RESUMO
Chronic obstructive pulmonary disease (COPD), as a common respiratory disease characterized by progressive development, not only has the incidence increased year by year, but also has a high disability and mortality rate, which brings serious economic burden to patients. Immune response plays an important role in the pathogenesis of COPD. Studies have shown that COPD is closely related to the disorder of autoimmune function, and traditional Chinese medicine (TCM) interferes with the disease process of COPD by mediating immune response. This paper mainly contains four kinds of research contents of TCM intervention on COPD immune response, namely T lymphocyte subsets count, immunoglobulin count, Th17/Treg dynamic balance, Th1/Th2 dynamic balance and related signaling pathways. In order to provide new reference and ideas for experimental research, a brief review is made at the end of this paper.
RESUMO
Chronic obstructive pulmonary disease (COPD) is a common respiratory disease with a high morbidity, disability and mortality. At the same time, COPD is always accompanied by pulmonary hypertension, pulmonary fibrosis, chronic pulmonary heart disease, right heart failure and other common serious complications. All of these cause serious financial burden for the family of patients. Airway remodeling plays an important role in the pathogenesis of COPD. It is the progressive development of airflow restriction that induces the main symptoms of COPD, such as cough, asthma and depression. Therefore, it is of great research value to explore the intervention of traditional Chinese medicine(TCM) in the development of COPD by alleviating airway remodeling. Studies have shown that multiple signaling pathways can induce progressive airway remodeling, and the therapeutic effect of TCM has been frequently confirmed by experimental studies. TCM often has a therapeutic effect on COPD through multi-target and multi-channel mediation. This paper mainly includes five signaling pathways that traditional Chinese medicine can intervene COPD airway remodeling, namely matrix metalloproteinases (MMPs)/tissue inhibitors of metalloproteinase (TIMPs), transforming growth factor (TGF)-beta 1/Smads, RhoA/Rho-associated kinase (ROCK), vascular endothelial growth factor (VEGF)/b-fibroblast growth factor (b-FGF) and nuclear factor (NF)-κB. This paper briefly reviews the research progress of these five signaling pathways, and discusses other signaling pathways that may be involved, in order to provide reference and ideas for future experimental research.
RESUMO
Objective: To observe the effect of modified Erchentang on GATA-binding protein-3(GATA3) and T-box expressed in T cells(T-bet) in lung tissue of rats with chronic obstructive pulmonary disease (COPD). Method: Seventy SD rats were randomly divided into seven groups, namely normal group, model group, low, medium and high-dose modified Erchentang group(5,10,20 g ·kg-1), Xiaokechuan group(5 g ·kg-1) and Erchentang group(5 g ·kg-1), with 10 in each group. The rat model of COPD was established by smoking combined with intratracheal dripping of lipopolysaccharide (LPS). After successful modeling, the treatment group was given intragastric administration, and the normal group and the model group were given intragastric administration of equal volume of saline. Enzyme-linked immunosorbent assay (ELISA) was used to determine the concentrations of interleukin-10 (IL-10) and interleukin-12 (IL-12) in rat serum. The expressions of GATA3 and T-bet were detected by real-time fluorescence quantitative polymerase chain reaction (Real-time PCR). The expressions of GATA3 and T-bet in lung tissue were detected by immunohistochemistry (IHC). Result: Compared with the control group, the serum levels of IL-10 in the model group was significantly decreased, while the IL-12 level was significantly increased (PPPPConclusion: Modified Erchentang may reduce the inflammation of lung tissue and improve lung function in COPD rats by reducing IL-12, increasing the content of IL-10, inhibiting the protein and gene expressions of T-bet, and stimulating the protein and gene expressions of GATA3.
RESUMO
Objective: To explore the effect of modified Erchentang on peroxisome proliferator-activated receptor gamma (PPARγ) protein and gene expressions in lung tissue of chronic obstructive pulmonary disease (COPD) rat model, and the expressions of interleukin-6 (IL-6), interleukin-10 (IL-10) and tumor necrosis factor-alpha (TNF-α) in serum, lung homogenate and bronchoalveolar lavage fluid. Method: Seventy SD rats were randomly divided into seven groups:normal group, model group, high, medium and low-dose modified Erchentang groups (40, 20, 10 g · kg-1 · d-1), Xiaokechuan group (5 g · kg-1 · d-1), and Erchentang group (5 g · kg-1 · d-1). The rat COPD model was established through smoking and intratracheal instillation of lipopolysaccharide (LPS). After successful modeling, the treatment group was given drug by gavage, while the normal group and the model group were given the same amount of saline. The concentrations of IL-6, IL-10 and TNF-α in serum, lung homogenate and bronchoalveolar lavage fluid(BALF) of rats were measured by enzyme-linked immunosorbent assay (ELISA). Real-time fluorescence quantitative PCR (Real-time PCR) was used to detect the expression of peroxisome proliferator-activated receptor gamma (PPARγ), and immunohistochemistry (IHC) and Western blot were used to detect the expression of PPARγ in lung tissue. Result: Compared with the normal group, the levels of IL-6 and TNF-α in serum, lung homogenate and BALF of the model group rats increased significantly (PPγ mRNA in lung tissue of rats in model group were significantly decreased (Pγ protein was significantly inhibited(Pα in serum, lung homogenate and BALF of each treatment group decreased to varying degrees(Pα in the middle-dose Erchentang group were particularly significant. The PPARγ mRNA and protein expressions in lung tissue of rats in each treatment group were increased to varying degrees (PConclusion: Modified Erchentang may improve pulmonary inflammation and pulmonary function in COPD rats by increasing the expression of PPARγ and the content of IL-10 and decreasing the contents of IL-6 and TNF-α.
RESUMO
Objective: To explore the effect of modified Erchentang on the signal pathway of β2 adrenergicreceptor(β2AR)/arrestin beta 2(β-arrestin2) in rats with chronic obstructive pulmonary disease (COPD), and the expression of interleukin-17(IL-17) in serum, lung homogenate and bronchoalveolar lavage fluid. Method: Seventy SD rats were randomly divided into seven groups:normal group, model group, modified Erchentang with high, medium and low doses (40, 20, 10 g · kg-1 · d-1), Xiaokechuan group (5 g · kg-1 · d-1), modified Erchentang group (5 g · kg-1 · d-1), 10 rats in each group. The rat model of COPD was established by smoking and lipopolysaccharide (LPS) intratracheal drip. After successful modeling, the treatment group was given intragastric administration, while the normal group and the model group were given the same amount of saline. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of IL-17 in serum, lung homogenate and bronchoalveolar lavage fluid of rats. Real-time fluorescence quantitative PCR (Real-time PCR) was used to detect the expression of β2AR gene. Western blot was used to detect the expression of β2AR protein in lung tissue. The expression of β2AR and β-arrestin2 in lung tissue was detected by immunohistochemistry. Result: Compared with the normal group, the expression of β2AR protein in lung tissue of model group was significantly decreased(Pβ2AR protein in lung tissue was significantly increased(PPβ2AR in model group was significantly lower(Pβ2AR in high, medium and low dose group, Xiaokechuan group and modified Erchentang group was significantly higher(PPPPConclusion: Modified Erchentang may increase the expression of β2AR and β-arrestin2 and decrease the content of IL-17 in order to resist inflammation and improve pulmonary function in COPD rats.
RESUMO
Objective: To observe the effects of Erchen on vascular endothelial growth factor (VEGF) and its receptor R2 (VEGFR2), interleukin (IL)-4 and endothelin-1 (ET-1) in rats with chronic obstructive pulmonary disease (COPD). Method: The 50 SD rats were randomly divided into 5 groups, 10 rats in each group, which were normal group, model group, Erchentang low, medium and high dose group (10, 20, 40 g · kg-1 · d-1). COPD rat model was established by smoking combined with lipopolysaccharide (LPS) intratracheal drip. After successful modeling, the treatment group was given intragastric administration, and the normal group and the model group were given intragastric distilled water of equal volume. The pathological changes of pulmonary vessels in rats were observed by light microscopy, and the thickness of pulmonary vascular wall was measured. The concentration of IL-4 in rat serum, bronchoalveolar lavage fluid (BALF) and lung homogenate was measured by enzyme-linked immunosorbent assay (ELISA). Real-time fluorescence quantitative polymerase chain reaction (Real-time PCR) was used to detect the expression of ET-1 and immunohistochemistry was used to detect the expression of VEGF,VEGFR2 and ET-1 in lung tissue. Result: Compared with normal group, the concentration of IL-4 in serum, BALF and lung homogenate of model group rats decreased significantly (PPPPPPConclusion: Modified Erchentang can alleviate the process of pulmonary inflammation and pulmonary vascular remodeling in COPD rats, and slow down the progress of COPD and its complications by increasing the content of IL-4, inhibiting the expression of VEGF, VEGFR2, ET-1.