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Article: The Short and Long Term Consequences of Delayed Cord Clamping on Late Pre-Term Infants.

Yan, Jie / Ren, Jian-Dong / Zhang, Jie / Li, Jun / Zhang, Xu / Ma, Yan / Gao, Li

2023 Volume 15, Page(s) 361–368

Abstract: Objective: To explore the effect of delayed cord clamping on preterm infants.: Methods: A retrospective analysis was conducted using the clinical data of 163 preterm infants with a gestational age of 34-36 weeks + 6 who were admitted to the ... ...

Abstract	Objective: To explore the effect of delayed cord clamping on preterm infants. Methods: A retrospective analysis was conducted using the clinical data of 163 preterm infants with a gestational age of 34-36 weeks + 6 who were admitted to the neonatology department within 2 hours after birth. The blood routine examination indices within 2 hours and at 3-5 days after birth, the biochemical indices and arterial blood gas (ABG) indices within 2 hours after birth, and the hemoglobin level 5-6 months after birth were compared between the early cord clamping (ECC) group and the delayed cord clamping (DCC) group. Results: Compared with the ECC group, the DCC group had significantly higher venous blood levels of red blood cells, hemoglobin, and hematocrit within 2 hours and at 3-5 days after birth. The ABG bicarbonate (HCO Conclusion: Delayed cord clamping can significantly increase the hemoglobin levels of preterm infants at birth and at 5-6 months after birth and can improve the oxygen circulation supply to the organs of such infants. Therefore, delayed cord clamping can improve the prognosis of preterm infants.
Language	English
Publishing date	2023-03-14
Publishing country	New Zealand
Document type	Journal Article
ZDB-ID	2508161-5
ISSN	1179-1411
ISSN	1179-1411
DOI	10.2147/IJWH.S385800
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Article ; Online: Nafamostat mesilate prevented caerulein-induced pancreatic injury by targeting HDAC6-mediated NLRP3 inflammasome activation.

Chen, Peng / Zhao, Li-Jun / Huang, Ling / He, Wen-Qi / Tang, Ying-Rui / Liu, Yi / Ren, Jian-Dong

Inflammation research : official journal of the European Histamine Research Society ... [et al.

2023 Volume 72, Issue 9, Page(s) 1919–1932

Abstract: Objective: Nafamostat mesilate (NM), a synthetic broad-spectrum serine protease inhibitor, has been commonly used for treating acute pancreatitis (AP) and other inflammatory-associated diseases in some East Asia countries. Although the potent inhibitory ...

Abstract	Objective: Nafamostat mesilate (NM), a synthetic broad-spectrum serine protease inhibitor, has been commonly used for treating acute pancreatitis (AP) and other inflammatory-associated diseases in some East Asia countries. Although the potent inhibitory activity against inflammation-related proteases (such as thrombin, trypsin, kallikrein, plasmin, coagulation factors, and complement factors) is generally believed to be responsible for the anti-inflammatory effects of NM, the precise target and molecular mechanism underlying its anti-inflammatory activity in AP treatment remain largely unknown. Methods: The protection of NM against pancreatic injury and inhibitory effect on the NOD-like receptor protein 3 (NLRP3) inflammasome activation were investigated in an experimental mouse model of AP. To decipher the molecular mechanism of NM, the effects of NM on nuclear factor kappa B (NF-κB) activity and NF-κB mediated NLRP3 inflammasome priming were examined in lipopolysaccharide (LPS)-primed THP-1 cells. Additionally, the potential of NM to block the activity of histone deacetylase 6 (HDAC6) and disrupt the association between HDAC6 and NLRP3 was also evaluated. Results: NM significantly suppressed NLRP3 inflammasome activation in the pancreas, leading to a reduction in pancreatic inflammation and prevention of pancreatic injury during AP. NM was found to interact with HDAC6 and effectively inhibit its function. This property allowed NM to influence HDAC6-dependent NF-κB transcriptional activity, thereby blocking NF-κB-driven transcriptional priming of the NLRP3 inflammasome. Furthermore, NM exhibited the potential to interfere the association between HDAC6 and NLRP3, impeding HDAC6-mediated intracellular transport of NLRP3 and ultimately preventing NLRP3 inflammasome activation. Conclusions: Our current work has provided valuable insight into the molecular mechanism underlying the immunomodulatory effect of NM in the treatment of AP, highlighting its promising application in the prevention of NLRP3 inflammasome-associated inflammatory pathological damage.
MeSH term(s)	Mice ; Animals ; Inflammasomes/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Pancreatitis/chemically induced ; Pancreatitis/drug therapy ; Pancreatitis/prevention & control ; NF-kappa B/metabolism ; Ceruletide/adverse effects ; NLR Proteins ; Histone Deacetylase 6/therapeutic use ; Acute Disease ; Inflammation/metabolism ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use
Chemical Substances	Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; NF-kappa B ; Ceruletide (888Y08971B) ; nafamostat (Y25LQ0H97D) ; NLR Proteins ; Histone Deacetylase 6 (EC 3.5.1.98) ; Anti-Inflammatory Agents
Language	English
Publishing date	2023-09-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1221794-3
ISSN	1420-908X ; 1023-3830
ISSN (online)	1420-908X
ISSN	1023-3830
DOI	10.1007/s00011-023-01794-0
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Article: Epigallocatechin-3-gallate attenuates acute pancreatitis induced lung injury by targeting mitochondrial reactive oxygen species triggered NLRP3 inflammasome activation

Luo, Zhu-Lin / Sun, Hong-Yu / Wu, Xiao-Bo / Cheng, Long / Ren, Jian-Dong

Food & function. 2021 June 21, v. 12, no. 12

2021

Abstract: Green tea has been considered as a health-promoting beverage and is widely consumed worldwide. Epigallocatechin-3-gallate (EGCG), the most abundant polyphenol derived from green tea leaves with potent antioxidative and chemopreventive activities, has ... ...

Abstract	Green tea has been considered as a health-promoting beverage and is widely consumed worldwide. Epigallocatechin-3-gallate (EGCG), the most abundant polyphenol derived from green tea leaves with potent antioxidative and chemopreventive activities, has been reported to offer protection against inflammation-driven tissue damage. Here, we evaluated the protective effects of EGCG against lung injury during acute pancreatitis (AP) and further revealed the detailed mechanism. The results showed that EGCG significantly attenuated l-arginine-induced AP and the consequent pulmonary damage in mice. Moreover, EGCG substantially attenuated oxidative stress and concurrently suppressed NOD-like receptor protein 3 (NLRP3) inflammasome activation in the lung. In vitro, EGCG considerably reduced the production of mitochondrial reactive oxygen species (mtROS) and oxidized mitochondrial DNA (ox-mtDNA) in alveolar macrophages (AMs) challenged with AP-conditioned plasma. Meanwhile, the amount of ox-mtDNA bound to NLRP3 decreased significantly by the treatment with EGCG, resulting in impaired NLRP3 inflammasome activation. In addition, the antagonism of NLRP3 signaling by EGCG was affected in the presence of the mtROS stimulant rotenone or scavenger Mito-TEMPO. Altogether, EGCG possesses potent activity to attenuate lung injury during AP progression by inhibiting NLRP3 inflammasome activation. As for the mechanism, the EGCG-conferred restriction of NLRP3 inflammasome activation probably arises from the elimination of mtROS as well as its oxidative product ox-mtDNA, which consequently enables the protection against AP-associated lung injury.
Keywords	antagonism ; beverages ; chemoprevention ; epigallocatechin gallate ; green tea ; health promotion ; inflammasomes ; lungs ; macrophages ; mitochondria ; mitochondrial DNA ; oxidative stress ; pancreatitis ; polyphenols ; reactive oxygen species ; rotenone
Language	English
Dates of publication	2021-0621
Size	p. 5658-5667.
Publishing place	The Royal Society of Chemistry
Document type	Article
ZDB-ID	2612033-1
ISSN	2042-650X ; 2042-6496
ISSN (online)	2042-650X
ISSN	2042-6496
DOI	10.1039/d1fo01154e
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Article ; Online: Epigallocatechin-3-gallate attenuates acute pancreatitis induced lung injury by targeting mitochondrial reactive oxygen species triggered NLRP3 inflammasome activation.

Luo, Zhu-Lin / Sun, Hong-Yu / Wu, Xiao-Bo / Cheng, Long / Ren, Jian-Dong

Food & function

2021 Volume 12, Issue 12, Page(s) 5658–5667

Abstract	Green tea has been considered as a health-promoting beverage and is widely consumed worldwide. Epigallocatechin-3-gallate (EGCG), the most abundant polyphenol derived from green tea leaves with potent antioxidative and chemopreventive activities, has been reported to offer protection against inflammation-driven tissue damage. Here, we evaluated the protective effects of EGCG against lung injury during acute pancreatitis (AP) and further revealed the detailed mechanism. The results showed that EGCG significantly attenuated l-arginine-induced AP and the consequent pulmonary damage in mice. Moreover, EGCG substantially attenuated oxidative stress and concurrently suppressed NOD-like receptor protein 3 (NLRP3) inflammasome activation in the lung. In vitro, EGCG considerably reduced the production of mitochondrial reactive oxygen species (mtROS) and oxidized mitochondrial DNA (ox-mtDNA) in alveolar macrophages (AMs) challenged with AP-conditioned plasma. Meanwhile, the amount of ox-mtDNA bound to NLRP3 decreased significantly by the treatment with EGCG, resulting in impaired NLRP3 inflammasome activation. In addition, the antagonism of NLRP3 signaling by EGCG was affected in the presence of the mtROS stimulant rotenone or scavenger Mito-TEMPO. Altogether, EGCG possesses potent activity to attenuate lung injury during AP progression by inhibiting NLRP3 inflammasome activation. As for the mechanism, the EGCG-conferred restriction of NLRP3 inflammasome activation probably arises from the elimination of mtROS as well as its oxidative product ox-mtDNA, which consequently enables the protection against AP-associated lung injury.
MeSH term(s)	Acute Lung Injury/metabolism ; Animals ; Antioxidants/pharmacology ; Catechin/analogs & derivatives ; Catechin/pharmacology ; DNA, Mitochondrial/metabolism ; Disease Models, Animal ; Inflammasomes/drug effects ; Inflammasomes/metabolism ; Inflammation/metabolism ; Lung/pathology ; Lung Injury/drug therapy ; Lung Injury/pathology ; Male ; Mice ; Mitochondria/drug effects ; NLR Family, Pyrin Domain-Containing 3 Protein/drug effects ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Pancreatitis/drug therapy ; Reactive Oxygen Species/metabolism ; Tea/chemistry
Chemical Substances	Antioxidants ; DNA, Mitochondrial ; Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nlrp3 protein, mouse ; Reactive Oxygen Species ; Tea ; Catechin (8R1V1STN48) ; epigallocatechin gallate (BQM438CTEL)
Language	English
Publishing date	2021-05-21
Publishing country	England
Document type	Journal Article
ZDB-ID	2612033-1
ISSN	2042-650X ; 2042-6496
ISSN (online)	2042-650X
ISSN	2042-6496
DOI	10.1039/d1fo01154e
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Article: Mangiferin loaded magnetic PCEC microspheres: preparation, characterization and antitumor activity studies in vitro

Xiao, WenJing / Hou, Jun / Ma, Jie / Yu, BoTao / Ren, JianDong / Jin, WeiHua / Wu, Juan / Zheng, DeZhi / Fan, KaiHua

Archives of pharmacal research. 2021 Aug., v. 44, no. 8

2021

Abstract: Mangiferin is a promising effective chemopreventive agent against various tumors. However, its clinical use is limited by poor water solubility and low bioavailability. In this article, mangiferin loaded magnetic PCEC microspheres (MG-MS) were designed, ... ...

Abstract	Mangiferin is a promising effective chemopreventive agent against various tumors. However, its clinical use is limited by poor water solubility and low bioavailability. In this article, mangiferin loaded magnetic PCEC microspheres (MG-MS) were designed, characterized and the antitumor activity of MG-MS was evaluated in vitro. The magnetic nanoparticles (MNP) were synthesized via the high-temperature reaction of iron acetylacetonate in phenyl ether in the presence of oleic acid and oleylamine. Poly (ε-caprolactone)-poly (ethyleneglycol)-poly (ε-caprolactone) (PCL-PEG-PCL, PCEC) copolymers were formed by ring-opening copolymerization of ε-CL initiated by PEG-diol using Sn(Oct)₂ as a catalyst and MG-MS were prepared by solvent diffusion method. MNP, PCEC copolymer, and MG-MS were characterized by GPC, TEM, XRD, FT-IR, ¹H-NMP and Malvern Laser Particle Sizer. Meanwhile, the antiproliferative activity in vitro and in vitro release behavior of this microspheres were studied in detail. The results indicate that the obtained magnetic microspheres might have great potential as an effective carrier for mangiferin used in cancer chemotherapy.
Keywords	antineoplastic activity ; bioavailability ; catalysts ; chemoprevention ; composite polymers ; copolymerization ; drug therapy ; magnetism ; microparticles ; oleic acid ; research ; solvents ; water solubility
Language	English
Dates of publication	2021-08
Size	p. 1-7.
Publishing place	Pharmaceutical Society of Korea
Document type	Article
ZDB-ID	447623-2
ISSN	1976-3786 ; 0253-6269
ISSN (online)	1976-3786
ISSN	0253-6269
DOI	10.1007/s12272-014-0485-3
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Article ; Online: Plasma-derived exosomes contribute to pancreatitis-associated lung injury by triggering NLRP3-dependent pyroptosis in alveolar macrophages.

Wu, Xiao-Bo / Sun, Hong-Yu / Luo, Zhu-Lin / Cheng, Long / Duan, Xing-Mei / Ren, Jian-Dong

Biochimica et biophysica acta. Molecular basis of disease

2020 Volume 1866, Issue 5, Page(s) 165685

Abstract: Progression of acute pancreatitis (AP) into a severe form usually results in a life-threatening condition with multiple organ dysfunction, and in particular acute lung injury (ALI), often contributes to the majority of AP-associated deaths. Increasing ... ...

Abstract	Progression of acute pancreatitis (AP) into a severe form usually results in a life-threatening condition with multiple organ dysfunction, and in particular acute lung injury (ALI), often contributes to the majority of AP-associated deaths. Increasing evidence has shown that uncontrolled activation of the immune system with rapid production of inflammatory cytokines play a dominant role in this process. As an intracellular inflammatory signaling platform, the NOD-like receptor protein 3 (NLRP3) inflammasome, is recently reported to be involved in the pathogenesis of AP progression, however, the relationship between NLRP3 inflammasome activation and AP-associated lung injury remains unclear yet. Here, we show that NLRP3 inflammasome activation and subsequent pyroptosis in alveolar macrophages (AMs) is responsible for the lung injury secondary to AP. In addition, plasma-derived exosomes from AP mice is capable of triggering NLRP3-dependent pyroptosis in AMs. Inhibition of exosome release or uptake in vivo by inhibitors substantially suppresses AMs pyroptosis and thereby alleviates AP-induced pulmonary lesion. Collectively, the current work reveals for the first time the involvement of NLRP3-dependent pyroptosis induced by plasma exosomes in the pathogenesis of AP-induced ALI, suggesting that the exosome-mediated NLRP3 inflammatory pathway is a potential therapeutic target for the treatment of lung injury during AP.
MeSH term(s)	Acute Lung Injury/blood ; Acute Lung Injury/immunology ; Acute Lung Injury/pathology ; Animals ; Arginine/administration & dosage ; Arginine/toxicity ; Bronchoalveolar Lavage Fluid/cytology ; Bronchoalveolar Lavage Fluid/immunology ; Disease Models, Animal ; Exosomes/immunology ; Exosomes/metabolism ; Humans ; Inflammasomes/immunology ; Macrophages, Alveolar/immunology ; Macrophages, Alveolar/pathology ; Male ; Mice ; Mice, Knockout ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Pancreatitis/blood ; Pancreatitis/chemically induced ; Pancreatitis/complications ; Pancreatitis/immunology ; Pyroptosis/immunology
Chemical Substances	Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nlrp3 protein, mouse ; Arginine (94ZLA3W45F)
Language	English
Publishing date	2020-01-15
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2020.165685
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Article: Molecular hydrogen inhibits lipopolysaccharide-triggered NLRP3 inflammasome activation in macrophages by targeting the mitochondrial reactive oxygen species.

Ren, Jian-Dong / Wu, Xiao-Bo / Jiang, Rui / Hao, Da-Peng / Liu, Yi

Biochimica et biophysica acta

2016 Volume 1863, Issue 1, Page(s) 50–55

Abstract: The NLRP3 inflammasome, an intracellular multi-protein complex controlling the maturation of cytokine interleukin-1β, plays an important role in lipopolysaccharide (LPS)-induced inflammatory cascades. Recently, the production of mitochondrial reactive ... ...

Abstract	The NLRP3 inflammasome, an intracellular multi-protein complex controlling the maturation of cytokine interleukin-1β, plays an important role in lipopolysaccharide (LPS)-induced inflammatory cascades. Recently, the production of mitochondrial reactive oxygen species (mtROS) in macrophages stimulated with LPS has been suggested to act as a trigger during the process of NLRP3 inflammasome activation that can be blocked by some mitochondria-targeted antioxidants. Known as a ROS scavenger, molecular hydrogen (H2) has been shown to possess therapeutic benefit on LPS-induced inflammatory damage in many animal experiments. Due to the unique molecular structure, H2 can easily target the mitochondria, suggesting that H2 is a potential antagonist of mtROS-dependent NLRP3 inflammasome activation. Here we have showed that, in mouse macrophages, H2 exhibited substantial inhibitory activity against LPS-initiated NLRP3 inflammasome activation by scavenging mtROS. Moreover, the elimination of mtROS by H2 resultantly inhibited mtROS-mediated NLRP3 deubiquitination, a non-transcriptional priming signal of NLRP3 in response to the stimulation of LPS. Additionally, the removal of mtROS by H2 reduced the generation of oxidized mitochondrial DNA and consequently decreased its binding to NLRP3, thereby inhibiting the NLRP3 inflammasome activation. Our findings have, for the first time, revealed the novel mechanism underlying the inhibitory effect of molecular hydrogen on LPS-caused NLRP3 inflammasome activation, highlighting the promising application of this new antioxidant in the treatment of LPS-associated inflammatory pathological damage.
MeSH term(s)	Animals ; Carrier Proteins/metabolism ; Cell Line ; Free Radical Scavengers/pharmacology ; Hydrogen/pharmacology ; Inflammasomes/metabolism ; Lipopolysaccharides/toxicity ; Macrophages/metabolism ; Mice ; Mitochondria/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein ; Reactive Oxygen Species/metabolism
Chemical Substances	Carrier Proteins ; Free Radical Scavengers ; Inflammasomes ; Lipopolysaccharides ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nlrp3 protein, mouse ; Reactive Oxygen Species ; lipopolysaccharide, Escherichia coli O111 B4 ; Hydrogen (7YNJ3PO35Z)
Language	English
Publishing date	2016-01
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbamcr.2015.10.012
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Article ; Online: The Role of Exogenous Hydrogen Sulfide in Free Fatty Acids Induced Inflammation in Macrophages.

Luo, Zhu-Lin / Ren, Jian-Dong / Huang, Zhu / Wang, Tao / Xiang, Ke / Cheng, Long / Tang, Li-Jun

Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

2017 Volume 42, Issue 4, Page(s) 1635–1644

Abstract: Background: This study aimed to investigate whether exogenous hydrogen sulfide (H2S) can protect the RAW264.7 macrophages against the inflammation induced by free fatty acids (FFA) by blunting NLRP3 inflammasome activation via a specific TLR4/NF-κB ... ...

Abstract	Background: This study aimed to investigate whether exogenous hydrogen sulfide (H2S) can protect the RAW264.7 macrophages against the inflammation induced by free fatty acids (FFA) by blunting NLRP3 inflammasome activation via a specific TLR4/NF-κB pathway. Methods: RAW264.7 macrophages were exposed to increasing concentrations of FFA for up to 3 days to induce FFA-induced inflammation. The cells were pretreated with NaHS (a donor of H2S) before exposure to FFA. Cell viability, cell apoptosis, TLR4, NF-κB, NLRP3 inflammasome, IL-1β, IL-18 and cleaved caspase-3 expression were measured by a combination of MTT assay, ELISA, and immunoblotting. Results: H2S attenuated FFA-induced cell apoptosis, and reduced the expression of NLRP3, ASC, pro-caspase-1, caspase-1, IL- 1β, IL-18 and caspase-3. In addition, H2S inhibited the FFA-induced activation of TLR4 and NF-κB. Furthermore, NLRP3 inflammasome activation was regulated by the TLR4 and NF-κB pathway. Conclusion: The present study demonstrated for the first time that H2S appears to suppress FFA-induced macrophage inflammation and apoptosis by inhibiting the TLR4/ NF-κB pathway and its downstream NLRP3 inflammasome activation. Thus H2S might possess potential in the treatment of diseases resulting from FFA overload like insulin resistance and type diabetes.
MeSH term(s)	Animals ; Anti-Inflammatory Agents, Non-Steroidal/chemistry ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Apoptosis/drug effects ; Caspase 3/genetics ; Caspase 3/immunology ; Cell Line ; Cell Survival/drug effects ; Fatty Acids, Nonesterified/antagonists & inhibitors ; Fatty Acids, Nonesterified/pharmacology ; Gene Expression Regulation ; Hydrogen Sulfide/chemistry ; Hydrogen Sulfide/pharmacology ; Inflammasomes/immunology ; Inflammasomes/metabolism ; Inflammation ; Interleukin-18/genetics ; Interleukin-18/immunology ; Interleukin-1beta/genetics ; Interleukin-1beta/immunology ; Macrophages/cytology ; Macrophages/drug effects ; Macrophages/immunology ; Mice ; NF-kappa B/antagonists & inhibitors ; NF-kappa B/genetics ; NF-kappa B/immunology ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/immunology ; Reactive Oxygen Species/antagonists & inhibitors ; Reactive Oxygen Species/metabolism ; Signal Transduction ; Sulfides/chemistry ; Sulfides/pharmacology ; Toll-Like Receptor 4/antagonists & inhibitors ; Toll-Like Receptor 4/genetics ; Toll-Like Receptor 4/immunology
Chemical Substances	Anti-Inflammatory Agents, Non-Steroidal ; Fatty Acids, Nonesterified ; IL1B protein, mouse ; Inflammasomes ; Interleukin-18 ; Interleukin-1beta ; NF-kappa B ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nlrp3 protein, mouse ; Reactive Oxygen Species ; Sulfides ; Tlr4 protein, mouse ; Toll-Like Receptor 4 ; Casp3 protein, mouse (EC 3.4.22.-) ; Caspase 3 (EC 3.4.22.-) ; sodium bisulfide (FWU2KQ177W) ; Hydrogen Sulfide (YY9FVM7NSN)
Language	English
Publishing date	2017-07-24
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1067572-3
ISSN	1421-9778 ; 1015-8987
ISSN (online)	1421-9778
ISSN	1015-8987
DOI	10.1159/000479405
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Article ; Online: Progressive balloon dilatation following hepaticojejunostomy improves outcome of bile duct stricture after iatrogenic biliary injury.

Luo, Zhu-lin / Cheng, Long / Ren, Jian-dong / Tang, Li-jun / Wang, Tao / Tian, Fu-zhou

BMC gastroenterology

2013 Volume 13, Page(s) 70

Abstract: Background: Iatrogenic biliary stricture (IBS) is a disastrous complication of cholecystectomy. Although the endoscopic treatments are well accepted as initial attempts for IBS, surgical hepaticojejunostomy (HJ) is often necessary for a considerable ... ...

Abstract	Background: Iatrogenic biliary stricture (IBS) is a disastrous complication of cholecystectomy. Although the endoscopic treatments are well accepted as initial attempts for IBS, surgical hepaticojejunostomy (HJ) is often necessary for a considerable proportion of patients. However, the anastomotic stricture after HJ also occurs. Methods: In the present study, a new procedure, progressive balloon dilation following HJ (HJPBD), was designed and utilized in the IBS treatment. We retrospectively compared HJPBD with the traditional HJ in term of the outcomes when used for IBS treatment. Results: Between January 1997 and December 2009, 112 patients with IBS attributed to cholecystectomy enrolled in our hospital were treated with surgical reconstruction with either HJ (n=58) or HJPBD (n=54). Of the 58 patients in HJ group, 48 patients (82.8%) had a successful outcome, while 52 out of 54 patients (96.3%) in HJPBD group achieved success. The successful surgical reconstruction rates were significantly different between these two groups, with a further improved outcome in patient undergone progressive balloon dilation following HJ. Additionally, 8 of the 10 failure cases in HJ group were successfully rescued by HJPBD procedure. Conclusions: Our findings suggest that the new procedure of HJPBD could be successfully applied to IBS patients, and significantly improve the outcome of IBS reconstruction.
MeSH term(s)	Adolescent ; Adult ; Aged ; Anastomosis, Surgical ; Bile Ducts/injuries ; Cholecystectomy/adverse effects ; Cholestasis/etiology ; Cholestasis/therapy ; Constriction, Pathologic/etiology ; Constriction, Pathologic/therapy ; Dilatation ; Female ; Hepatic Duct, Common/surgery ; Humans ; Jejunum/surgery ; Male ; Middle Aged ; Retrospective Studies ; Young Adult
Language	English
Publishing date	2013-04-22
Publishing country	England
Document type	Journal Article
ISSN	1471-230X
ISSN (online)	1471-230X
DOI	10.1186/1471-230X-13-70
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Article ; Online: Experimental evidence supporting the lack of primary stem cells in adult pancreatic tissue.

Gong, JiaQing / Tian, FuZhou / Ren, JianDong / Luo, GuoDe

Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.

2010 Volume 10, Issue 5, Page(s) 620–630

Abstract: Purpose: To investigate the origin and localization of pancreatic stem cells in adult pancreatic tissues and to determine the primary mechanism underlying the participation of these cells in repairing pancreatic injuries.: Methods: Sprague-Dawley ... ...

Abstract	Purpose: To investigate the origin and localization of pancreatic stem cells in adult pancreatic tissues and to determine the primary mechanism underlying the participation of these cells in repairing pancreatic injuries. Methods: Sprague-Dawley rats were divided into experimental and control groups. The experimental group was given intraperitoneal injections of cerulein to induce acute pancreatitis. At 6 h, 1, 2, 3, 5 and 7 days, 5 rats from the experimental group and 2 rats from the control group were sacrificed; all sacrificed animals were intraperitoneally injected with 5-bromo-2'-deoxyuracil nucleotides (BrdU) 6 and 3 h prior to sacrifice. The pathological changes of pancreatic tissue were observed. The stem cell marker nestin and the cell proliferation marker BrdU were detected with immunohistochemistry. Pancreatic duodenal homeobox-1 (PDX-1) was determined by real-time PCR. Results: (1) The pathological changes of acute pancreatitis can be divided into three phases: the edema and apoptosis phase, the hemorrhagic necrosis phase, and the reconstruction phase. (2) Nestin-positive cells mainly appeared in the interlobular vascular lumen after cerulein injection, and they peaked at day 3 when the positive cells spread all over the pancreatic tissues. (3) BrdU-positive cells began to appear in the area surrounding the interlobular region, and the number of positive cells peaked on day 7. (4) The expression of PDX-1 mRNA initially increased, then decreased and gradually got close to a normal level. Conclusion: Primary pancreatic stem cells may not exist in the adult pancreatic tissues. The so-called pancreatic stem cells may actually originate from bone marrow stem cells. When pancreatic tissue is injured, bone marrow stem cells may participate in the repair.
MeSH term(s)	Adult Stem Cells/metabolism ; Animals ; Bone Marrow Cells/metabolism ; Bromodeoxyuridine/metabolism ; Ceruletide ; Homeodomain Proteins/metabolism ; Intermediate Filament Proteins/metabolism ; Nerve Tissue Proteins/metabolism ; Nestin ; Pancreas/cytology ; Pancreas/pathology ; Pancreatitis/chemically induced ; Pancreatitis/pathology ; Rats ; Rats, Sprague-Dawley ; Stem Cells/metabolism ; Trans-Activators/metabolism
Chemical Substances	Homeodomain Proteins ; Intermediate Filament Proteins ; Nerve Tissue Proteins ; Nes protein, rat ; Nestin ; Trans-Activators ; pancreatic and duodenal homeobox 1 protein ; Ceruletide (888Y08971B) ; Bromodeoxyuridine (G34N38R2N1)
Language	English
Publishing date	2010
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2056680-3
ISSN	1424-3911 ; 1424-3903
ISSN (online)	1424-3911
ISSN	1424-3903
DOI	10.1159/000321586
Database	MEDical Literature Analysis and Retrieval System OnLINE

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