Abstract

Asthma is an inflammatory disease caused by an imbalance of Th1 and Th2 cells. In general, asthma is characterized by a stronger Th2 response. Most conventional asthma treatment focuses on improving airway flow or suppression of airway inflammation. To reduce the side effects of currently used asthma medicines, we have conducted studies on natural products that have no side effects. 2,3,5,4′-tetrahydroxystilbene-2-O-β-d-glucoside (TSG), the main compound of Polygonum multiflorum (PM), has various biological activities, including anti-inflammation and anti-oxidation activities. However, the effect of TSG on asthma has not been studied yet. We examined the effects of TSG on Th2 immune responses using an OVA-induced asthma animal model. OVA-sensitized mice were treated with TSG. 24 h after the last intranasal challenge, airway hyperresponsiveness (AHR) was measured or serum and bronchoalveolar lavage fluid (BALF) were harvested. We measured typical Th1 and Th2 cytokines in serum and BALF. As a result, TSG suppressed Th2 responses, as shown by the lower levels of IL-4, IL-5, total IgE, OVA-specific IgE, and OVA-specific IgG1. On the other hand, TSG increased Th1 responses, as shown by the levels of IFN-gamma. Collectively, these results confirm the potential of TSG for asthma treatment through modulation of inflammatory responses. Considering that the cytotoxic effect of PM extract is due to the cis isomer of TSG, if the effect of TSG on asthma treatment is found to be non-toxic in clinical trials, it would be more effective to use it as a purified component than PM extract as an asthma treatment agent.

Highlights

  • Asthma is an inflammatory disease caused by an allergic reaction

  • TSG inhibits the levels of total IgE, OVA-specific IgE, and OVA-specific IgG1. These results indicated that the reduction of antigen (OVA)-specific IgE and IgG1 shows a decrease in IL-4, demonstrating that TSG reduces the Th2 immune response

  • In the asthmatic mice induced by sensitization and provocation of airway inflammation with OVA, production of IL-4 and IL-5 in the bronchoalveolar lavage fluid (BALF) and inflammatory cells such as leukocytes, neutrophils, lymphocytes, monocytes, eosinophils, and basophils were increased, which enhanced airway hyperresponsiveness (AHR)

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Summary

Introduction

Asthma is an inflammatory disease caused by an allergic reaction. Symptoms include wheezing, coughing, chest tightness, and dyspnea due to airway obstruction [1]. 95% of asthmatic patients respond effectively to corticosteroids and β2-agonists, and their proper use does not adversely affect them. Despite this treatment accounting for 50% of asthma health care costs, 5–10% of patients do not respond well to this therapy [8]. 2. Results into asthmatic mice alleviates asthma symptoms by inhibiting the Th2 immune response. In order to determine the effect of TSG on the changes of inflammatory cell populations, we measu3r.e2d. Tnhde e6n0hamncge/mkegnt (oFf itgheuBreAL2F).toAtallscoel,l nwuhmibteer binlothoedOVceAllgsro(uFpigwuarsede3cAre)a,sendeutrophils (Figure 3Bb),ylyexmpopshuroecoyfteTsSG(F3i0guanred 360Cm),gm/kogn(Foicgyutrees2)(.FAiglsuor, ew3hDite),belooosdinceolplsh(Filisgu(Freig3Aur),en3eEut)r,oapnhidls basophils (Figure 3F)(Fiingutrhee3BO),VlyAmapshtohcmyteast(iFciggurroeu3pC)w, meorneosciygtensi(fiFcigaunrtely3Dh),igeohseinrotphhailns (iFnigtuhree 3cEo)n, atnrodlbgasroopuhpil.s this upregu(Fliagtuioren3Fo)finththeeiOnVflAamasmthamtaotricygcroeullppwoepreusliagtniiofincainntlythheigOheVr Athagnrionuthpe wconatsrorlegvreoruspe.dHobwyetvheer, treatment this upregulation of the inflammatory cell population in the OVA group was reversed by the with TSG. Tefhfeecetffsecotfs TofSTGSGononththee ppooppuullaatitoionnofoinf filnamflammatmoraytocerlyls cineltlhseibnlotohde. (bAlo) owdh.ite(Abl)owodhcietell,blood cell, (B(B) )nneeuuttrroophhiill,,(C(C) )lylmymphpohcyotcey, t(De,)(mDo)nmocoynteo, c(Ey)te,os(iEn)opeohisli,naonpdh(Fil),baansodp(hFil)wbearseoapnhaillyzwederbeyatnhealyzed by theHHEMEMAVAEVTE9T509.5G0r.ouGprdoautpa adraeteaxparreesseexdparsemsseeadnsa±s SmDefaonr sfiv±e mSDicefoprerfigvroeump.iac,ebp, ce,rangdrodu:pT.hea, b, c, and d:mTehaensmneoatnshsanrointgsahacorimnmg oancloemttemr aorne sleigtnteifricaarnetlsyigdnififfierceannttblyetdwiefefenrgernotubpestawt epe

Effects of TSG on the Production of Cytokines in OVA-Induced Asthmatic Mice
Effects of TSG on Histological Changes in Asthmatic Mice
Discussion
Reagents
Animals
Sensitization and Provocation of Airway Inflammation with OVA
Findings
Statistical Analysis
Conclusions

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