LI shows good clinical effect in treating bronchial asthma, and its mechanism might be related to the suppression of the synthesis of IL-4, thus leading to the inhibition of TH2 cell subset preponderant response and immune equilibrium regulation.
IntroductionmiRNAs play an important role in cardiovascular abnormalities such as heart failure. In the present work we evaluated the role of miR-200a in the condition of chronic heart failure and also the mechanism involved.Material and methodsIn the study 180 subjects, among whom 100 were reported for chronic heart failure and 80 as normal, were included. ELISA and qRT-PCR was done to evaluate levels of HMGB1 and miR-200a in subjects. The cardiac hemodynamics and functioning, oxidative stress and expression of mediators of inflammation were studied in rats with chronic heart failure induced after transfecting them with miR-200a or HMGB1. Luciferase activity was measured to establish any correlation between HMGB1 and miR-200a.ResultsThe chronic heart failure patients included in the study showed suppressed levels of miR-200a and elevated HMGB1 compared to normal subjects. In chronic heart failure rats, the transfection of miR-200a attenuated the cardiac function and other hemodynamic parameters. In addition, improvement in oxidative stress as well as inflammatory mediators was observed. The outcomes also confirmed that HMGB1 was the potential target of miR-200a. It was also noted that upon transfection miR-200a resulted in suppression of protein as well as mRNA levels of HMGB1 in the cardiac tissue of chronic heart failure rats. Also overexpression of HMGB1 decreased the effects of miR-200a.ConclusionsThe outcomes indicate that miR-200a exerts a protective effect on cardiac cell injury via the HMGB1 pathway.
Purpose: To investigate the inhibitory effects of caffeoylxanthiazonoside (CYT) on airway inflammation in mice and its mechanism of action.
Methods: An allergic asthma mice model was established by intraperitoneal injection and aerosol nebulization with ovalbumin (OVA). After treatment with CYT, the blood and bronchoalveolar lavage fluid (BALF) were collected from the mice. The leukocytes were classified and counted with Giemsa solution. Enzyme-linked immunosorbent assay (ELISA) was used to determine the serum levels of IgE, and IL-4, IL-5, IL-13 and IFN-γ in the BALF of mice. Lung tissues were obtained from the mice and MUC5AC protein expression was measured by western blot.
Results: CYT significantly decreased the serum level of IgE in asthmatic mice. Inflammatory cells in BALF of mice were markedly reduced (p < 0.05) by CYT treatment at varying doses (10, 20, and 40 mg/kg). Treatment with CYT also significantly suppressed the cytokines of IL-4, IL-5 and IL-13 and increased the IFN-γ in the BLAF of OVA-induced allergic asthma mice (p < 0.05). Western blot results indicate that CYT treatment significantly decreased the expression of MUC5AC protein in the lung tissues of asthmatic mice. In addition, no significant effects on the body weight of the mice were found after CYT treatment.
Conclusion: Caffeoylxanthiazonoside inhibits airway inflammation in allergic asthma mice by altering Th1/Th2 via re-balancing of related cytokines and downregulation of lung MUC5AC protein expression. Therefore, this compound can potentially be developed for the therapeutic management of inflammation in allergic asthma.
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