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

Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

Article Title: Gu-Ben-Fang-Xiao decoction modulates lipid metabolism by activating the AMPK pathway in asthma remission.

doi: 10.1016/j.biopha.2021.111403

Figure Lengend Snippet: Fig. 2. (a) Lungs were stained with H&E (×200) to analyse inflammatory cell infiltration. (b) Histopathological inflammation score. Inflammatory responses in airways, blood vessels, and interstitial spaces. (c,d) GBFXD regulated TNF-α and periostin levels in the lung, as determined by ELISA. Results are presented as means ± SD (n = 3), and statistical significance was determined by one-way ANOVA with Dunnett’s multiple comparison post hoc tests implemented in GraphPad Prism; #p < 0.05 compared with the control group, and *p < 0.05 compared with the model group.

Article Snippet: An ELISA kit for TNF-α was obtained from Multisciences (catalogue number: EK282/3-96; Hangzhou, China) and an ELISA for periostin from BOSTER (catalogue number: EK1187; Pleasanton, CA, USA).

Techniques: Staining, Enzyme-linked Immunosorbent Assay, Comparison, Control

Journal: Genes & diseases

Article Title: Vitamin D-binding protein in plasma microglia-derived extracellular vesicles as a potential biomarker for major depressive disorder.

doi: 10.1016/j.gendis.2023.02.049

Figure Lengend Snippet: Figure 2 Concentration and diagnostic performance of VDBP in plasma BCDEVs from MDD patients and HCs. (A) VDBP protein level in plasma MDEVs, NDEVs, and ADEVs from MDD and HCs in the discovery cohort, as measured by ELISA. (B) Diagnostic accuracy of VDBP in plasma BCDEVs of MDD in the discovery cohort, as calculated by the AUC of the ROC curve. Pearson correlation analysis showed the relationships between the VDBP level in plasma MDEVs (C), NDEVs (D), or ADEVs (E) and HAMD-24 scores in MDD patients of the discovery cohort. (F) VDBP level in plasma MDEVs from MDD patients was confirmed in the validation cohort. (G) Diagnostic accuracy of VDBP in plasma BCDEVs of MDD in the validation cohort. Pearson correlation analysis showed the relationships between VDBP level in plasma MDEVs (H), NDEVs (I), or ADEVs (J) and HAMD-24 scores in MDD patients of the validation cohort. HAMD-24: Hamilton Depression Rating Scale-24 item. ***P < 0.001, n. s.: Z not significant. Results are presented as mean SEM.

Article Snippet: The VDBP level in the exosome preparation from each brain cell type was normalized to the total protein (measured by the BCA assay) as previously reported.28 VDBP was measured using a commercial ELISA kit (human and rhesus macaque samples: EH2937, Fine Biotech, China; mouse samples: EK2063, BOSTER, China) in accordance with the manufacturer’s protocol.

Techniques: Concentration Assay, Diagnostic Assay, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Biomarker Discovery

Journal: Genes & diseases

Article Title: Vitamin D-binding protein in plasma microglia-derived extracellular vesicles as a potential biomarker for major depressive disorder.

doi: 10.1016/j.gendis.2023.02.049

Figure Lengend Snippet: Figure 3 Characterization and VDBP evaluation of plasma MDEVs from chronic glucocorticoid-induced depressed rhesus macaque model. (A) Sucrose preference test (SPT) and (B) accumulated behavior scores of chronic glucocorticoid and saline-treated rhesus macaque. Isolated plasma MDEVs from rhesus macaque were characterized by TEM (C) and NTA (D). The red arrow indicates MDEVs in a representative TEM image. (E) Western blot showing the presence of the exosome marker ALIX and VDBP in isolated rhesus macaque plasma MDEVs. VDBP concentrations in plasma MDEVs (F) and cerebrospinal fluid (CSF) (G) of rhesus macaque at baseline were measured by ELISA. VDBP concentrations in plasma MDEVs (H) and CSF (I) of rhesus macaque after saline or chronic gluco- corticoid treatment were measured by ELISA. (J) Pearson correlation analysis showing the relationships between VDBP in plasma MDEVs and CSF of rhesus macaque after treatment with saline or chronic glucocorticoid. *P < 0.05, n. s. Z not significant. Results are presented as mean SEM.

Article Snippet: The VDBP level in the exosome preparation from each brain cell type was normalized to the total protein (measured by the BCA assay) as previously reported.28 VDBP was measured using a commercial ELISA kit (human and rhesus macaque samples: EH2937, Fine Biotech, China; mouse samples: EK2063, BOSTER, China) in accordance with the manufacturer’s protocol.

Techniques: Clinical Proteomics, Saline, Isolation, Western Blot, Marker, Enzyme-linked Immunosorbent Assay

Journal: Genes & diseases

Article Title: Vitamin D-binding protein in plasma microglia-derived extracellular vesicles as a potential biomarker for major depressive disorder.

doi: 10.1016/j.gendis.2023.02.049

Figure Lengend Snippet: Figure 4 VDBP level in plasma MDEVs and microglia in PrL of LPS-induced depressed mice. (A) Schematic diagram of the experimental procedure for LPS-induced depressed mouse model. (B) Body weight loss in LPS-induced depressed mice. Sucrose preference test (C), tail suspension test (D), and forced swimming test (E) of mice treated with saline (Control) or LPS. Isolation and characterization of plasma MDEVs by TEM (F), NTA (G) of LPS-induced depressed mice. The red arrow points to the plasma MDEV successfully isolated. (H) Western blotting showing the enriched VDBP and exosome marker ALIX in isolated mice plasma MDEVs. (I) VDBP in plasma MDEVs from LPS-induced depressed mice as measured by ELISA. (J) Immunofluorescence images showing the microglial VDBP level (green) in the PrL of LPS-induced depressed mice. The nucleus was stained with DAPI (blue). Microglia were labeled with Iba-1 antibody (red). (K) Colocalization of VDBP in Iba-1þ cells was calculated. (L) Pearson correlation analysis showing the relationships between VBBP in plasma MDEVs and PrL microglia. *P < 0.05, **P < 0.01, ***P < 0.001. Results are presented as mean SEM.

Article Snippet: The VDBP level in the exosome preparation from each brain cell type was normalized to the total protein (measured by the BCA assay) as previously reported.28 VDBP was measured using a commercial ELISA kit (human and rhesus macaque samples: EH2937, Fine Biotech, China; mouse samples: EK2063, BOSTER, China) in accordance with the manufacturer’s protocol.

Techniques: Clinical Proteomics, Suspension, Saline, Control, Isolation, Western Blot, Marker, Enzyme-linked Immunosorbent Assay, Staining, Labeling

Journal: Cells

Article Title: Anti-Inflammatory Effects of C1q/Tumor Necrosis Factor-Related Protein 3 (CTRP3) in Endothelial Cells

doi: 10.3390/cells10082146

Figure Lengend Snippet: Tissue expression of Ctrp3. Ctrp3 (C1q/TNF-related protein 3) mRNA levels in different murine tissues and organs were determined by Real-time PCR and CTRP3 serum level by ELISA. n = 4–6 mice.

Article Snippet: Supernatant from MyEnd cells and murine blood serum was analyzed for TNF-α, sVCAM-1, and sICAM-1 applying mouse-specific ELISA kits from R&D Systems (Minneapolis, MN, USA) and CTRP3 was quantified in murine blood serum applying a mouse-specific ELISA kit (LSBio, Seattle, WA, USA).

Techniques: Expressing, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

Journal: Cells

Article Title: Anti-Inflammatory Effects of C1q/Tumor Necrosis Factor-Related Protein 3 (CTRP3) in Endothelial Cells

doi: 10.3390/cells10082146

Figure Lengend Snippet: Characterization of recombinant CTRP3. ( A ) Indicated quantities of recombinant CTRP3 (C1q/TNF-related protein 3) were run on SDS-PAGE (left) and 1000 ng CTRP3 for a longer gel run (right). Gels were subsequently stained with Coomassie. M = protein size marker. ( B ) THP-1 monocyte-like cells were stimulated with LPS (10 ng/mL) alone or pretreated with CTRP3 (10 µg/mL, for 30 min) and with CTRP3 alone for 18 h. CCL2 (C-C motif chemokine ligand 2) and IL-6 (interleukin-6) protein levels in the cell supernatant were analyzed by ELISA ** p < 0.01 vs. con = unstimulated control, # p < 0.05 vs. LPS, n = 5–6.

Article Snippet: Supernatant from MyEnd cells and murine blood serum was analyzed for TNF-α, sVCAM-1, and sICAM-1 applying mouse-specific ELISA kits from R&D Systems (Minneapolis, MN, USA) and CTRP3 was quantified in murine blood serum applying a mouse-specific ELISA kit (LSBio, Seattle, WA, USA).

Techniques: Recombinant, SDS Page, Staining, Marker, Enzyme-linked Immunosorbent Assay

Journal: Cells

Article Title: Anti-Inflammatory Effects of C1q/Tumor Necrosis Factor-Related Protein 3 (CTRP3) in Endothelial Cells

doi: 10.3390/cells10082146

Figure Lengend Snippet: LPS-induced endothelial adhesion molecule expression is inhibited by CTRP3. ( A ) MyEnd (myocardial endothelial) cells were stimulated with LPS (lipopolysaccharides, 50 ng/mL) for the indicated period. Vcam-1 (vascular cell adhesion molecule-1) and Icam-1 (intercellular adhesion molecule-1) mRNA levels were analyzed by real-time PCR. * p < 0.05, ** p < 0.01 vs. con = unstimulated control, n = 5–6. ( B ) MyEnd cells were stimulated with LPS (50 ng/mL) alone or pretreated with CTRP3 (C1q/TNF-related protein 3, 10 µg/mL, pre-incubation for 30 min) and with CTRP3 alone for 3 h; Vcam-1 and Icam-1 mRNA levels were analyzed by real-time PCR. * p < 0.05, ** p < 0.01 vs. con = unstimulated control, # p < 0.05, ## p < 0.01 vs. LPS, n = 4–6. ( C ) MyEnd cells were stimulated with LPS (50 ng/mL) alone or pretreated with CTRP3 (10 µg/mL, for 30 min) and with CTRP3 alone for 3 h. The sVCAM-1 (soluble vascular cell adhesion molecule-1) and sICAM-1 (soluble intercellular adhesion molecule-1) protein levels in the cell supernatant were analyzed by ELISA. * p < 0.05 vs. con = unstimulated control, # p < 0.05 vs. LPS, n = 3–5.

Article Snippet: Supernatant from MyEnd cells and murine blood serum was analyzed for TNF-α, sVCAM-1, and sICAM-1 applying mouse-specific ELISA kits from R&D Systems (Minneapolis, MN, USA) and CTRP3 was quantified in murine blood serum applying a mouse-specific ELISA kit (LSBio, Seattle, WA, USA).

Techniques: Expressing, Real-time Polymerase Chain Reaction, Incubation, Enzyme-linked Immunosorbent Assay

Journal: Cells

Article Title: Anti-Inflammatory Effects of C1q/Tumor Necrosis Factor-Related Protein 3 (CTRP3) in Endothelial Cells

doi: 10.3390/cells10082146

Figure Lengend Snippet: LPS-induced systemic markers of endothelial inflammation are not affected by CTRP3 in vivo. Male C57BL/6J wild-type mice were treated with i.p. injection of recombinant CTRP3 (C1q/TNF-related protein 3, 10 µg/animal) 30 min prior to i.p. LPS-injection (lipopolysaccharides, 1 µg/animal) for 2 h. LPS and CTRP3 alone were used as controls. ( A ) TNF-α (tumor necrosis factor-α), ( B ) sICAM-1 (soluble intercellular adhesion molecule-1) and ( C ) sVCAM-1 (soluble vascular cell adhesion molecule-1) protein levels in blood serum were quantified by ELISA. * p < 0.05 con = unstimulated control, n = 3–9.

Article Snippet: Supernatant from MyEnd cells and murine blood serum was analyzed for TNF-α, sVCAM-1, and sICAM-1 applying mouse-specific ELISA kits from R&D Systems (Minneapolis, MN, USA) and CTRP3 was quantified in murine blood serum applying a mouse-specific ELISA kit (LSBio, Seattle, WA, USA).

Techniques: In Vivo, Injection, Recombinant, Enzyme-linked Immunosorbent Assay