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1.
Phytomedicine ; 126: 155273, 2024 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-38342020

RESUMO

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is defined by persistent airway and lung inflammation, excessive mucus production, remodeling of the airways, and damage to the alveolar tissue. Based on clinical experience, it has been observed that Jianpiyifei II (JPYF II) granules exhibit a significant therapeutic impact on individuals suffering from stable COPD. Nevertheless, the complete understanding of JPYF II's potential mode of action against COPD remains to be further clarified. PURPOSE: To further investigate the underlying mechanism of JPYF II for treating COPD and clarify the role of the IL-17 pathway in the treatment. METHODS: A variety of databases were utilized to acquire JPYF II's bioactive components, as well as related targets of JPYF II and COPD. Cytoscape was utilized to establish multiple interaction networks for the purpose of topological analyses and core-target screening. The Metascape was utilized to identify the function of target genes and crucial signaling pathways. To evaluate the interactions between bioactive ingredients and central target proteins, molecular docking simulations were conducted. Following that, a sequence of experiments was conducted both in the laboratory and in living organisms, which included analyzing the cell counts in bronchoalveolar lavage fluid (BALF), examining lung tissue for histopathological changes, conducting immunohistochemistry, RT‒qPCR, ELISA, and Western blotting. RESULTS: In JPYF II, 88 bioactive ingredients were predicted to have a total of 342 targets. After conducting Venn analysis, it was discovered that 284 potential targets of JPYF II were linked to the provision of defensive benefits against COPD. The PPI network yielded a total of twenty-four core targets. The findings from the analysis of enrichment and gene‒pathway network suggested that JPYF II targeted Hsp90, MAPKs, ERK, AP-1, TNF-α, IL-6, COX-2, CXCL8, and MMP-9 as crucial elements for COPD treatment through the IL-17 pathway. Additionally, JPYF II might modulate MAPK signaling pathways and the downstream transcription factor AP-1 via IL-17 regulation. According to the findings from molecular docking, it was observed that the 24 core target proteins exhibited robust binding affinities towards the top 10 bioactive compounds. Furthermore, the treatment of COPD through the regulation of MAPKs in the IL-17 pathway was significantly influenced by flavonoids and sterols found in JPYF II. In vitro, these observations were further confirmed. In vivo results demonstrated that JPYF II reduced inflammatory cell infiltration in pulmonary tissues and the quantity of inflammatory cells in BALF obtained from LPS- and CS-stimulated mice. Moreover, the administration of JPYF II resulted in the inhibition of IL-17 mRNA and protein levels, phosphorylation levels of MAPK proteins, and expression of phosphorylated AP-1 proteins. It also suppressed the expression of downstream effector genes and proteins associated with the IL-17/MAPK/AP-1 signaling axis in lung tissues and BALF. CONCLUSION: This research reveals that JPYF II improves COPD by controlling the IL-17/MAPK/AP-1 signaling axis within the IL-17 pathway for the first time. These findings offer potential approaches for the creation of novel medications that specifically target IL-17 and proteins involved in the IL-17 pathway to address COPD.


Assuntos
Medicamentos de Ervas Chinesas , Doença Pulmonar Obstrutiva Crônica , Animais , Camundongos , Simulação de Acoplamento Molecular , Interleucina-17 , Farmacologia em Rede , Fator de Transcrição AP-1 , Doença Pulmonar Obstrutiva Crônica/tratamento farmacológico , Medicamentos de Ervas Chinesas/farmacologia , Medicamentos de Ervas Chinesas/uso terapêutico
2.
Front Pharmacol ; 12: 603863, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34887746

RESUMO

Aims: The occurrence of vascular permeability pulmonary edema in acute lung injury (ALI) is related to the imbalance of alveolar fluid transport. Regulating the active transport of alveolar fluid by aquaporins (AQPs), epithelial sodium channels (ENaCs), and Na+-K+-ATPase can effectively reduce the edema fluid in the alveolar cavity and protect against ALI. We evaluated the therapeutic effects of total flavonoids, extracted from Nervilia fordii (TFENF), and investigated its potential mechanisms of alveolar fluid transport in a rat ALI model. Materials and methods: A model of lipopolysaccharide (LPS, 5 mg/kg)-induced ALI was established in Sprague-Dawley (SD) rats through the arteriae dorsalis penis. SD rats were divided into six groups, including the vehicle, LPS model, TFENF (6 mg/kg, 12 mg/kg, 24 mg/kg), and dexamethasone group (DEX group, 5 mg/kg). The wet-to-dry (W/D) lung weight ratio, oxygenation index, and histopathological observation were used to evaluate the therapeutic effect of TFENF. The mRNA expression of AQPs, ENaCs, and pro-inflammatory cytokines was determined using real-time polymerase chain reaction, whereas protein expression was determined using immunohistochemistry. The Na + -K + -ATPase activity was assessed using enzyme-linked immunosorbent assay. Results: LPS significantly stimulated the production of inflammatory mediators including tumor necrosis factor (TNF)-α and interleukin (IL)-1ß, and disrupted the water transport balance in the alveolar cavity by inhibiting AQPs/ENaCs/Na + -K + -ATPase. Pretreatment with TFENF reduced the pathological damage and W/D ratio of the lungs and ameliorated the arterial blood oxygen partial pressure (PaO2) and oxygenation index. TFENF further decreased the mRNA level of TNF-α and IL-1ß; increased the expression of AQP-1, AQP-5, αENaC, and ßENaC; and increased Na + -K + -ATPase activity. Moreover, the regulation of AQPs, ßENaC, and Na + -K + -ATPase and the inhibition of TNF-α and IL-1ß by TFENF were found to be dose dependent. Conclusion: TFENF protects against LPS-induced ALI, at least in part, through the suppression of inflammatory cytokines and regulation of the active transport capacity of AQPs/ENaCs/Na + -K + -ATPase. These findings suggest the therapeutic potential of TFENF as phytomedicine to treat inflammation and pulmonary edema in ALI.

3.
Clin Sci (Lond) ; 135(14): 1733-1750, 2021 07 30.
Artigo em Inglês | MEDLINE | ID: mdl-34236078

RESUMO

Chronic obstructive pulmonary disease (COPD) is a worldwide chronic inflammatory lung disease, and influenza A virus (IAV) infection is a common cause of acute exacerbations of COPD (AECOPD). Therefore, targeting viral infections represents a promising strategy to prevent the occurrence and development of inflammatory flare ups in AECOPD. Jianpiyifei II (JPYFII) is a traditional herbal medicine used in China to treat patients with COPD, and its clinical indications are not well understood. However, investigation of the anti-inflammatory effects and underlying mechanism using an animal model of smoking have been reported in a previous study by our group. In addition, some included herbs, such as Radix astragali and Radix aupleuri, were reported to exhibit antiviral effects. Therefore, the aim of the present study was to investigate whether JPYFII formulation relieved acute inflammation by clearing the IAV in a mouse model that was exposed to cigarette smoke experimentally. JPYFII formulation treatment during smoke exposure and IAV infection significantly reduced the number of cells observed in bronchoalveolar lavage fluid (BALF), expression of proinflammatory cytokines, chemokines, superoxide production, and viral load in IAV-infected and smoke-exposed mice. However, JPYFII formulation treatment during smoke exposure alone did not reduce the number of cells in BALF or the expression of Il-6, Tnf-a, and Il-1ß. The results demonstrated that JPYFII formulation exerted an antiviral effect and reduced the exacerbation of lung inflammation in cigarette smoke (CS)-exposed mice infected with IAV. Our results suggested that JPYFII formulation could potentially be used to treat patients with AECOPD associated with IAV infection.


Assuntos
Medicina Herbária , Vírus da Influenza A/patogenicidade , Pneumonia/terapia , Doença Pulmonar Obstrutiva Crônica/terapia , Animais , Citocinas/metabolismo , Modelos Animais de Doenças , Feminino , Humanos , Influenza Humana/complicações , Pulmão/metabolismo , Camundongos Endogâmicos BALB C , Doença Pulmonar Obstrutiva Crônica/metabolismo , Fumaça/efeitos adversos , Fumar/efeitos adversos
4.
Front Pharmacol ; 11: 581, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32425799

RESUMO

Jianpiyifei II granules (JPYF II), a herbal formula, are used for the treatment of chronic obstructive pulmonary disease (COPD) in Guangdong Provincial Hospital of Chinese Medicine. The protective effects of JPYF II against bronchial epithelial cell apoptosis in mice exposed to cigarette smoke (CS) and apoptosis of human bronchial epithelial cell lines (BEAS-2B and 16-HBE) stimulated with cigarette smoke extract (CSE) were investigated. Mice were exposed to CS generated from four cigarettes/day for 30 days and administered a dose of JPYF II (0.75, 1.5, and 3 g/kg/d) from the 3rd week of CS exposure. In mice exposed to CS, JPYF II significantly inhibited CS-induced apoptosis and overexpression of endoplasmic reticulum (ER) stress-related markers in bronchial epithelial cells of the lung tissues. In CSE-stimulated BEAS-2B and 16-HBE cells, JPYF II attenuated apoptosis and cell cycle arrest in the G0/G1 phase. Mechanistically, CSE initially induced intracellular reactive oxygen species (ROS) production, which then triggered ER stress, leading to the release of Ca2+ from ER inositol trisphosphate receptor (IP3R)-mediated stores and finally cell death. Treatment with JPYF II resulted in a significant reduction in CSE-induced apoptosis through interruption of the ROS-ER stress-Ca2+ signaling pathway. Therefore, the results of this study have revealed the underlying mechanism of action of JPYF II in the treatment of COPD.

5.
J Eukaryot Microbiol ; 66(6): 869-881, 2019 11.
Artigo em Inglês | MEDLINE | ID: mdl-30977159

RESUMO

The biodiversity of peritrich ciliates from brackish biotopes is rarely investigated, especially members of the genus Pseudovorticella. Here, the morphology of three species of Pseudovorticella, i.e. P. cf. vestita (Stokes, 1883) Jankowski, 1976, P. spathulata sp. n., and P. qinghaiensis sp. n. isolated from brackish waters were studied. Pseudovorticella cf. vestita is characterized by inverted bell-shaped cell; a J-shaped macronucleus; a single contractile vacuole ventrally located; P3 three-rowed; pellicle striated with highly developed pellicular vesicles; 18-22 transverse silverlines between peristome and aboral trochal band, and 9-13 between aboral trochal band and scopula. Pseudovorticella spathulata sp. n. differs from its congeners by the following combination of characters: elongate-elliptical cell; a single contractile vacuole near ventral wall of infundibulum; a J-shaped macronucleus; P3 three-rowed; 24-34 silverlines between oral area and aboral trochal band and 6-10 between aboral trochal band and scopula. Pseudovorticella qinghaiensis sp. n. is characterized by: cell with an oval outline; a single contractile vacuole near ventral wall of infundibulum; a C-shaped macronucleus; P3 three-rowed; 30-35 and 9-11 transverse silverlines above and below the trochal band, respectively. The SSU rDNA sequences of five Pseudovorticella species, namely P. annulata, P. monilata, P. parakenti, P. spathulata sp. n., and P. cf. vestita, plus that of Zoothamnium hartwigi, are reported for the first time and their evolutionary relationships are investigated. Five undefined Pseudovorticella forms are considered might be conspecific with P. monilata. Two congeners are conspecific with P. spathulata sp. n. Phylogenetic analyses based on SSU rDNA sequences reveal that Pseudovorticella is not monophyletic and Z. hartwigi clusters with its congeners as expected.


Assuntos
Lagos/parasitologia , Oligoimenóforos/classificação , Água do Mar/parasitologia , China , Oligoimenóforos/citologia , Oligoimenóforos/genética , Filogenia , RNA de Protozoário/análise , Águas Salinas , Áreas Alagadas
6.
J Eukaryot Microbiol ; 66(2): 267-280, 2019 03.
Artigo em Inglês | MEDLINE | ID: mdl-30025176

RESUMO

Four new species of Vorticella, V. parachiangi sp. n., V. scapiformis sp. n., V. sphaeroidalis sp. n., and V. paralima sp. n., were isolated from coastal brackish waters of southern China. Their morphology, infraciliature, and silverline system were investigated based on observations of specimens both in vivo and following silver staining. Vorticella parachiangi sp. n. is distinguished by: a J-shaped macronucleus; a single dorsally located contractile vacuole; a two-rowed infundibular polykinetid 3, in which row 1 is shorter than row 2; 21-31 silverlines between peristome and aboral trochal band, 6-11 between aboral trochal band and scopula. Vorticella scapiformis sp. n. is characterized by its conspicuously thin and irregularly edged peristomial lip; a J-shaped macronucleus; a single, ventrally located contractile vacuole; row 1 of the infundibular polykinetid 3 proximally shortened; 18-25 silverlines between peristome and aboral trochal band, 8-12 between aboral trochal band and scopula. Vorticella sphaeroidalis sp. n. can be identified by its small, sub-spherical zooid; a C-shaped macronucleus; a ventrally located contractile vacuole; an aboral trochal band adjacent to the scopula; 16-18 silverlines between persitome and aboral trochal band, two between aboral trochal band and scopula. Vorticella paralima sp. n. can be identified by its ovoidal zooid; a J-shaped macronucleus; a dorsally positioned contractile vacuole; rows 1 and 2 of the infundibular polykinetid 3 proximally shortened; 26-35 silverlines from peristome to aboral trochal band, and 7-13 from aboral trochal band to scopula. The SSU rDNA genes of these four species were sequenced and their phylogeny was analyzed.


Assuntos
Oligoimenóforos/classificação , Oligoimenóforos/citologia , China , DNA de Protozoário/análise , Macronúcleo/fisiologia , Águas Salinas , Análise de Sequência de DNA , Especificidade da Espécie
7.
Artigo em Inglês | MEDLINE | ID: mdl-30174706

RESUMO

Jianpiyifei II granule (JPYF II) is an oriental herbal formula used clinically in China to treat chronic obstructive pulmonary disease (COPD). The aim of the present study was to investigate the anti-inflammatory and antioxidative activities of JPYF II in a mouse model of COPD induced by lipopolysaccharide (LPS) and cigarette smoke (CS) and in RAW264.7 cells stimulated with cigarette smoke extract (CSE). Mice were given LPS via intratracheal instillation on days 1 and 15 and exposed to CS generated from 4 cigarettes/day for 28 days. The mice were treated with 0.75, 1.5, or 3 g/kg/d JPYF II by intragastric administration in low, middle, and high dose groups, respectively, for two weeks. RAW264.7 cells were stimulated by CSE and treated with JPYF II at doses of 12.5, 25, or 50 µg/mL. In the mouse model of LPS and CS-induced COPD, JPYF II decreased inflammatory cell counts in broncho alveolar lavage fluid (BALF), in addition to mRNA expression of proinflammatory cytokines and metalloproteinases (MMPs) in lung tissues. In addition, JPYF II elevated catalase (CAT) and glutathione peroxidase (GSH-Px) activities and reduced the levels of malondialdehyde (MDA) and IκBα and p65 phosphorylation and inflammatory cell infiltration in the lung tissues. In RAW264.7 cells stimulated with CSE, JPYF II inhibited the mRNA levels of inflammatory mediators and the phosphorylation of IκBα and p65. Our results suggest that JPYF II enhanced anti-inflammatory and antioxidative activities in a mouse model of COPD induced by LPS and CS and in RAW264.7 cells stimulated with CSE via inhibition of the NF-κB pathway.

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