Journal: Molecular Biomedicine

Article Title: Deleting fibroblast growth factor 2 in macrophages aggravates septic acute lung injury by increasing M1 polarization and inflammatory cytokine secretion

doi: 10.1186/s43556-024-00203-0

Figure Lengend Snippet: Effect of FGF2 deficiency on BMDM apoptosis and polarization. a – c FGF2 deletion increased BMDM apoptosis. a Apoptosis in BMDM deprived of FBS for 24 h was assessed by flow cytometry ( n = 4). b - c Percentage of PI + Annexin V + and PI- Annexin V + BMDM after starvation. d - k FGF2 deletion in BMDM promoted M1 polarization. d - g Flow cytometric analysis of macrophage markers in BMDM treated with LPS or IL4, including CD86, iNOS, CD206, and Arg1 ( n = 3). h - k The levels of CD86, iNOS, CD206 and Arg1 in BMDM after treatment with LPS or IL4. N represents no treatment; * p < 0.05, vs. WT; Ψ p < 0.05, vs. N + WT; Ω p < 0.05, vs. N + FGF2 KO

Article Snippet: The tissue sections were incubated overnight at 4°C with primary antibodies, including the rabbit polyclonal antibody CD206 (1:200, Cat No. A02285-2, Boster, Wuhan, China), rabbit monoclonal antibody CD86 (1:100, Cat No. BM4121, Boster, Wuhan, China), rabbit polyclonal antibody F4/80 (1:100, Cat No. 29414-1-AP, Proteintech, Wuhan, China), anti-mouse NLRP3 (1:200, Cat No.68102-1-Ig, Proteintech, Wuhan, China), Caspase-1 p20 Rabbit pAb (1:400, Cat No.bs-10743R, Bioss, Beijing, China) and ASC/TMS1 Rabbit PolyAb (1:200, Cat No.10500-1-AP, Proteintech, Wuhan, China).

Techniques: Flow Cytometry

Journal: Molecular Biomedicine

Article Title: Deleting fibroblast growth factor 2 in macrophages aggravates septic acute lung injury by increasing M1 polarization and inflammatory cytokine secretion

doi: 10.1186/s43556-024-00203-0

Figure Lengend Snippet: Mice reconstituted with FGF2 KO macrophages and subjected to CLP demonstrate increased M1 polarization in lung tissue. a - f The presence and levels of CD206, CD86, and F4/80 markers on macrophages within lung tissue were identified and quantitatively assessed using immunofluorescence staining. Bar is 20 μm. * p < 0.05, vs. WT; Δ p < 0.05 vs. WT + LPS; # p < 0.05 vs. FGF2 KO

Article Snippet: The tissue sections were incubated overnight at 4°C with primary antibodies, including the rabbit polyclonal antibody CD206 (1:200, Cat No. A02285-2, Boster, Wuhan, China), rabbit monoclonal antibody CD86 (1:100, Cat No. BM4121, Boster, Wuhan, China), rabbit polyclonal antibody F4/80 (1:100, Cat No. 29414-1-AP, Proteintech, Wuhan, China), anti-mouse NLRP3 (1:200, Cat No.68102-1-Ig, Proteintech, Wuhan, China), Caspase-1 p20 Rabbit pAb (1:400, Cat No.bs-10743R, Bioss, Beijing, China) and ASC/TMS1 Rabbit PolyAb (1:200, Cat No.10500-1-AP, Proteintech, Wuhan, China).

Techniques: Immunofluorescence, Staining

Journal: Iranian Journal of Basic Medical Sciences

Article Title: Sanguinarine, identified as a natural alkaloid LSD1 inhibitor, suppresses lung cancer cell growth and migration

doi: 10.22038/IJBMS.2022.62541.13851

Figure Lengend Snippet: Sanguinarine increased cellular levels of H3K4me2 and H3K9me2 and up-regulated the expression of CD86 in NSCLC cell lines. (A) and (B) Expression of H3K4me2 and H3K9me2 in H1975 and H1299 cells treated with sanguinarine for 48 hr, respectively, with H3 as loading control; (C) and (D) The expression of CD86 was detected, GADPH was used as a loading control. Data are the mean ± SEM of three independent experiments. * P <0.05, ** P <0.01, *** P <0.005

Article Snippet: Antibodies used were against GAPDH (GOOD HERE, AB-P-R 001), H3 (HUABIO, EM30605), H3K4me2 (HUABIO, R1110-3), H3K9me2 (HUABIO, ET1611-51), CD86 (BOSTER, BM4121), E-Cadherin (HUABIO, ET1607-75), N-Cadherin (HUABIO, ET1607-37), Bax (HUABIO, ER0907), Bcl-2 (HUABIO, ER1082-97).

Techniques: Expressing, Control

Journal: Iranian Journal of Basic Medical Sciences

Article Title: Sanguinarine, identified as a natural alkaloid LSD1 inhibitor, suppresses lung cancer cell growth and migration

doi: 10.22038/IJBMS.2022.62541.13851

Figure Lengend Snippet: Sanguinarine increased cellular levels of H3K4me2 and H3K9me2 and up-regulated the expression of CD86 in NSCLC cell lines. (A) and (B) Expression of H3K4me2 and H3K9me2 in H1975 and H1299 cells treated with sanguinarine for 48 hr, respectively, with H3 as loading control; (C) and (D) The expression of CD86 was detected, GADPH was used as a loading control. Data are the mean ± SEM of three independent experiments. * P <0.05, ** P <0.01, *** P <0.005

Article Snippet: Antibodies used were against GAPDH (GOOD HERE, AB-P-R 001), H3 (HUABIO, EM30605), H3K4me2 (HUABIO, R1110-3), H3K9me2 (HUABIO, ET1611-51), CD86 (BOSTER, BM4121), E-Cadherin (HUABIO, ET1607-75), N-Cadherin (HUABIO, ET1607-37), Bax (HUABIO, ER0907), Bcl-2 (HUABIO, ER1082-97).

Techniques: Expressing, Control

Journal: Frontiers in Immunology

Article Title: Effect and mechanism of chlorogenic acid on cognitive dysfunction in mice by lipopolysaccharide-induced neuroinflammation

doi: 10.3389/fimmu.2023.1178188

Figure Lengend Snippet: Chlorogenic acid downregulated the expression of core targets in the TNF signaling pathway. BV-2 cells were exposed to LPS (1 μg·ml -1 ) for 24 h with or without CGA pretreatment for 24 h. (A–G) Western blotting analysis of the protein expression of p-Akt1, Akt1, p-NF-κB, NF-κB, p-p38, p38, p-ERK1/2, ERK1/2, PTGS2, and TNF-α. **P < 0.01, ***P < 0.001 vs. the control group, #P < 0.05, ##P < 0.01 vs. the LPS group.(n=5).

Article Snippet: Anti-CD86 (1:1000, BM4121), anti-Arg-1 (1:1000, M01106-4), anti-IL-10 (1:1000, RP1015), anti-CD206 (1:1000, A02285-2), anti-CXCL12 (1:1000, BA1389), anti-CXCR4 (1:1000, A00031-4), anti-PTGS2 (1:1000, A00084), and anti-TNF (1:1000, BA0131) were purchased from Boster Biological Technology Co. Ltd. (Shanghai, China).

Techniques: Expressing, Western Blot

Journal: Iranian Journal of Basic Medical Sciences

Article Title: Sanguinarine, identified as a natural alkaloid LSD1 inhibitor, suppresses lung cancer cell growth and migration

doi: 10.22038/IJBMS.2022.62541.13851

Figure Lengend Snippet: Effects of sanguinarine on cell migration, invasion in H1975 and H1299 cells. (A) and (B) Wound healing assay of H1975 and H1299 treated with different concentrations of sanguinarine for 36 hours; (C) and (D) Inhibition of H1975 and H1299 migration by sanguinarine; (E) and (F) Sanguinarine reverses the expression of E-Cadherin and N-Cadherin in NSCLC cell line H1975 and H1299, respectively. *( P < 0.05), **( P < 0.01) vs control. All experiments were carried out at least three times

Article Snippet: Antibodies used were against GAPDH (GOOD HERE, AB-P-R 001), H3 (HUABIO, EM30605), H3K4me2 (HUABIO, R1110-3), H3K9me2 (HUABIO, ET1611-51), CD86 (BOSTER, BM4121), E-Cadherin (HUABIO, ET1607-75), N-Cadherin (HUABIO, ET1607-37), Bax (HUABIO, ER0907), Bcl-2 (HUABIO, ER1082-97).

Techniques: Migration, Wound Healing Assay, Inhibition, Expressing, Control