Anti-inflammatory effects and mechanism of the total flavonoids from Artemisia scoparia Waldst. et kit. in vitro and in vivo.
Identifieur interne : 000A24 ( Main/Merge ); précédent : 000A23; suivant : 000A25Anti-inflammatory effects and mechanism of the total flavonoids from Artemisia scoparia Waldst. et kit. in vitro and in vivo.
Auteurs : Xue Wang [République populaire de Chine] ; Hua Huang [République populaire de Chine] ; Xueping Ma [République populaire de Chine] ; Linlin Wang [République populaire de Chine] ; Chong Liu [République populaire de Chine] ; Biyu Hou [République populaire de Chine] ; Shengqian Yang [République populaire de Chine] ; Li Zhang [République populaire de Chine] ; Guanhua Du [République populaire de Chine]Source :
- Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie [ 1950-6007 ] ; 2018.
Descripteurs français
- KwdFr :
- Animaux, Anti-inflammatoires (pharmacologie), Artemisia (), Cellules RAW 264.7, Chimiokine CCL2 (métabolisme), Espèces réactives de l'oxygène (métabolisme), Facteur de nécrose tumorale alpha (métabolisme), Facteur de transcription NF-kappa B (métabolisme), Flavonoïdes (pharmacologie), Granulocytes neutrophiles (), Granulocytes neutrophiles (métabolisme), Infiltration par les neutrophiles (), Interleukine-6 (métabolisme), Lignée cellulaire, Lésion pulmonaire aigüe (métabolisme), Lésion pulmonaire aigüe (traitement médicamenteux), Macrophages (), Macrophages (métabolisme), Mitogen-Activated Protein Kinases (métabolisme), Mâle, Poumon (), Poumon (métabolisme), Scoparia (), Souris, Souris de lignée BALB C, Stress oxydatif (), Transduction du signal ().
- MESH :
- métabolisme : Chimiokine CCL2, Espèces réactives de l'oxygène, Facteur de nécrose tumorale alpha, Facteur de transcription NF-kappa B, Granulocytes neutrophiles, Interleukine-6, Lésion pulmonaire aigüe, Macrophages, Mitogen-Activated Protein Kinases, Poumon.
- pharmacologie : Anti-inflammatoires, Flavonoïdes.
- traitement médicamenteux : Lésion pulmonaire aigüe.
- Animaux, Artemisia, Cellules RAW 264.7, Granulocytes neutrophiles, Infiltration par les neutrophiles, Lignée cellulaire, Macrophages, Mâle, Poumon, Scoparia, Souris, Souris de lignée BALB C, Stress oxydatif, Transduction du signal.
English descriptors
- KwdEn :
- Acute Lung Injury (drug therapy), Acute Lung Injury (metabolism), Animals, Anti-Inflammatory Agents (pharmacology), Artemisia (chemistry), Cell Line, Chemokine CCL2 (metabolism), Flavonoids (pharmacology), Interleukin-6 (metabolism), Lung (drug effects), Lung (metabolism), Macrophages (drug effects), Macrophages (metabolism), Male, Mice, Mice, Inbred BALB C, Mitogen-Activated Protein Kinases (metabolism), NF-kappa B (metabolism), Neutrophil Infiltration (drug effects), Neutrophils (drug effects), Neutrophils (metabolism), Oxidative Stress (drug effects), RAW 264.7 Cells, Reactive Oxygen Species (metabolism), Scoparia (chemistry), Signal Transduction (drug effects), Tumor Necrosis Factor-alpha (metabolism).
- MESH :
- chemical , metabolism : Chemokine CCL2, Interleukin-6, Mitogen-Activated Protein Kinases, NF-kappa B, Reactive Oxygen Species, Tumor Necrosis Factor-alpha.
- chemical , pharmacology : Anti-Inflammatory Agents, Flavonoids.
- chemistry : Artemisia, Scoparia.
- drug effects : Lung, Macrophages, Neutrophil Infiltration, Neutrophils, Oxidative Stress, Signal Transduction.
- drug therapy : Acute Lung Injury.
- metabolism : Acute Lung Injury, Lung, Macrophages, Neutrophils.
- Animals, Cell Line, Male, Mice, Mice, Inbred BALB C, RAW 264.7 Cells.
Abstract
Artemisia scoparia Waldst. et Kit. is traditionally used for the treatment of jaundice urinary retention, itching wet sores, infectious icteric hepatitis and influenza in Uighur medicine. This study aimed to further illuminate the anti-inflammatory effects and mechanism of the total flavonoids (ASTF) from Artemisia scoparia Waldst. et Kit. In vitro, RAW 264.7 cells were pretreated with ASTF 1 h before stimulation with LPS (1 μg/mL) for 24 h. Then, the concentrations of NO, PGE2, TNF-α, IL-6 and MCP-1 in the medium were determined. Intracellular oxidative stress was detected using DCFH-DA. Immunofluorescent analysis, western blot and qRT-PCR were carried out to illuminate the mechanism of anti-inflammatory effects of ASTF. In vivo, mice were given an intragastric administration of ASTF 1 h before an intranasal administration of LPS. After 24 h, bronchoalveolar lavage fluid (BALF) was collected to measure the number of total cells, macrophage and neutrophils. The levels of TNF-α and IL-6 in BALF were quantified by ELISA kits. Lung specimens were isolated for histopathological examinations and lung wet-to-dry weight (W/D) ratio. We found that ASTF significantly inhibited the production of NO, PGE2, TNF-α, IL-6, MCP-1 and reactive oxygen species (ROS) in LPS-stimulated RAW 264.7 cells. ASTF can obviously inhibit the degredation of IκBa and inhibit the nucleus translocations of p-NF-κB p65, p-ERK1/2 and p-p38 in RAW 264.7 cells stimulated by LPS. ASTF also markedly decreased the protein and mRNA expression of TNF-α and IL-6 in a dose-dependent manner. When pretreated with ASTF, alveolar hemorrhage and neutrophil infiltration, as well as pulmonary histopathologic changes, were substantially suppressed in lung tissues in the murine acute lung injury model. The lung wet-to-dry weight (W/D) ratio was strongly decreased. These results suggested that ASTF showed important anti-inflammatory activity and might provide protective effects against LPS-induced ALI. The anti-inflammatory effect of ASTF might attribute to its suppression of NF-κB and MAPK signaling pathway.
DOI: 10.1016/j.biopha.2018.05.054
PubMed: 29787986
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acute Lung Injury (drug therapy)</term>
<term>Acute Lung Injury (metabolism)</term>
<term>Animals</term>
<term>Anti-Inflammatory Agents (pharmacology)</term>
<term>Artemisia (chemistry)</term>
<term>Cell Line</term>
<term>Chemokine CCL2 (metabolism)</term>
<term>Flavonoids (pharmacology)</term>
<term>Interleukin-6 (metabolism)</term>
<term>Lung (drug effects)</term>
<term>Lung (metabolism)</term>
<term>Macrophages (drug effects)</term>
<term>Macrophages (metabolism)</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Mitogen-Activated Protein Kinases (metabolism)</term>
<term>NF-kappa B (metabolism)</term>
<term>Neutrophil Infiltration (drug effects)</term>
<term>Neutrophils (drug effects)</term>
<term>Neutrophils (metabolism)</term>
<term>Oxidative Stress (drug effects)</term>
<term>RAW 264.7 Cells</term>
<term>Reactive Oxygen Species (metabolism)</term>
<term>Scoparia (chemistry)</term>
<term>Signal Transduction (drug effects)</term>
<term>Tumor Necrosis Factor-alpha (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Anti-inflammatoires (pharmacologie)</term>
<term>Artemisia ()</term>
<term>Cellules RAW 264.7</term>
<term>Chimiokine CCL2 (métabolisme)</term>
<term>Espèces réactives de l'oxygène (métabolisme)</term>
<term>Facteur de nécrose tumorale alpha (métabolisme)</term>
<term>Facteur de transcription NF-kappa B (métabolisme)</term>
<term>Flavonoïdes (pharmacologie)</term>
<term>Granulocytes neutrophiles ()</term>
<term>Granulocytes neutrophiles (métabolisme)</term>
<term>Infiltration par les neutrophiles ()</term>
<term>Interleukine-6 (métabolisme)</term>
<term>Lignée cellulaire</term>
<term>Lésion pulmonaire aigüe (métabolisme)</term>
<term>Lésion pulmonaire aigüe (traitement médicamenteux)</term>
<term>Macrophages ()</term>
<term>Macrophages (métabolisme)</term>
<term>Mitogen-Activated Protein Kinases (métabolisme)</term>
<term>Mâle</term>
<term>Poumon ()</term>
<term>Poumon (métabolisme)</term>
<term>Scoparia ()</term>
<term>Souris</term>
<term>Souris de lignée BALB C</term>
<term>Stress oxydatif ()</term>
<term>Transduction du signal ()</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Chemokine CCL2</term>
<term>Interleukin-6</term>
<term>Mitogen-Activated Protein Kinases</term>
<term>NF-kappa B</term>
<term>Reactive Oxygen Species</term>
<term>Tumor Necrosis Factor-alpha</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anti-Inflammatory Agents</term>
<term>Flavonoids</term>
</keywords>
<keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Artemisia</term>
<term>Scoparia</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Lung</term>
<term>Macrophages</term>
<term>Neutrophil Infiltration</term>
<term>Neutrophils</term>
<term>Oxidative Stress</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Acute Lung Injury</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Acute Lung Injury</term>
<term>Lung</term>
<term>Macrophages</term>
<term>Neutrophils</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Chimiokine CCL2</term>
<term>Espèces réactives de l'oxygène</term>
<term>Facteur de nécrose tumorale alpha</term>
<term>Facteur de transcription NF-kappa B</term>
<term>Granulocytes neutrophiles</term>
<term>Interleukine-6</term>
<term>Lésion pulmonaire aigüe</term>
<term>Macrophages</term>
<term>Mitogen-Activated Protein Kinases</term>
<term>Poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Anti-inflammatoires</term>
<term>Flavonoïdes</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Lésion pulmonaire aigüe</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Line</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>RAW 264.7 Cells</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Artemisia</term>
<term>Cellules RAW 264.7</term>
<term>Granulocytes neutrophiles</term>
<term>Infiltration par les neutrophiles</term>
<term>Lignée cellulaire</term>
<term>Macrophages</term>
<term>Mâle</term>
<term>Poumon</term>
<term>Scoparia</term>
<term>Souris</term>
<term>Souris de lignée BALB C</term>
<term>Stress oxydatif</term>
<term>Transduction du signal</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Artemisia scoparia Waldst. et Kit. is traditionally used for the treatment of jaundice urinary retention, itching wet sores, infectious icteric hepatitis and influenza in Uighur medicine. This study aimed to further illuminate the anti-inflammatory effects and mechanism of the total flavonoids (ASTF) from Artemisia scoparia Waldst. et Kit. In vitro, RAW 264.7 cells were pretreated with ASTF 1 h before stimulation with LPS (1 μg/mL) for 24 h. Then, the concentrations of NO, PGE<sub>2</sub>
, TNF-α, IL-6 and MCP-1 in the medium were determined. Intracellular oxidative stress was detected using DCFH-DA. Immunofluorescent analysis, western blot and qRT-PCR were carried out to illuminate the mechanism of anti-inflammatory effects of ASTF. In vivo, mice were given an intragastric administration of ASTF 1 h before an intranasal administration of LPS. After 24 h, bronchoalveolar lavage fluid (BALF) was collected to measure the number of total cells, macrophage and neutrophils. The levels of TNF-α and IL-6 in BALF were quantified by ELISA kits. Lung specimens were isolated for histopathological examinations and lung wet-to-dry weight (W/D) ratio. We found that ASTF significantly inhibited the production of NO, PGE<sub>2</sub>
, TNF-α, IL-6, MCP-1 and reactive oxygen species (ROS) in LPS-stimulated RAW 264.7 cells. ASTF can obviously inhibit the degredation of IκBa and inhibit the nucleus translocations of p-NF-κB p65, p-ERK1/2 and p-p38 in RAW 264.7 cells stimulated by LPS. ASTF also markedly decreased the protein and mRNA expression of TNF-α and IL-6 in a dose-dependent manner. When pretreated with ASTF, alveolar hemorrhage and neutrophil infiltration, as well as pulmonary histopathologic changes, were substantially suppressed in lung tissues in the murine acute lung injury model. The lung wet-to-dry weight (W/D) ratio was strongly decreased. These results suggested that ASTF showed important anti-inflammatory activity and might provide protective effects against LPS-induced ALI. The anti-inflammatory effect of ASTF might attribute to its suppression of NF-κB and MAPK signaling pathway.</div>
</front>
</TEI>
</record>
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