Fig 1.
Suppression of airway hyper-responsiveness after administration of LRE in HDM-induced mouse model of asthma.
(A) Airway resistance was measured by whole body plethysmography. Data are expressed as mean ± SD (n = 5). *p<0.05 is significantly different from HDM group.
Fig 2.
Effects of different doses of LRE (125, 250, 500 mg/kg) on serum IgE levels.
Data are expressed as means ± SD (n = 5/group). # p < 0.05 indicates significance difference from the normal group. * p < 0.05 indicates significant difference from OVA control group.
Fig 3.
Effects of different doses of LRE (125, 250, 500 mg/kg) on Th2 cytokines level in BALF.
Data are expressed as means ± SD (n = 5 per group). # p < 0.05 indicates significance difference from the normal group. * p < 0.05 indicates significant difference from OVA control group.
Fig 4.
Effects of different doses of LRE (125, 250, 500 mg/kg) on airway inflammation in the peribronchiole region and perivascular connective tissue in OVA-induced allergic asthma model (H&E staining, original magnification 50×).
Representative photomicrographs showing (A) Normal; (B) OVA control group; (C) LRE 125 mg/kg; (D) LRE 250 mg/kg; (F) LRE 500 mg/kg (F) Graphs represent inflammation score. Black arrows indicate the presence of infiltration with eosinophils or leukocytes surrounding the bronchiole.
Fig 5.
Attenuation of mucus production and goblet cell hyperplasia following administration of LRE in OVA-induced rat model of asthma.
(A) Representative photomicrographs showing periodic acid–Schiff (PAS) staining (magnification ×40) staining for measuring mucus production in the airways. The black arrows indicate the presence of stained goblet cells. (B) Quantitative analysis of scoring on mucus production was done by scoring with a subjective scale of 0–4. Data was expressed as mean ± SD (n = 5 per group). # p < 0.05 indicates significance difference from the normal group. * p < 0.05 indicates significant difference from OVA control group.
Fig 6.
The effects of LRE on the CD4+ population of BALF cells in OVA-induced rat model of asthma.
Representative dot plot showing (A) unstained (B) CD4+ cells. Data was expressed as mean ± SD (n = 5 per group). # p < 0.05 indicates significance difference from the normal group. *p < 0.05 indicates significant difference from OVA control group.
Fig 7.
The effects of LRE on the CD4+CD25+Foxp3+ Treg population in BALF of OVA-induced rat model of asthma.
Representative dot plot showing (A) unstained, (B) CD4+ cells, (C) CD4+CD25+ cells and (D) CD4+CD25+Foxp3+ Treg cells. Data was expressed as mean ± SD (n = 5 per group). # p < 0.05 indicates significance difference from the normal group. * p < 0.05 indicates significant difference from OVA control group.
Fig 8.
The effects of LRE on eosinophils and neutrophils population in BALF of OVA-induced rat model of asthma.
Representative dot plot showing (A) unstained and (B) RP-1+ HIS48+ positive cells. BALF was stained with specific antibodies for CD3 FITC (T-cells), HIS48 FITC stained to detect (C) eosinophils population and RP-1, PE stained to detect (D) neutrophils population. Data was expressed as mean ± SD (n = 5 per group). # p < 0.05 indicates significance difference from the normal group. * p < 0.05 indicates significance different from OVA control group.
Fig 9.
Scatter plots of asthma genes expression of the lungs tissue in OVA-induced rat model of asthma following (A) OVA sensitization and (B) OVA sensitization + LRE. Fold-change values of less than one indicates a down-regulation and that the fold-regulation is the negative inverse of the fold-change.
Table 1.
Up-regulation of genes following OVA induction in rats.
Table 2.
Up and down-regulation of genes following LRE administration in OVA-induced asthma in rats.