Fig 1: Expression of serum OVA-specific IgE and inflammatory cytokines in BALF. (A) Expression of OVA-specific IgE in serum. Expression of (B) IL-4, (C) IL-5, (D) IL-13 and (E) IFN-? in BALF. Data are expressed as the mean ± SD; n=12; *P<0.05 vs. Control; ?P<0.05 vs. PM2.5; #P<0.05 vs. OVA. OVA, ovalbumin; BALF, bronchoalveolar lavage fluid; PM2.5, 2.5 µm particulate matter; IFN-?, interferon; IL-, interleukin.
Fig 2: SIRT3 reduced apoptosis and inflammation caused by oxidative stress in 16HBE cells. (A) Western blotting was used to detected the expression of SIRT3 in 16HBE cells of each group. (B) Following stimulation with different concentrations of H2O2 for 12 h, flow cytometry was used to analyze apoptosis. (C and D) After stimulating with 100 µmol/l H2O2 for 12 h, the apoptosis of 16HBE cells before and after the knockdown or overexpression of SIRT3 was analyzed by flow cytometry. (E) The expression of cytokines (TNF-a, IL-4, IL-5 and IL-13) mRNA was detected by reverse transcription-quantitative PCR. Each experiment was repeated three times and data were shown as mean ± SD. The P-values were calculated by calculated by Student's t-test in A, C and E and by post-hoc comparisons in B. ***P<0.001 vs. NC-shRNA group; ###P<0.001 vs. NC-AAV group; and &&&P<0.001 vs. 0 µmol/l H2O2. SIRT3, sirtuin 3; sh, short hairpin; NC, negative control.
Fig 3: Upregulation of SIRT3 reduced increased inflammation of BALF in asthmatic mice. (A) The number of cells in BALF as determined by Wright's Giemsa staining. (B) The expression of cytokines (TNF-a, IL-4, IL-5 and IL-13) mRNA in cells of BALF determined by reverse transcription-quantitative PCR. (C) The secretion levels of cytokines (TNF-a, IL-4, IL-5 and IL-13) in BALF determined with ELISA assay. DEX treatment was used as the positive control. There were seven mice in each group, the data were shown as mean ± SD and the P-value was calculated by calculated by post-hoc comparisons. ns, P>0.05, *P>0.05, **P<0.01 and ***P<0.001 vs. Asthma group. SIRT3, sirtuin 3; BALF, bronchoalveolar lavage fluid; DEX, dexamethasone.
Fig 4: Histopathological analysis of the back skin tissues. Dorsal skin sections were stained with H&E (magnification, ×100). (A) Skin tissues following treatment for 1 day. (B) Skin tissues following treatment for 4 days. (C) Skin tissues following treatment for 7 days. (D) Epidermal thickness in the dorsal skin. Levels of (E) IL-4, (F) IL-5, (G) IL-13, (H) IL-1ß and (I) TNF-a in dorsal skin tissues. Data are presented as the mean ± standard deviation. *P<0.05, **P<0.001 vs. control; #P<0.05, ##P<0.001 vs. AD. AD, atopic dermatitis; AD + Q, AD group treated with quinine; C + Q, control group treated with quinine; IL, interleukin; TNF, tumor necrosis factor.
Fig 5: NF-?B and p38 MAPK inhibitors suppress inflammatory response in allergic rhinitis mice. The expression levels of (A) IL-4, (B) IL-5, (C) IL-13, (D) IL-17, (E) TNF-a, (F) IL-2 and (G) IFN-? in the serum of different groups. **P<0.01 vs. AR group. AR, allergic rhinitis.
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