Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

Article Title: Bifidobacterium infantis Relieves Allergic Asthma in Mice by Regulating Th1/Th2

doi: 10.12659/MSM.920583

Figure Lengend Snippet: The summary results inflammation cytokines level by ELISA.

Article Snippet: Total IgE and OVA-specific IgE in the serum of each group of mice were measured using a Mouse IgE ELISA Kit (CSB-E07983m, Cusabio, China) and a Mouse OVA sIgE ELISA Kit (CSB-E08914m, Cusabio, China).

Techniques: Enzyme-linked Immunosorbent Assay, Control

Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

Article Title: Bifidobacterium infantis Relieves Allergic Asthma in Mice by Regulating Th1/Th2

doi: 10.12659/MSM.920583

Figure Lengend Snippet: B. infantis reduced the expression of IgE in the serum of allergic asthma mice. ( A ) ELISA was used to measure the total IgE content (ng/ml) in the serum of mice. ( B ) ELISA was used to detect the content of OVA-specific IgE (ng/ml) in the serum of mice. All experiments were repeated in triplicate to average (n=10). ## p <0.001 vs. control; ** p <0.001 vs. OVA.

Article Snippet: Total IgE and OVA-specific IgE in the serum of each group of mice were measured using a Mouse IgE ELISA Kit (CSB-E07983m, Cusabio, China) and a Mouse OVA sIgE ELISA Kit (CSB-E08914m, Cusabio, China).

Techniques: Expressing, Enzyme-linked Immunosorbent Assay, Control

Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

Article Title: Bifidobacterium infantis Relieves Allergic Asthma in Mice by Regulating Th1/Th2

doi: 10.12659/MSM.920583

Figure Lengend Snippet: B. infantis regulated the balance of Th1/Th2-related cytokines in BALF and lung tissues. ( A–E ) ELISA was used to detect the contents of IFN-γ, IL-2, IL-4, IL-5, and IL-13 in BALF. ( F–J ) QRT-PCR was used to detect the expression of IFN-γ, IL-2, IL-4, IL-5, and IL-13 in lung tissues. β-actin served as a reference gene. All experiments were repeated in triplicate to average (n=10). # p <0.05, ## p <0.001 vs. control; * p <0.05, ** p <0.001 vs. OVA.

Article Snippet: Total IgE and OVA-specific IgE in the serum of each group of mice were measured using a Mouse IgE ELISA Kit (CSB-E07983m, Cusabio, China) and a Mouse OVA sIgE ELISA Kit (CSB-E08914m, Cusabio, China).

Techniques: Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR, Expressing, Control

Journal: Bioactive Materials

Article Title: A new osteogenic protein isolated from Dioscorea opposita Thunb accelerates bone defect healing through the mTOR signaling axis

doi: 10.1016/j.bioactmat.2023.04.018

Figure Lengend Snippet: HKUOT-S2-induced osteoblast activity enhanced bone defect repairs. A-D) Relative expression of osteogenic markers, Alp, Bglap1, Bglap1, and Runx2 expressions in the bone defect sites of the sham control and HKUOT-S2 treatment groups. E-H) ELISA analysis of BALP and OCN proteins levels in both serum and bone lysates from the bone defect site of the sham control and HKUOT-S2 treatment groups. I–K) Representative immunofluorescent and measurement of ALP, OCN, and RUNX2 expression at the bone defect sites of the sham control and HKUOT-S2 treatment groups. The values were shown as mean ± SEM. X, 2X, and 4X = 1.09 mg/kg, 2.18 mg/kg, and 4.36 mg/kg HKUOT-S2 treatments respectively. *p < 0.05, **p < 0.01.

Article Snippet: The HKUOT-S2-induced ALP and OCN levels in the bone defect sites were evaluated by mouse BALP (CUSABIO) and mouse osteocalcin (Novus Biological) ELISA kits according to the manufacturer's instructions.

Techniques: Activity Assay, Expressing, Control, Enzyme-linked Immunosorbent Assay

Journal: Life Metabolism

Article Title: Blockade of Arf1-mediated lipid metabolism in cancers promotes tumor infiltration of cytotoxic T cells via the LPE-PPARγ-NF-κB-CCL5 pathway

doi: 10.1093/lifemeta/load036

Figure Lengend Snippet: The Arf1 inhibitors promote T-cell infiltration by upregulating CCL5 chemokine. (a) Chord diagram of gene correlation in the Arf1-ablated MYC-ON liver tumors ( n = 4 in each group). (b) qRT-PCR for chemokines in CT26 cells treated with DMSO, DU101, or DU102. (c) Serum CCL5 levels in the CT26 allografts with the indicated treatments ( n = 6 in each group). (d) CCL5 mRNA levels in the liver tumors of MYC-ON mice that were treated with DMSO, DU101, or DU102 ( n = 9 in each group). (e) Experimental design for the co-culture system. (f) FACS analysis of the migration of CD3 + T cells in CT26 cells that were treated with DMSO, DU101, or DU102. (g) The mRNA levels of CCL5 in CT26 cells with the indicated knockdowns and treatments. (h) FACS analysis of CD3 + T-cell migration in CT26 cells with the indicated knockdowns and treatments. (i and j) Tumor volumes (i) and tumor weights (j) of CT26 allografts with the indicated knockdowns and treatments ( n = 10 in each group). (k) Percentages of infiltrated CD3 + T cells in CT26 allografts with the indicated knockdowns and treatments ( n = 3 in each group). Data are shown as mean ± SEM. Student’s t test. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. n.s., no significance.

Article Snippet: The level of chemokine CCL5 in cultured medium and mouse serum was detected by Mouse RANTES ELISA Kit (BOSTER, Cat# EK0495) according to the manufacturer’s instructions.

Techniques: Quantitative RT-PCR, Co-Culture Assay, Migration

Journal: Life Metabolism

Article Title: Blockade of Arf1-mediated lipid metabolism in cancers promotes tumor infiltration of cytotoxic T cells via the LPE-PPARγ-NF-κB-CCL5 pathway

doi: 10.1093/lifemeta/load036

Figure Lengend Snippet: The Arf1 inhibitors activate the PPARγ pathway by inducing unsaturated fatty acid (LPE). (a) Heatmap of different lipid fractions in the Arf1-deficient CT26 cells. (b) The mRNA levels of downstream genes of PPARγ were detected in CT26 cells treated with different concentrations of LPE (0, 100, 200, 250, and 300 μmol/L for 24 h) by qRT-PCR. (c and d) The mRNA levels of PPARγ in CT26 cells (c) and MYC-ON liver tumors (d) treated with DMSO or Arf1 inhibitors were detected by qRT-PCR. (e) The CCL5 mRNA levels in CT26 cells treated with different concentrations of LPE were detected by qRT-PCR. (f) The CCL5 mRNA levels in CT26 cells with vesicle or GW9662 treatment were detected by qRT-PCR. (g) The CCL5 levels in cell medium collected from CT26 cells with the indicated treatments were determined by ELISA. (h) The percentages of the infiltrated CD3 + T cells in CT26 cells with the indicated treatments. Data are shown as mean ± SEM. Student’s t test. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. n.s., no significance.

Article Snippet: The level of chemokine CCL5 in cultured medium and mouse serum was detected by Mouse RANTES ELISA Kit (BOSTER, Cat# EK0495) according to the manufacturer’s instructions.

Techniques: Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay

Journal: Life Metabolism

Article Title: Blockade of Arf1-mediated lipid metabolism in cancers promotes tumor infiltration of cytotoxic T cells via the LPE-PPARγ-NF-κB-CCL5 pathway

doi: 10.1093/lifemeta/load036

Figure Lengend Snippet: The Arf1 inhibitors promote T-cell tumor infiltration by activating the NF-κB-CCL5 pathway. (a) The phosphorylated p65 in CT26 cells treated with vesicle, DU101, or DU102 was detected by western blot analysis. (b) The phosphorylated p65 in MYC-ON liver tumors after DMSO, DU101, or DU102 treatment was detected by IHC staining. The right was the statistical analysis of p-p65 + cells per field. (c) The relative CCL5 enrichment in CT26 cells with the indicated treatments was analyzed by ChIP-PCR assay. (d) The CCL5 mRNA levels in CT26 cells with the indicated treatments were detected by qRT-PCR. (e) The CCL5 levels in the cell medium collected from CT26 cells with the indicated treatments were detected by the mouse CCL5 ELISA kit. (f) FACS analysis of the infiltrated CD3 + T cells in CT26 cells with the indicated treatments. (g and h) The proportions of the infiltrated CD3 + T cells (g) and CD3 + CCR5 + T (h) cells in Hepa1-6 cells with the indicated treatments were detected by FACS analysis. Data are shown as mean ± SEM. Student’s t test. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. n.s., no significance.

Article Snippet: The level of chemokine CCL5 in cultured medium and mouse serum was detected by Mouse RANTES ELISA Kit (BOSTER, Cat# EK0495) according to the manufacturer’s instructions.

Techniques: Western Blot, Immunohistochemistry, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay

Journal: Atmosphere

Article Title: Combined Effects of Particulate Matter Exposure and Exercise Training on Neuroplasticity-Related Growth Factors and Blood–Brain Barrier Integrity

doi: 10.3390/atmos16020220

Figure Lengend Snippet: Figure 4. Changes in serum biomarkers related to BBB integrity following PM exposure and exercise training interventions. Values are expressed as the mean ± SD. (A) S100β, S100 calcium-binding protein β; (B) NSE, neuron-specific enolase; CON, control group; PM, particulate matter exposure group; EX, exercise training group; PMEX, particulate matter exposure with exercise training group. * Versus CON and EX (p < 0.05); # versus PM and PMEX (p < 0.05).

Article Snippet: The serum levels of MDA (Catalog No. MBS741034, MyBioSource, San Diego, CA, USA), SOD (Catalog No. MBS034842, MyBioSource, San Diego, CA, USA), IL-6 (Catalog No. DY406, R&D Systems, Minneapolis, MN, USA), TNF-α (Catalog No. DY410, R&D Systems, Minneapolis, MN, USA), IGF-1 (Catalog No. MG100, R&D Systems, Minneapolis, MN, USA), BDNF (Catalog No. DY248, R&D Systems, Minneapolis, MN, USA), VEGF (Catalog No. MMV00, R&D Systems, Minneapolis, MN, USA), S100β (Catalog No. CSB-EL020643MO, CUSABIO, Wuhan, China), and NSE (#CSB-E07962m, CUSABIO, Wuhan, China) were measured using enzyme-linked immunosorbent assay (ELISA) kits according to the manufacturers’ instructions.

Techniques: Binding Assay, Control

Journal: Oxidative Medicine and Cellular Longevity

Article Title: HO-1 Is Essential for Tetrahydroxystilbene Glucoside Mediated Mitochondrial Biogenesis and Anti-Inflammation Process in LPS-Treated RAW264.7 Macrophages

doi: 10.1155/2017/1818575

Figure Lengend Snippet: TSG reduced RAW264.7 cells activation and proinflammatory cytokines release induced by LPS. RAW264.7 cells were exposed to various concentrations of TSG (0–480 μ M) for 6 hours. (a) Cell viability was analyzed by WST assay. (b) Annexin V-PI method was used to detect the cell death rate. (c-d) RAW264.7 cells were exposed to 1 μ g/mL LPS for 12 hours with or without TSG (120 μ M) pretreatment for 6 hours. Then, the morphological change was captured under a microscope. Bar = 50 μ m (×30). The percentage of activated cells in total cell population was calculated. (e-f) In the presence and absence of TSG (0, 30, 60, and 120 μ M) or Dex (100 μ M) for 6 hours, RAW264.7 macrophages were stimulated with 1 μ g/mL LPS for 12 hours. The concentration of TNF- α and IL-6 production in the culture medium were assessed by specific ELISA kits. All data were expressed as the means ± SEM of three independent experiments. ∗ P < 0.05 and ∗∗∗ P < 0.001 versus control; # P < 0.05 versus LPS treatment group.

Article Snippet: Mouse specific ELISA kit for IL-6 and TNF- α level was purchased from CUSABIO Biotechnology Corp. (Wuhan, China).

Techniques: Activation Assay, WST Assay, Microscopy, Concentration Assay, Enzyme-linked Immunosorbent Assay, Control