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Figure 2. mRNA expression levels of <t>VEGF</t> and MMP‑13 in the knee articular cartilage of mice among the Sham, Dmm and Dmm+Th groups (n=4 in each group). (A) Relative mRNA expression levels of VEGF in the medial articular cartilage. (B) Relative mRNA expression levels of MMP‑13 in the medial articular cartilage. The values are presented as the mean ± standard deviation. *P<0.05 compared with the Sham group; #P<0.05 compared with the Dmm group. Dmm, destabilization of the medial meniscus; MMP‑13, matrix metalloproteinase‑13; Th, thalidomide; VEGF, vascular endothelial growth factor.
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Figure 2. mRNA expression levels of <t>VEGF</t> and MMP‑13 in the knee articular cartilage of mice among the Sham, Dmm and Dmm+Th groups (n=4 in each group). (A) Relative mRNA expression levels of VEGF in the medial articular cartilage. (B) Relative mRNA expression levels of MMP‑13 in the medial articular cartilage. The values are presented as the mean ± standard deviation. *P<0.05 compared with the Sham group; #P<0.05 compared with the Dmm group. Dmm, destabilization of the medial meniscus; MMP‑13, matrix metalloproteinase‑13; Th, thalidomide; VEGF, vascular endothelial growth factor.
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Figure 2. mRNA expression levels of <t>VEGF</t> and MMP‑13 in the knee articular cartilage of mice among the Sham, Dmm and Dmm+Th groups (n=4 in each group). (A) Relative mRNA expression levels of VEGF in the medial articular cartilage. (B) Relative mRNA expression levels of MMP‑13 in the medial articular cartilage. The values are presented as the mean ± standard deviation. *P<0.05 compared with the Sham group; #P<0.05 compared with the Dmm group. Dmm, destabilization of the medial meniscus; MMP‑13, matrix metalloproteinase‑13; Th, thalidomide; VEGF, vascular endothelial growth factor.
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Figure 2. mRNA expression levels of <t>VEGF</t> and MMP‑13 in the knee articular cartilage of mice among the Sham, Dmm and Dmm+Th groups (n=4 in each group). (A) Relative mRNA expression levels of VEGF in the medial articular cartilage. (B) Relative mRNA expression levels of MMP‑13 in the medial articular cartilage. The values are presented as the mean ± standard deviation. *P<0.05 compared with the Sham group; #P<0.05 compared with the Dmm group. Dmm, destabilization of the medial meniscus; MMP‑13, matrix metalloproteinase‑13; Th, thalidomide; VEGF, vascular endothelial growth factor.
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Figure 2. mRNA expression levels of <t>VEGF</t> and MMP‑13 in the knee articular cartilage of mice among the Sham, Dmm and Dmm+Th groups (n=4 in each group). (A) Relative mRNA expression levels of VEGF in the medial articular cartilage. (B) Relative mRNA expression levels of MMP‑13 in the medial articular cartilage. The values are presented as the mean ± standard deviation. *P<0.05 compared with the Sham group; #P<0.05 compared with the Dmm group. Dmm, destabilization of the medial meniscus; MMP‑13, matrix metalloproteinase‑13; Th, thalidomide; VEGF, vascular endothelial growth factor.
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Figure 2. mRNA expression levels of <t>VEGF</t> and MMP‑13 in the knee articular cartilage of mice among the Sham, Dmm and Dmm+Th groups (n=4 in each group). (A) Relative mRNA expression levels of VEGF in the medial articular cartilage. (B) Relative mRNA expression levels of MMP‑13 in the medial articular cartilage. The values are presented as the mean ± standard deviation. *P<0.05 compared with the Sham group; #P<0.05 compared with the Dmm group. Dmm, destabilization of the medial meniscus; MMP‑13, matrix metalloproteinase‑13; Th, thalidomide; VEGF, vascular endothelial growth factor.
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Figure 2. mRNA expression levels of <t>VEGF</t> and MMP‑13 in the knee articular cartilage of mice among the Sham, Dmm and Dmm+Th groups (n=4 in each group). (A) Relative mRNA expression levels of VEGF in the medial articular cartilage. (B) Relative mRNA expression levels of MMP‑13 in the medial articular cartilage. The values are presented as the mean ± standard deviation. *P<0.05 compared with the Sham group; #P<0.05 compared with the Dmm group. Dmm, destabilization of the medial meniscus; MMP‑13, matrix metalloproteinase‑13; Th, thalidomide; VEGF, vascular endothelial growth factor.
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<t>VEGFC</t> and VEGFR2 protein levels in conditioned media of stable cell lines indicated <t>by</t> <t>ELISA.</t> (A) VEGFC; (B) VEGFR2. VEGF, vascular endothelial growth factor; ELISA, enzyme-linked immunosorbent assay.
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<t>VEGFC</t> and VEGFR2 protein levels in conditioned media of stable cell lines indicated <t>by</t> <t>ELISA.</t> (A) VEGFC; (B) VEGFR2. VEGF, vascular endothelial growth factor; ELISA, enzyme-linked immunosorbent assay.
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<t>VEGFC</t> and VEGFR2 protein levels in conditioned media of stable cell lines indicated <t>by</t> <t>ELISA.</t> (A) VEGFC; (B) VEGFR2. VEGF, vascular endothelial growth factor; ELISA, enzyme-linked immunosorbent assay.
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TGF-α (A, B) and VEGF-B (C, D) levels as well as AHR agonistic activity (G, H) in serum samples of patients with RRMS in remission (n = 98), SPMS (n = 44), PPMS (n = 36), and their respective controls (A, C, E, G: n = 43; B, D, F, H: n = 16) were assessed. TGF-α and VEGF-B levels were measured in pg/mL using a human TGF-α or VEGF-B <t>ELISA.</t> TGF-α/VEGF-B ratio (E, F) was determined by dividing TGF-α levels by VEGF-B levels. An AHR ligand–sensitive luciferase assay was used. Relative activity was calculated by dividing firefly luciferase activity (pGud-Luc) by Renilla luciferase activity (pTK-Renilla). Values are means of duplicate measurements. Lines represent median and interquartile range. Significance levels were derived using nonparametric tests (Mann-Whitney test and Kruskal-Wallis test with the Dunn multiple comparison test correcting for multiple comparisons). **** p < 0.0001, *** p < 0.001, ** p < 0.001, * p < 0.01, and ns = nonsignificant. AHR = aryl hydrocarbon receptor; MS = multiple sclerosis; PPMS = primary progressive MS; RRMS = relapsing-remitting MS; SPMS = secondary progressive MS; TGF-α = transforming growth factor alpha; VEGF-B = vascular endothelial growth factor B.
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Image Search Results


Figure 2. mRNA expression levels of VEGF and MMP‑13 in the knee articular cartilage of mice among the Sham, Dmm and Dmm+Th groups (n=4 in each group). (A) Relative mRNA expression levels of VEGF in the medial articular cartilage. (B) Relative mRNA expression levels of MMP‑13 in the medial articular cartilage. The values are presented as the mean ± standard deviation. *P<0.05 compared with the Sham group; #P<0.05 compared with the Dmm group. Dmm, destabilization of the medial meniscus; MMP‑13, matrix metalloproteinase‑13; Th, thalidomide; VEGF, vascular endothelial growth factor.

Journal: Molecular medicine reports

Article Title: Intraperitoneal injection of thalidomide alleviates early osteoarthritis development by suppressing vascular endothelial growth factor expression in mice.

doi: 10.3892/mmr.2018.8980

Figure Lengend Snippet: Figure 2. mRNA expression levels of VEGF and MMP‑13 in the knee articular cartilage of mice among the Sham, Dmm and Dmm+Th groups (n=4 in each group). (A) Relative mRNA expression levels of VEGF in the medial articular cartilage. (B) Relative mRNA expression levels of MMP‑13 in the medial articular cartilage. The values are presented as the mean ± standard deviation. *P<0.05 compared with the Sham group; #P<0.05 compared with the Dmm group. Dmm, destabilization of the medial meniscus; MMP‑13, matrix metalloproteinase‑13; Th, thalidomide; VEGF, vascular endothelial growth factor.

Article Snippet: An ELISA kit of VEGF (E-EL-M1292c) was purchased from Elabscience Biotechnology Co., Ltd., Wuhan, China.

Techniques: Expressing, Standard Deviation

Figure 3. Immunohistochemical analysis of VEGF expression in the knee articular cartilage of mice among the Sham, Dmm and Dmm+Th groups (n=4 in each group). (A) Immunohistochemistry staining of VEGF in the articular cartilage of the medial tibial plateau (magnification, x400, scale bar=100 µm). (B) Quantification of VEGF positive cells, based on the results of immunohistochemistry staining. The values are presented as the mean ± standard deviation. *P<0.05 compared with the Sham group; #P<0.05 compared with the Dmm group. Dmm, destabilization of the medial meniscus; Th, thalidomide; VEGF, vascular endothelial growth factor.

Journal: Molecular medicine reports

Article Title: Intraperitoneal injection of thalidomide alleviates early osteoarthritis development by suppressing vascular endothelial growth factor expression in mice.

doi: 10.3892/mmr.2018.8980

Figure Lengend Snippet: Figure 3. Immunohistochemical analysis of VEGF expression in the knee articular cartilage of mice among the Sham, Dmm and Dmm+Th groups (n=4 in each group). (A) Immunohistochemistry staining of VEGF in the articular cartilage of the medial tibial plateau (magnification, x400, scale bar=100 µm). (B) Quantification of VEGF positive cells, based on the results of immunohistochemistry staining. The values are presented as the mean ± standard deviation. *P<0.05 compared with the Sham group; #P<0.05 compared with the Dmm group. Dmm, destabilization of the medial meniscus; Th, thalidomide; VEGF, vascular endothelial growth factor.

Article Snippet: An ELISA kit of VEGF (E-EL-M1292c) was purchased from Elabscience Biotechnology Co., Ltd., Wuhan, China.

Techniques: Immunohistochemical staining, Expressing, Immunohistochemistry, Staining, Standard Deviation

Figure 5. ELISA analysis of serum VEGF concentration of mice among the Sham, Dmm and Dmm+Th groups (n=8 in each group). The values are presented as the mean ± standard deviation. *P<0.05 compared with the Sham group; #P<0.05 compared with the Dmm group. Dmm, destabilization of the medial meniscus; Th, thalidomide; VEGF, vascular endothelial growth factor.

Journal: Molecular medicine reports

Article Title: Intraperitoneal injection of thalidomide alleviates early osteoarthritis development by suppressing vascular endothelial growth factor expression in mice.

doi: 10.3892/mmr.2018.8980

Figure Lengend Snippet: Figure 5. ELISA analysis of serum VEGF concentration of mice among the Sham, Dmm and Dmm+Th groups (n=8 in each group). The values are presented as the mean ± standard deviation. *P<0.05 compared with the Sham group; #P<0.05 compared with the Dmm group. Dmm, destabilization of the medial meniscus; Th, thalidomide; VEGF, vascular endothelial growth factor.

Article Snippet: An ELISA kit of VEGF (E-EL-M1292c) was purchased from Elabscience Biotechnology Co., Ltd., Wuhan, China.

Techniques: Enzyme-linked Immunosorbent Assay, Concentration Assay, Standard Deviation

VEGFC and VEGFR2 protein levels in conditioned media of stable cell lines indicated by ELISA. (A) VEGFC; (B) VEGFR2. VEGF, vascular endothelial growth factor; ELISA, enzyme-linked immunosorbent assay.

Journal: Chinese Journal of Cancer Research

Article Title: Tim-3 promotes cell aggressiveness and paclitaxel resistance through NF-κB/STAT3 signalling pathway in breast cancer cells

doi: 10.21147/j.issn.1000-9604.2020.05.02

Figure Lengend Snippet: VEGFC and VEGFR2 protein levels in conditioned media of stable cell lines indicated by ELISA. (A) VEGFC; (B) VEGFR2. VEGF, vascular endothelial growth factor; ELISA, enzyme-linked immunosorbent assay.

Article Snippet: ELISA was performed using the human VEGFC (cat. no. E-EL-H1600; Elabscience) and vascular endothelial growth factor receptor 2 (VEGFR2) ELISA kit (cat. no. E-EL-H1603; Elabscience), according to the manufacturer’s protocol.

Techniques: Stable Transfection, Enzyme-linked Immunosorbent Assay

TGF-α (A, B) and VEGF-B (C, D) levels as well as AHR agonistic activity (G, H) in serum samples of patients with RRMS in remission (n = 98), SPMS (n = 44), PPMS (n = 36), and their respective controls (A, C, E, G: n = 43; B, D, F, H: n = 16) were assessed. TGF-α and VEGF-B levels were measured in pg/mL using a human TGF-α or VEGF-B ELISA. TGF-α/VEGF-B ratio (E, F) was determined by dividing TGF-α levels by VEGF-B levels. An AHR ligand–sensitive luciferase assay was used. Relative activity was calculated by dividing firefly luciferase activity (pGud-Luc) by Renilla luciferase activity (pTK-Renilla). Values are means of duplicate measurements. Lines represent median and interquartile range. Significance levels were derived using nonparametric tests (Mann-Whitney test and Kruskal-Wallis test with the Dunn multiple comparison test correcting for multiple comparisons). **** p < 0.0001, *** p < 0.001, ** p < 0.001, * p < 0.01, and ns = nonsignificant. AHR = aryl hydrocarbon receptor; MS = multiple sclerosis; PPMS = primary progressive MS; RRMS = relapsing-remitting MS; SPMS = secondary progressive MS; TGF-α = transforming growth factor alpha; VEGF-B = vascular endothelial growth factor B.

Journal: Neurology® Neuroimmunology & Neuroinflammation

Article Title: The Aryl Hydrocarbon Receptor–Dependent TGF-α/VEGF-B Ratio Correlates With Disease Subtype and Prognosis in Multiple Sclerosis

doi: 10.1212/NXI.0000000000001043

Figure Lengend Snippet: TGF-α (A, B) and VEGF-B (C, D) levels as well as AHR agonistic activity (G, H) in serum samples of patients with RRMS in remission (n = 98), SPMS (n = 44), PPMS (n = 36), and their respective controls (A, C, E, G: n = 43; B, D, F, H: n = 16) were assessed. TGF-α and VEGF-B levels were measured in pg/mL using a human TGF-α or VEGF-B ELISA. TGF-α/VEGF-B ratio (E, F) was determined by dividing TGF-α levels by VEGF-B levels. An AHR ligand–sensitive luciferase assay was used. Relative activity was calculated by dividing firefly luciferase activity (pGud-Luc) by Renilla luciferase activity (pTK-Renilla). Values are means of duplicate measurements. Lines represent median and interquartile range. Significance levels were derived using nonparametric tests (Mann-Whitney test and Kruskal-Wallis test with the Dunn multiple comparison test correcting for multiple comparisons). **** p < 0.0001, *** p < 0.001, ** p < 0.001, * p < 0.01, and ns = nonsignificant. AHR = aryl hydrocarbon receptor; MS = multiple sclerosis; PPMS = primary progressive MS; RRMS = relapsing-remitting MS; SPMS = secondary progressive MS; TGF-α = transforming growth factor alpha; VEGF-B = vascular endothelial growth factor B.

Article Snippet: Commercial TGF-α ELISA Kit (EHTGF-Α, Thermo Scientific) and VEGF-B ELISA Kit (CSB-E04758h, CUSABIO) were used for the quantitative determination of TGF-α and VEGF-B levels.

Techniques: Activity Assay, Enzyme-linked Immunosorbent Assay, Luciferase, Derivative Assay, MANN-WHITNEY, Comparison

TGF-α (A) and VEGF-B (B) levels as well as AHR agonistic activity (D) were assessed in serum samples of patients with RRMS in remission (n = 98), RRMS during relapse (n = 54), and controls (n = 44). TGF-α and VEGF-B levels were measured in pg/mL using a human TGF-α or VEGF-B ELISA. TGF-α/VEGF-B ratio (C) was determined by dividing TGF-α levels by VEGF-B levels. An AHR ligand–sensitive luciferase assay was used. Relative activity was calculated by dividing firefly luciferase activity (pGud-Luc) by Renilla luciferase activity (pTK-Renilla). Values are means of duplicate measurements. Lines represent median and interquartile range. Significance levels were derived using the nonparametric Kruskal-Wallis test with the Dunn multiple comparison test correcting for multiple comparisons. **** p < 0.0001, *** p < 0.001, ** p < 0.001, * p < 0.01, and ns = nonsignificant. AHR = aryl hydrocarbon receptor; RRMS = relapsing-remitting multiple sclerosis; TGF-α = transforming growth factor alpha; VEGF-B = vascular endothelial growth factor B.

Journal: Neurology® Neuroimmunology & Neuroinflammation

Article Title: The Aryl Hydrocarbon Receptor–Dependent TGF-α/VEGF-B Ratio Correlates With Disease Subtype and Prognosis in Multiple Sclerosis

doi: 10.1212/NXI.0000000000001043

Figure Lengend Snippet: TGF-α (A) and VEGF-B (B) levels as well as AHR agonistic activity (D) were assessed in serum samples of patients with RRMS in remission (n = 98), RRMS during relapse (n = 54), and controls (n = 44). TGF-α and VEGF-B levels were measured in pg/mL using a human TGF-α or VEGF-B ELISA. TGF-α/VEGF-B ratio (C) was determined by dividing TGF-α levels by VEGF-B levels. An AHR ligand–sensitive luciferase assay was used. Relative activity was calculated by dividing firefly luciferase activity (pGud-Luc) by Renilla luciferase activity (pTK-Renilla). Values are means of duplicate measurements. Lines represent median and interquartile range. Significance levels were derived using the nonparametric Kruskal-Wallis test with the Dunn multiple comparison test correcting for multiple comparisons. **** p < 0.0001, *** p < 0.001, ** p < 0.001, * p < 0.01, and ns = nonsignificant. AHR = aryl hydrocarbon receptor; RRMS = relapsing-remitting multiple sclerosis; TGF-α = transforming growth factor alpha; VEGF-B = vascular endothelial growth factor B.

Article Snippet: Commercial TGF-α ELISA Kit (EHTGF-Α, Thermo Scientific) and VEGF-B ELISA Kit (CSB-E04758h, CUSABIO) were used for the quantitative determination of TGF-α and VEGF-B levels.

Techniques: Activity Assay, Enzyme-linked Immunosorbent Assay, Luciferase, Derivative Assay, Comparison

TGF-α (A) and VEGF-B (B) levels as well as AHR agonistic activity (D) were assessed in serum samples of patients with RRMS in remission (n = 98), CIS (n = 20), and controls (n = 44). TGF-α and VEGF-B levels were measured in pg/mL using a human TGF-α or VEGF-B ELISA. TGF-α/VEGF-B ratio (C) was determined by dividing TGF-α levels by VEGF-B levels. An AHR ligand–sensitive luciferase assay was used. Relative activity was calculated by dividing firefly luciferase activity (pGud-Luc) by Renilla luciferase activity (pTK-Renilla). Values are means of duplicate measurements. Lines represent median and interquartile range. Significance levels were derived using the nonparametric Kruskal-Wallis test with the Dunn multiple comparison test correcting for multiple comparisons. **** p < 0.0001, *** p < 0.001, ** p < 0.001, * p < 0.01, and ns = nonsignificant. AHR = aryl hydrocarbon receptor; CIS = clinically isolated syndrome; RRMS = relapsing-remitting multiple sclerosis; TGF-α = transforming growth factor alpha; VEGF-B = vascular endothelial growth factor B.

Journal: Neurology® Neuroimmunology & Neuroinflammation

Article Title: The Aryl Hydrocarbon Receptor–Dependent TGF-α/VEGF-B Ratio Correlates With Disease Subtype and Prognosis in Multiple Sclerosis

doi: 10.1212/NXI.0000000000001043

Figure Lengend Snippet: TGF-α (A) and VEGF-B (B) levels as well as AHR agonistic activity (D) were assessed in serum samples of patients with RRMS in remission (n = 98), CIS (n = 20), and controls (n = 44). TGF-α and VEGF-B levels were measured in pg/mL using a human TGF-α or VEGF-B ELISA. TGF-α/VEGF-B ratio (C) was determined by dividing TGF-α levels by VEGF-B levels. An AHR ligand–sensitive luciferase assay was used. Relative activity was calculated by dividing firefly luciferase activity (pGud-Luc) by Renilla luciferase activity (pTK-Renilla). Values are means of duplicate measurements. Lines represent median and interquartile range. Significance levels were derived using the nonparametric Kruskal-Wallis test with the Dunn multiple comparison test correcting for multiple comparisons. **** p < 0.0001, *** p < 0.001, ** p < 0.001, * p < 0.01, and ns = nonsignificant. AHR = aryl hydrocarbon receptor; CIS = clinically isolated syndrome; RRMS = relapsing-remitting multiple sclerosis; TGF-α = transforming growth factor alpha; VEGF-B = vascular endothelial growth factor B.

Article Snippet: Commercial TGF-α ELISA Kit (EHTGF-Α, Thermo Scientific) and VEGF-B ELISA Kit (CSB-E04758h, CUSABIO) were used for the quantitative determination of TGF-α and VEGF-B levels.

Techniques: Activity Assay, Enzyme-linked Immunosorbent Assay, Luciferase, Derivative Assay, Comparison, Isolation

TGF-α/VEGF-B ratio (A) and AHR agonistic activity (B) in serum samples of patients with RRMS in remission (n = 98) were assessed. TGF-α and VEGF-B levels were measured in pg/mL using a human TGF-α or VEGF-B ELISA. TGF-α/VEGF-B ratio was determined by dividing TGF-α levels by VEGF-B levels. An AHR ligand–sensitive luciferase assay was used. Relative activity was calculated by dividing firefly luciferase activity (pGud-Luc) by Renilla luciferase activity (pTK-Renilla). Values are presented as means of duplicate measurements. Line shows linear regression of the TGF-α/VEGF-B ratio or AHR agonistic activity and patients' EDSS. Significance levels were derived using Spearman correlation analysis (A: Spearman r = −0.2427; R 2 = 0.059; B: Spearman r = −0.2433; R 2 = 0.059). AHR = aryl hydrocarbon receptor; EDSS = Expanded Disability Status Scale; RRMS = relapsing-remitting multiple sclerosis; TGF-α = transforming growth factor alpha; VEGF-B = vascular endothelial growth factor B.

Journal: Neurology® Neuroimmunology & Neuroinflammation

Article Title: The Aryl Hydrocarbon Receptor–Dependent TGF-α/VEGF-B Ratio Correlates With Disease Subtype and Prognosis in Multiple Sclerosis

doi: 10.1212/NXI.0000000000001043

Figure Lengend Snippet: TGF-α/VEGF-B ratio (A) and AHR agonistic activity (B) in serum samples of patients with RRMS in remission (n = 98) were assessed. TGF-α and VEGF-B levels were measured in pg/mL using a human TGF-α or VEGF-B ELISA. TGF-α/VEGF-B ratio was determined by dividing TGF-α levels by VEGF-B levels. An AHR ligand–sensitive luciferase assay was used. Relative activity was calculated by dividing firefly luciferase activity (pGud-Luc) by Renilla luciferase activity (pTK-Renilla). Values are presented as means of duplicate measurements. Line shows linear regression of the TGF-α/VEGF-B ratio or AHR agonistic activity and patients' EDSS. Significance levels were derived using Spearman correlation analysis (A: Spearman r = −0.2427; R 2 = 0.059; B: Spearman r = −0.2433; R 2 = 0.059). AHR = aryl hydrocarbon receptor; EDSS = Expanded Disability Status Scale; RRMS = relapsing-remitting multiple sclerosis; TGF-α = transforming growth factor alpha; VEGF-B = vascular endothelial growth factor B.

Article Snippet: Commercial TGF-α ELISA Kit (EHTGF-Α, Thermo Scientific) and VEGF-B ELISA Kit (CSB-E04758h, CUSABIO) were used for the quantitative determination of TGF-α and VEGF-B levels.

Techniques: Activity Assay, Enzyme-linked Immunosorbent Assay, Luciferase, Derivative Assay