Objective. To systematically review the efficacy and safety of Ligustrazine in the treatment of idiopathic pulmonary fibrosis (IPF). Methods. The electronic literature databases (PubMed, EMbase, CNKI, WanFang database, and VIP) were retrieved through a computer to find out the randomized controlled trials (RCT) of Ligustrazine in the treatment of IPF according to the inclusion/exclusion criteria screening test. Cochrane’s bias risk table was also used to evaluate the quality of the study and to extract effective data. RevMan 5.3 was used for statistical analysis. Results. A total of 7 RCTs (a total of 366 patients, including 196 in experimental and 170 in control group). Compared with the control group, Ligustrazine could improve the clinical symptoms ([OR] = 2.20, 95% CI [1.40, 3.46], P = 0.0006 ), lung function (VC % [MD] = 3.92, 95% CI [0.68, 7.17], P = 0.02 ), (TLC% [MD] = 4.94, 95% CI [0.37, 9.52], P = 0.03 ), the pulmonary diffusion function (DLCO % [MD] = 9.12, 95% CI [5.70, 12.55], P < 0.00001 ), and arterial blood gas analysis (PaO2 [MD] = 7.11, 95% CI [1.96, 12.25], P = 0.007 ) (PaCO2 [MD] = −2.42, 95% CI [−4.36, −0.49], P = 0.01 ) of IPF patients, respectively. However, FEV1/FVC % ([MD] = 9.37, 95% CI [−1.23, 19.97], P = 0.08 ) and adverse reactions ([MD] = 0.35, 95% CI [0.02, 5.36], P = 0.45 ) were not significantly improved. Conclusion. Ligustrazine has certain clinical efficacy in the treatment of IPF, but the safety of applying it and the adverse reactions need to be further analyzed and determined. It can be considered as a new alternative and complementary medicine to be promoted and recommended for use in medical units in various countries in the world and it solved the difficult problem of conventional drug treatment of IPF; therefore, more research strength can be put in the treatment of the pathological mechanism of IPF for further exploration. The study was registered under registration number CRD42020193626.
Bufei decoction (BFD) has been applied to treat chronic obstructive pulmonary disease (COPD) for centuries as a recognized traditional Chinese herbal formula. However, mechanisms of BFD on COPD are unclear. This study conducts an inquiry into the underlying mechanisms of the therapeutic effect of BFD on COPD. A COPD rat model with qi deficiency in lungs was established through induction using cigarette and sawdust smoking combined with intratracheal instillation of lipopolysaccharide following BFD treatment for 28 days. Changes in Th17/Treg cells of COPD rats with the syndrome of lung qi deficiency after BFD administration were verified using pulmonary function, ELISA, flow cytometry, histopathology, and Western blotting assays. The findings showed that BFD protected COPD rats from decreased lung function and lung injury. BFD administration reduced proinflammatory cytokines IL-6 and IL-17 secretion, promoted inhibitory cytokines IL-10 and TGF-β secretion, decreased Th17/Treg cell ratio, markedly downregulated the Th17 cell transcription factor ROR-γt expression, and upregulated transcription factor Foxp3 expression in Treg cells. We speculate that lung tonic soup improved pulmonary qi deficiency in rats with COPD by regulating the balance of Th17/Treg cells.
Objective. The purpose of the present study was to explore the mechanism of Astragalus membranaceus in the treatment of sepsis. Methods. We searched the active components and targets of Astragalus membranaceus using the TCMSP and BATMAN databases. Then, the GeneCards, MalaCards, and OMIM databases were used to screen out relevant targets of sepsis. The common targets of the former two gene sets were uploaded to the STRING database to create an interaction network. DAVID was used to perform KEGG enrichment analysis of the core targets. Based on the results of KEGG and previous studies, key pathways for the development of sepsis were identified and experimentally validated. Result. We obtained 3,370 sepsis-related targets in databases and 59 active components in Astragalus membranaceus through data mining, corresponding to 1,130 targets. The intersection of the two types of targets led to a total of 318 common targets and 84 core targets were obtained after screening again. The KEGG and previous studies showed that these 84 core targets were involved in sepsis by regulating TNF, MAPK, and PI3K pathways. TNF, MAPK8, NF-κB, and IκBα are crucial in sepsis. Experimental validation demonstrated that some markers in sepsis model rats were improved after the intervention with Astragalus granules and their chemical components. Among them, IL-1β, IL-6, and TNF-α in rat serum were reduced. The mRNA and protein expression of TNF-α, IL-6, MMP9, MAPK8, and NF-κB were reduced in rat blood. However, the mRNA and protein expression of IκBα and PI3K were increased in rat blood. Conclusion. The AST could affect the TNF, PI3K, and MAPK pathway cascade responses centred on IκBα and NF-κB, attenuate the expression of IL-6 and MMP9, and interfere with the inflammatory response during sepsis.
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