the proliferation and migration of KSHV-infected cells.

Luo, Ting / Pan, Yangyang / Liu, Yuhao / Zheng, Jun / Zhuang, Zhaowei / Ren, Zuodong / Zhu, Jiaojiao / Gu, Yongqing / Zeng, Yan

Journal of medical virology

2022 Volume 95, Issue 1, Page(s) e28255

Abstract: ... infected cells by regulating the miR-155/GATA3 axis. Regarding the molecular mechanism, c-Jun and c-Fos ... interact to form a complex. LANA upregulates the expression of c-Jun and c-Fos and enhances the formation ... of c-Jun/c-Fos complex. The complex binds to the -95∼-100 bp site of miR-155 promoter and ...

Abstract	Kaposi's sarcoma (KS) is the second most common tumor in people infected with human immunodeficiency virus worldwide, but its pathogenesis is still unclear. In this study, we discovered that the expression of GATA-binding protein 3 (GATA3) was lowly expressed in KS tissues and KSHV-infected cells, while microRNA-155 (miR-155) was highly expressed in KS serum and KSHV-infected cells. miR-155 promoted the proliferation, migration and invasion of KSHV infection by targeting GATA3. Further, The KSHV-encoded protein, the Latency associated nuclear antigen (LANA), promotes the proliferation, migration and invasion of KSHV-infected cells by regulating the miR-155/GATA3 axis. Regarding the molecular mechanism, c-Jun and c-Fos interact to form a complex. LANA upregulates the expression of c-Jun and c-Fos and enhances the formation of c-Jun/c-Fos complex. The complex binds to the -95∼-100 bp site of miR-155 promoter and transcriptionally activates miR-155. All in all, LANA enhances the c-Jun/c-Fos interaction, resulting in enhanced transcriptional regulation of miR-155 by the c-Jun/c-Fos complex, thereby downregulating GATA3 and promoting the proliferation, migration and invasion of KSHV-infected cells. The discovery of LANA/c-Jun/c-Fos/miR-155/GATA3 further refines the pathogenesis of KS, potentially opening a new avenue for developing effective drugs against KS.
MeSH term(s)	Humans ; Herpesvirus 8, Human/physiology ; Cell Line ; Sarcoma, Kaposi ; Antigens, Viral/metabolism ; Antigens, Nuclear/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Cell Proliferation ; GATA3 Transcription Factor/genetics ; GATA3 Transcription Factor/metabolism
Chemical Substances	Antigens, Viral ; Antigens, Nuclear ; MicroRNAs ; GATA3 protein, human ; GATA3 Transcription Factor ; MIRN155 microRNA, human
Language	English
Publishing date	2022-11-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	752392-0
ISSN	1096-9071 ; 0146-6615
ISSN (online)	1096-9071
ISSN	0146-6615
DOI	10.1002/jmv.28255
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 1320: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Retraction Note: MicroRNA-30d promotes angiogenesis and tumor growth via MYPT1/c-JUN/VEGFA pathway and predicts aggressive outcome in prostate cancer.

Lin, Zhuo-Yuan / Chen, Guo / Zhang, Yan-Qiong / He, Hui-Chan / Liang, Yu-Xiang / Ye, Jian-Heng / Liang, Ying-Ke / Mo, Ru-Jun / Lu, Jian-Ming / Zhuo, Yang-Jia / Zheng, Yu / Jiang, Fu-Neng / Han, Zhao-Dong / Wu, Shu-Lin / Zhong, Wei-de / Wu, Chin-Lee

Molecular cancer

2023 Volume 22, Issue 1, Page(s) 56

Language	English
Publishing date	2023-03-20
Publishing country	England
Document type	Retraction of Publication
ZDB-ID	2091373-4
ISSN	1476-4598 ; 1476-4598
ISSN (online)	1476-4598
ISSN	1476-4598
DOI	10.1186/s12943-023-01763-5
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Salidroside ameliorated the pulmonary inflammation induced by cigarette smoke via mitigating M1 macrophage polarization by JNK/c-Jun.

Feng, Haoshen / Zhang, Dan / Yin, Yan / Kang, Jian / Zheng, Rui

Phytotherapy research : PTR

2023 Volume 37, Issue 9, Page(s) 4251–4264

Abstract: ... salidroside mitigated M1 polarization induced by CS. CSE activated the JNK/c-Jun in AMs and the M1 ... c-Jun, which indicated that salidroside mitigated the M1 polarization of AMs induced by CS via ... inhibiting JNK/c-Jun. Salidroside treatment ameliorated the pulmonary inflammation and M1 polarization of AMs ...

Abstract	Pulmonary inflammation induced by cigarette smoke (CS) promoted the development of chronic obstructive pulmonary disease (COPD), and macrophage polarization caused by CS modulated inflammatory response. Previous studies indicated that salidroside exerted therapeutic effects in COPD, but the anti-inflammatory mechanisms were not clear. This study aimed to explore the effects and mechanisms of salidroside on macrophage polarization induced by CS. Wistar rats received passively CS exposure and were treated intraperitoneally with salidroside at a low, medium or high dose. Lung tissues were stained with hematoxylin-eosin. Emphysema and inflammatory scores were evaluated by histomorphology. Lung function, cytokines, and cell differential counts in BALF were detected. The macrophage polarization was determined by immunohistochemistry in lung tissues. Alveolar macrophages (AMs) were isolated and treated with cigarette smoke extract (CSE), salidroside or inhibitors of relative pathways. The polarization status was determined by qPCR, and the protein level was detected by Western blotting. CS exposure induced emphysema and lung function deterioration. The inflammatory scores, cytokines level and neutrophils counts were elevated after CS exposure. Salidroside treatment partly ameliorated above abnormal. CS exposure activated M1 and M2 polarization of AMs in vivo and in vitro, and salidroside mitigated M1 polarization induced by CS. CSE activated the JNK/c-Jun in AMs and the M1 polarization of AMs was inhibited by the inhibitors of JNK and AP-1. Salidroside treatment deactivated the JNK/c-Jun, which indicated that salidroside mitigated the M1 polarization of AMs induced by CS via inhibiting JNK/c-Jun. Salidroside treatment ameliorated the pulmonary inflammation and M1 polarization of AMs induced by CS, and the process might be mediated by the deactivation of JNK/c-Jun.
MeSH term(s)	Rats ; Animals ; Cigarette Smoking ; Rats, Wistar ; Lung ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Pneumonia ; Pulmonary Emphysema/chemically induced ; Pulmonary Emphysema/metabolism ; Macrophages/metabolism ; Cytokines/metabolism ; Emphysema/metabolism
Chemical Substances	rhodioloside (M983H6N1S9) ; Cytokines
Language	English
Publishing date	2023-05-30
Publishing country	England
Document type	Journal Article
ZDB-ID	639136-9
ISSN	1099-1573 ; 0951-418X
ISSN (online)	1099-1573
ISSN	0951-418X
DOI	10.1002/ptr.7905
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.B 3092: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Low-Dose Trans-Resveratrol Ameliorates Diabetes-Induced Retinal Ganglion Cell Degeneration via TyrRS/c-Jun Pathway.

Xiao, Ke / Ma, Xiao-Hong / Zhong, Zheng / Zhao, Yin / Chen, Xu-Hui / Sun, Xu-Fang

Investigative ophthalmology & visual science

2023 Volume 64, Issue 7, Page(s) 2

Abstract: ... on the binding of TyrRS to the transcription factor c-Jun and the binding of c-Jun to pro-apoptotic genes were ... and HG-treated N2a cells. Trans-RSV promoted TyrRS binding to c-Jun, inhibited the phosphorylation ... of Ser-63 of c-Jun, and downregulated pro-apoptotic gene transcription.: Conclusions: Low-dose trans ...

Abstract	Purpose: The purpose of this study was to investigate the protective effect of low-dose trans-resveratrol (trans-RSV) on diabetes-induced retinal ganglion cell (RGC) degeneration and its possible mechanism. Methods: A streptozotocin-induced diabetic mouse model was established and treated with or without trans-RSV intragastric administration (10 mg/kg body weight/day) for 12 weeks. Oscillatory potentials (Ops) of the dark-adapted electroretinogram (ERG) were recorded. The number of RGCs was detected by Tuj1 and TUNEL staining. The apoptosis markers in the retina were analyzed by Western blot. The cross sections of optic nerves were observed by transmission electron microscopy. In addition, mouse neuroblastoma N2a cells were injured by high-glucose (HG) treatment. Cell viability and apoptosis were measured with or without low-dose trans-RSV treatment. The intracellular localization of tyrosyl transfer-RNA synthetase (TyrRS) was observed in both mouse retinas and N2a cells. The effects of low-dose trans-RSV on the binding of TyrRS to the transcription factor c-Jun and the binding of c-Jun to pro-apoptotic genes were analyzed by co-IP and ChIP assays in HEK 293 cells. Results: Trans-RSV relieved electrophysiological injury of retinas and inhibited RGC apoptosis in diabetic mice. It also protected N2a cells from HG-induced apoptosis. Additionally, it promoted TyrRS nuclear translocation in both diabetic mouse retinas and HG-treated N2a cells. Trans-RSV promoted TyrRS binding to c-Jun, inhibited the phosphorylation of Ser-63 of c-Jun, and downregulated pro-apoptotic gene transcription. Conclusions: Low-dose trans-RSV can ameliorate diabetes-induced RGC degeneration via the TyrRS/c-Jun pathway. It can promote TyrRS nuclear translocation and bind to c-Jun, downregulating c-Jun phosphorylation and downstream pro-apoptotic genes.
MeSH term(s)	Mice ; Humans ; Animals ; Retinal Ganglion Cells/metabolism ; Resveratrol/pharmacology ; Diabetes Mellitus, Experimental/complications ; Diabetes Mellitus, Experimental/drug therapy ; Diabetes Mellitus, Experimental/metabolism ; HEK293 Cells ; Retina/metabolism ; Apoptosis
Chemical Substances	Resveratrol (Q369O8926L)
Language	English
Publishing date	2023-06-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	391794-0
ISSN	1552-5783 ; 0146-0404
ISSN (online)	1552-5783
ISSN	0146-0404
DOI	10.1167/iovs.64.7.2
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 45: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: C-Jun/C7ORF41/NF-κB axis mediates hepatic inflammation and lipid accumulation in NAFLD.

Yan, Feng-Juan / Wang, Xu / Wang, Song-En / Hong, Hai-Ting / Lu, Jun / Ye, Qin / Zheng, Yuan-Lin / Wang, Yong-Jian

The Biochemical journal

2020 Volume 477, Issue 3, Page(s) 691–708

Abstract: ... activation, which promotes c-Jun-mediated transcriptional repression of C7ORF41. In conclusion, our findings ... suggested that a c-Jun/C7ORF41/NF-κB regulatory network controls the inflammatory response and lipid ...

Abstract	Nonalcoholic fatty liver disease (NAFLD) is an expanding health problem worldwide. Although many studies have made great efforts to elucidate the pathogenesis of NAFLD, the molecular basis remains poorly understood. Here, we showed that hepatic C7ORF41, a critical regulator of innate immune response, was markedly decreased in diet or genetic-induced NAFLD model. We also demonstrated that C7ORF41 overexpression significantly ameliorated hepatic inflammation and lipid accumulation in palmitic acid (PA)-treated hepatocytes, whereas C7ORF41 knockdown showed the opposite effects. Mechanistically, we found the anti-inflammatory role of C7ORF41 was attributed to the suppression of NF-κB p65-mediated induction of inflammatory cytokines. Moreover, we demonstrated that the suppression of C7ORF41 expression in hepatocytes is due to JNK activation, which promotes c-Jun-mediated transcriptional repression of C7ORF41. In conclusion, our findings suggested that a c-Jun/C7ORF41/NF-κB regulatory network controls the inflammatory response and lipid accumulation in NAFLD and may benefit the development of novel and promising therapeutic targets for NAFLD.
MeSH term(s)	Animals ; Cytokines/metabolism ; Disease Models, Animal ; Hepatocytes/pathology ; Immunity, Innate ; Inflammation/metabolism ; JNK Mitogen-Activated Protein Kinases/metabolism ; Lipid Metabolism ; Liver/pathology ; Mice ; NF-kappa B/metabolism ; Non-alcoholic Fatty Liver Disease/metabolism ; Signal Transduction
Chemical Substances	Cytokines ; NF-kappa B ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2020-01-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2969-5
ISSN	1470-8728 ; 0006-2936 ; 0306-3275 ; 0264-6021
ISSN (online)	1470-8728
ISSN	0006-2936 ; 0306-3275 ; 0264-6021
DOI	10.1042/BCJ20190799
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.110: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Impinging Flow Induces Expression of Monocyte Chemoattractant Protein-1 in Endothelial Cells Through Activation of the c-Jun N-terminal Kinase/c-Jun/p38/c-Fos Pathway.

Zhu, Huaxin / Hao, Zheng / Xing, Zelong / Tan, Jiacong / Zhao, Yeyu / Li, Meihua

World neurosurgery

2022 Volume 164, Page(s) e681–e693

Abstract: ... of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), p38, activator protein-1, and MCP-1 were detected ... the phosphorylation levels of ERK, JNK, and p38, as well as the protein levels of MCP-1, c-Jun, and c-Fos, increased ... factors are regulated through the JNK/c-Jun/p38/c-Fos pathway and participate in EC inflammation. ...

Abstract	Objective: Monocyte chemoattractant protein-1 (MCP-1) is an important regulator of the formation and development of intracranial aneurysms. This study explored the molecular mechanisms underlying the induction of MCP-1 and related inflammatory factors in human umbilical vein endothelial cells (HUVECs) under hemodynamic conditions. Methods: A modified T chamber was used to simulate fluid flow at the bifurcation of the artery and wall shear stress on HUVECs in vitro. Changes in HUVECs were analyzed in response to impinging flow. And HUVECs without impinging flow were used as the control group. Protein expression levels of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), p38, activator protein-1, and MCP-1 were detected by Western blot, and the messenger RNA expression levels of MCP-1, interleukin (IL)-1β, and IL-6 were determined by quantitative reverse transcription polymerase chain reaction. Results: Under impinging flow, the phosphorylation levels of ERK, JNK, and p38, as well as the protein levels of MCP-1, c-Jun, and c-Fos, increased. The messenger RNA expression of MCP-1, IL-1β, and IL-6 also increased in HUVECs. Pretreatment of the HUVECs with inhibitors of JNK and p38 significantly attenuated the increased expression of MCP-1, IL-1β, and IL-6, while ERK inhibitors had no obvious effect. Conclusions: Under impinging flow, MCP-1 and inflammatory factors are regulated through the JNK/c-Jun/p38/c-Fos pathway and participate in EC inflammation.
MeSH term(s)	Cells, Cultured ; Chemokine CCL2/genetics ; Chemokine CCL2/metabolism ; Extracellular Signal-Regulated MAP Kinases ; Human Umbilical Vein Endothelial Cells ; Humans ; Interleukin-6/metabolism ; JNK Mitogen-Activated Protein Kinases/metabolism ; RNA, Messenger/metabolism
Chemical Substances	Chemokine CCL2 ; Interleukin-6 ; RNA, Messenger ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2022-05-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2534351-8
ISSN	1878-8769 ; 1878-8750
ISSN (online)	1878-8769
ISSN	1878-8750
DOI	10.1016/j.wneu.2022.05.032
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1159: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: FK866 attenuates sepsis-induced acute lung injury through c-jun-N-terminal kinase (JNK)-dependent autophagy.

Zheng, Qiang / Wang, Yu-Chang / Liu, Qin-Xin / Dong, Xi-Jie / Xie, Zhen-Xing / Liu, Xing-Hua / Gao, Wei / Bai, Xiang-Jun / Li, Zhan-Fei

Life sciences

2020 Volume 250, Page(s) 117551

Abstract: Aims: Increasing evidence indicates that FK866, a specific noncompetitive nicotinamide phosphoribosyl transferase inhibitor, exhibits a protective effect on acute lung injury (ALI). Autophagy plays a pivotal role in sepsis-induced ALI. However, the ... ...

Abstract	Aims: Increasing evidence indicates that FK866, a specific noncompetitive nicotinamide phosphoribosyl transferase inhibitor, exhibits a protective effect on acute lung injury (ALI). Autophagy plays a pivotal role in sepsis-induced ALI. However, the contribution of autophagy and the underlying mechanism by which FK866-confered lung protection remains elusive. Herein, we aimed to study whether FK866 could alleviate sepsis-induced ALI via the JNK-dependent autophagy. Main methods: Male C57BL/6 mice were subjected to cecal ligation and puncture (CLP) to establish the polymicrobial sepsis mice model, and treated with FK866 (10 mg/kg) at 24, 12 and 0.5 h before the CLP procedure. The lung protective effects were measured by lung histopathology, tissue edema, vascular leakage, inflammation infiltration, autophagy-related protein expression and JNK activity. A549 cells were stimulated with LPS (1000 ng/ml) to generate the ALI cell model, and pretreated with FK866 or SP600125 for 30 min to measure the autophagy-related protein expression and JNK activity. Key findings: Our results demonstrated that FK866 reduced lung injury score, tissue edema, vascular leakage, and inflammatory infiltration, and upregulated autophagy. The protective effect of autophagy conferred by FK866 on ALI was further clarified by using 3-methyladenine (3MA) and rapamycin. Additionally, the activity of JNK was suppressed by FK866, and inhibition of JNK promoted autophagy and showed a benefit effect. Significance: Our study indicates that FK866 protects against sepsis-induced ALI by induction of JNK-dependent autophagy. This may provide new insights into the functional mechanism of NAMPT inhibition in sepsis-induced ALI.
MeSH term(s)	A549 Cells ; Acrylamides/therapeutic use ; Acute Lung Injury/complications ; Acute Lung Injury/drug therapy ; Animals ; Autophagy ; Bronchoalveolar Lavage Fluid ; Capillary Permeability ; Disease Models, Animal ; Humans ; Lung/drug effects ; MAP Kinase Kinase 4/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Piperidines/therapeutic use ; Sepsis/complications ; Sepsis/drug therapy ; Signal Transduction ; Up-Regulation
Chemical Substances	Acrylamides ; N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide ; Piperidines ; MAP Kinase Kinase 4 (EC 2.7.12.2)
Language	English
Publishing date	2020-03-13
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2020.117551
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.368: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Danggui Buxue Tang potentiates the cytotoxicity of 5-fluorouracil on colorectal adenocarcinoma cells: A signaling mediated by c-Jun N-terminal kinase.

Gong, Guowei / Zheng, Yuzhong / Ganesan, Kumar / Xiong, Qingping / Tsim, Karl Wah Keung

Phytotherapy research : PTR

2023 Volume 37, Issue 7, Page(s) 2864–2876

Abstract: ... The inhibition of proliferation induced by DBT and 5-FU was shown to be mediated by c-Jun N-terminal kinase ...

Abstract	Danggui Buxue Tang (DBT) is a well-known Chinese herbal recipe often prescribed in clinical treatment for menopausal and cardiovascular symptoms. 5-Fluorouracil (5-FU) is a chemotherapy drug that treats several cancers; however, it causes severe adverse effects and multidrug resistance. Combining natural medications can reduce the side effects of 5-FU use. Hence, we aimed to determine the role of DBT in strengthening the anticancer capabilities of 5-FU in a cultured colorectal adenocarcinoma cell line (HT-29 cell) and xenograft nude mice. HT-29 cells cultured with DBT did not exhibit cytotoxicity. However, co-administration of DBT with 5-FU significantly increased apoptosis and the expression of apoptotic markers. The inhibition of proliferation induced by DBT and 5-FU was shown to be mediated by c-Jun N-terminal kinase signaling. In addition, the potentiation effect of 5-FU and DBT was demonstrated in reducing tumor size, expressions of Ki67 and CD34 in HT-29 xenograft mice. This finding suggests that DBT can work with 5-FU as a novel chemotherapeutic strategy for treating colon cancer.
MeSH term(s)	Humans ; Mice ; Animals ; Fluorouracil/pharmacology ; JNK Mitogen-Activated Protein Kinases ; Mice, Nude ; Drugs, Chinese Herbal/pharmacology ; Colonic Neoplasms ; Adenocarcinoma/drug therapy
Chemical Substances	danggui buxue decoction ; Fluorouracil (U3P01618RT) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Drugs, Chinese Herbal
Language	English
Publishing date	2023-02-22
Publishing country	England
Document type	Journal Article
ZDB-ID	639136-9
ISSN	1099-1573 ; 0951-418X
ISSN (online)	1099-1573
ISSN	0951-418X
DOI	10.1002/ptr.7782
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.B 3092: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito