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plasma levels of il-6 e-el-h0102c  (Elabscience Biotechnology)


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    Elabscience Biotechnology plasma levels of il-6 e-el-h0102c
    Plasma Levels Of Il 6 E El H0102c, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Treatment of rats and NHBE cells with LPS downregulates miR-16 expression. (A) Hematoxylin and eosin staining revealed histological differences between the lung tissues from rats in the LPS and control groups. The lung tissues from the LPS group showed lung injury, including hemorrhage (clear arrow), interstitial edema (red arrow) and infiltration of inflammatory cells (black arrow). Scale bar, 100 µm. (B) Differences in miR-16 expression between rats in the LPS and control groups were assessed by reverse transcription-quantitative PCR. The levels of (C) TNF-α, (D) IL-1β and <t>(E)</t> <t>IL-6</t> were measured in rats treated with LPS or PBS (control) using ELISA. * P<0.05 vs. Control. (F) miR-16 expression was decreased following treatment of NHBE cells with increasing concentrations of LPS (0, 1, 2, 3, 4, 8 and 16 µg/ml) for 12 h as assessed by reverse transcription-quantitative PCR. * P<0.05 vs. 0 group. (G) miR-16 expression was gradually reduced in NHBE cells incubated with 2 µg/ml LPS for a range of indicated time durations (0, 6, 12, 24, 36 and 48 h) as assessed by reverse transcription-quantitative PCR. * P<0.05 vs. 0 group. * P<0.05. LPS, lipopolysaccharide; ALI, acute lung injury; TNF-α, tumor necrosis factor α; IL, interleukin; NHBE, normal human bronchial epithelial; NC, negative control; miR, microRNA.
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    Treatment of rats and NHBE cells with LPS downregulates miR-16 expression. (A) Hematoxylin and eosin staining revealed histological differences between the lung tissues from rats in the LPS and control groups. The lung tissues from the LPS group showed lung injury, including hemorrhage (clear arrow), interstitial edema (red arrow) and infiltration of inflammatory cells (black arrow). Scale bar, 100 µm. (B) Differences in miR-16 expression between rats in the LPS and control groups were assessed by reverse transcription-quantitative PCR. The levels of (C) TNF-α, (D) IL-1β and <t>(E)</t> <t>IL-6</t> were measured in rats treated with LPS or PBS (control) using ELISA. * P<0.05 vs. Control. (F) miR-16 expression was decreased following treatment of NHBE cells with increasing concentrations of LPS (0, 1, 2, 3, 4, 8 and 16 µg/ml) for 12 h as assessed by reverse transcription-quantitative PCR. * P<0.05 vs. 0 group. (G) miR-16 expression was gradually reduced in NHBE cells incubated with 2 µg/ml LPS for a range of indicated time durations (0, 6, 12, 24, 36 and 48 h) as assessed by reverse transcription-quantitative PCR. * P<0.05 vs. 0 group. * P<0.05. LPS, lipopolysaccharide; ALI, acute lung injury; TNF-α, tumor necrosis factor α; IL, interleukin; NHBE, normal human bronchial epithelial; NC, negative control; miR, microRNA.
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    Treatment of rats and NHBE cells with LPS downregulates miR-16 expression. (A) Hematoxylin and eosin staining revealed histological differences between the lung tissues from rats in the LPS and control groups. The lung tissues from the LPS group showed lung injury, including hemorrhage (clear arrow), interstitial edema (red arrow) and infiltration of inflammatory cells (black arrow). Scale bar, 100 µm. (B) Differences in miR-16 expression between rats in the LPS and control groups were assessed by reverse transcription-quantitative PCR. The levels of (C) TNF-α, (D) IL-1β and <t>(E)</t> <t>IL-6</t> were measured in rats treated with LPS or PBS (control) using ELISA. * P<0.05 vs. Control. (F) miR-16 expression was decreased following treatment of NHBE cells with increasing concentrations of LPS (0, 1, 2, 3, 4, 8 and 16 µg/ml) for 12 h as assessed by reverse transcription-quantitative PCR. * P<0.05 vs. 0 group. (G) miR-16 expression was gradually reduced in NHBE cells incubated with 2 µg/ml LPS for a range of indicated time durations (0, 6, 12, 24, 36 and 48 h) as assessed by reverse transcription-quantitative PCR. * P<0.05 vs. 0 group. * P<0.05. LPS, lipopolysaccharide; ALI, acute lung injury; TNF-α, tumor necrosis factor α; IL, interleukin; NHBE, normal human bronchial epithelial; NC, negative control; miR, microRNA.
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    Treatment of rats and NHBE cells with LPS downregulates miR-16 expression. (A) Hematoxylin and eosin staining revealed histological differences between the lung tissues from rats in the LPS and control groups. The lung tissues from the LPS group showed lung injury, including hemorrhage (clear arrow), interstitial edema (red arrow) and infiltration of inflammatory cells (black arrow). Scale bar, 100 µm. (B) Differences in miR-16 expression between rats in the LPS and control groups were assessed by reverse transcription-quantitative PCR. The levels of (C) TNF-α, (D) IL-1β and <t>(E)</t> <t>IL-6</t> were measured in rats treated with LPS or PBS (control) using ELISA. * P<0.05 vs. Control. (F) miR-16 expression was decreased following treatment of NHBE cells with increasing concentrations of LPS (0, 1, 2, 3, 4, 8 and 16 µg/ml) for 12 h as assessed by reverse transcription-quantitative PCR. * P<0.05 vs. 0 group. (G) miR-16 expression was gradually reduced in NHBE cells incubated with 2 µg/ml LPS for a range of indicated time durations (0, 6, 12, 24, 36 and 48 h) as assessed by reverse transcription-quantitative PCR. * P<0.05 vs. 0 group. * P<0.05. LPS, lipopolysaccharide; ALI, acute lung injury; TNF-α, tumor necrosis factor α; IL, interleukin; NHBE, normal human bronchial epithelial; NC, negative control; miR, microRNA.
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    Treatment of rats and NHBE cells with LPS downregulates miR-16 expression. (A) Hematoxylin and eosin staining revealed histological differences between the lung tissues from rats in the LPS and control groups. The lung tissues from the LPS group showed lung injury, including hemorrhage (clear arrow), interstitial edema (red arrow) and infiltration of inflammatory cells (black arrow). Scale bar, 100 µm. (B) Differences in miR-16 expression between rats in the LPS and control groups were assessed by reverse transcription-quantitative PCR. The levels of (C) TNF-α, (D) IL-1β and <t>(E)</t> <t>IL-6</t> were measured in rats treated with LPS or PBS (control) using ELISA. * P<0.05 vs. Control. (F) miR-16 expression was decreased following treatment of NHBE cells with increasing concentrations of LPS (0, 1, 2, 3, 4, 8 and 16 µg/ml) for 12 h as assessed by reverse transcription-quantitative PCR. * P<0.05 vs. 0 group. (G) miR-16 expression was gradually reduced in NHBE cells incubated with 2 µg/ml LPS for a range of indicated time durations (0, 6, 12, 24, 36 and 48 h) as assessed by reverse transcription-quantitative PCR. * P<0.05 vs. 0 group. * P<0.05. LPS, lipopolysaccharide; ALI, acute lung injury; TNF-α, tumor necrosis factor α; IL, interleukin; NHBE, normal human bronchial epithelial; NC, negative control; miR, microRNA.
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    miR-149-5p mimics inhibited TNF-α-induced growth inhibition and inflammation. After transfection with miR-149-5p mimics or miR-149-5p mimics combined with TRADD vector into chondrocytes with or without TNF-α treatment, cell viability was measured by CCK8 assays ( A ); the production of inflammatory cytokines, including <t>IL-1β,</t> <t>IL-6</t> and IL-18, was detected by ELISA assays ( B–D ). n = 3 in each group, * p < 0.05
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    miR-149-5p mimics inhibited TNF-α-induced growth inhibition and inflammation. After transfection with miR-149-5p mimics or miR-149-5p mimics combined with TRADD vector into chondrocytes with or without TNF-α treatment, cell viability was measured by CCK8 assays ( A ); the production of inflammatory cytokines, including <t>IL-1β,</t> <t>IL-6</t> and IL-18, was detected by ELISA assays ( B–D ). n = 3 in each group, * p < 0.05
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    Treatment of rats and NHBE cells with LPS downregulates miR-16 expression. (A) Hematoxylin and eosin staining revealed histological differences between the lung tissues from rats in the LPS and control groups. The lung tissues from the LPS group showed lung injury, including hemorrhage (clear arrow), interstitial edema (red arrow) and infiltration of inflammatory cells (black arrow). Scale bar, 100 µm. (B) Differences in miR-16 expression between rats in the LPS and control groups were assessed by reverse transcription-quantitative PCR. The levels of (C) TNF-α, (D) IL-1β and (E) IL-6 were measured in rats treated with LPS or PBS (control) using ELISA. * P<0.05 vs. Control. (F) miR-16 expression was decreased following treatment of NHBE cells with increasing concentrations of LPS (0, 1, 2, 3, 4, 8 and 16 µg/ml) for 12 h as assessed by reverse transcription-quantitative PCR. * P<0.05 vs. 0 group. (G) miR-16 expression was gradually reduced in NHBE cells incubated with 2 µg/ml LPS for a range of indicated time durations (0, 6, 12, 24, 36 and 48 h) as assessed by reverse transcription-quantitative PCR. * P<0.05 vs. 0 group. * P<0.05. LPS, lipopolysaccharide; ALI, acute lung injury; TNF-α, tumor necrosis factor α; IL, interleukin; NHBE, normal human bronchial epithelial; NC, negative control; miR, microRNA.

    Journal: Experimental and Therapeutic Medicine

    Article Title: MicroRNA-16 regulates lipopolysaccharide-induced inflammatory factor expression by targeting TLR4 in normal human bronchial epithelial cells

    doi: 10.3892/etm.2021.10414

    Figure Lengend Snippet: Treatment of rats and NHBE cells with LPS downregulates miR-16 expression. (A) Hematoxylin and eosin staining revealed histological differences between the lung tissues from rats in the LPS and control groups. The lung tissues from the LPS group showed lung injury, including hemorrhage (clear arrow), interstitial edema (red arrow) and infiltration of inflammatory cells (black arrow). Scale bar, 100 µm. (B) Differences in miR-16 expression between rats in the LPS and control groups were assessed by reverse transcription-quantitative PCR. The levels of (C) TNF-α, (D) IL-1β and (E) IL-6 were measured in rats treated with LPS or PBS (control) using ELISA. * P<0.05 vs. Control. (F) miR-16 expression was decreased following treatment of NHBE cells with increasing concentrations of LPS (0, 1, 2, 3, 4, 8 and 16 µg/ml) for 12 h as assessed by reverse transcription-quantitative PCR. * P<0.05 vs. 0 group. (G) miR-16 expression was gradually reduced in NHBE cells incubated with 2 µg/ml LPS for a range of indicated time durations (0, 6, 12, 24, 36 and 48 h) as assessed by reverse transcription-quantitative PCR. * P<0.05 vs. 0 group. * P<0.05. LPS, lipopolysaccharide; ALI, acute lung injury; TNF-α, tumor necrosis factor α; IL, interleukin; NHBE, normal human bronchial epithelial; NC, negative control; miR, microRNA.

    Article Snippet: The secretion levels of TNF-α (cat. no. E-EL-R0019c), IL-1β (cat. no. E-EL-H0149c) and IL-6 (cat. no. E-EL-H0102c) were determined using the corresponding ELISA kits (Elabscience Biotechnology Co., Ltd.) in peripheral blood samples of rats and cell culture medium of NHBE cells.

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

    miR-16 overexpression attenuates LPS-induced secretion of IL-1β, TNF-α and IL-6. NHBE cells were treated with 2 µg/ml LPS for 12 h after transfection 48 h. (A) Transfection of NHBE cells with miR-16 mimics sufficiently overexpressed miR-16. * P<0.05 vs. miR-NC. Secretion of (B) TNF-α, (C) IL-1β and (D) IL-6 by NHBE cells was determined following cell transfection with miR-16 mimics for 48 h using ELISA. mRNA expression levels of (E) TNF-α, (F) IL-1β and (G) IL-6 were measured in NHBE cells by reverse transcription-quantitative PCR. * P<0.05. LPS, lipopolysaccharide; TNF-α, tumor necrosis factor α; IL-1β, interleukin 1β; NHBE, normal human bronchial epithelial; NC, negative control; miR, microRNA.

    Journal: Experimental and Therapeutic Medicine

    Article Title: MicroRNA-16 regulates lipopolysaccharide-induced inflammatory factor expression by targeting TLR4 in normal human bronchial epithelial cells

    doi: 10.3892/etm.2021.10414

    Figure Lengend Snippet: miR-16 overexpression attenuates LPS-induced secretion of IL-1β, TNF-α and IL-6. NHBE cells were treated with 2 µg/ml LPS for 12 h after transfection 48 h. (A) Transfection of NHBE cells with miR-16 mimics sufficiently overexpressed miR-16. * P<0.05 vs. miR-NC. Secretion of (B) TNF-α, (C) IL-1β and (D) IL-6 by NHBE cells was determined following cell transfection with miR-16 mimics for 48 h using ELISA. mRNA expression levels of (E) TNF-α, (F) IL-1β and (G) IL-6 were measured in NHBE cells by reverse transcription-quantitative PCR. * P<0.05. LPS, lipopolysaccharide; TNF-α, tumor necrosis factor α; IL-1β, interleukin 1β; NHBE, normal human bronchial epithelial; NC, negative control; miR, microRNA.

    Article Snippet: The secretion levels of TNF-α (cat. no. E-EL-R0019c), IL-1β (cat. no. E-EL-H0149c) and IL-6 (cat. no. E-EL-H0102c) were determined using the corresponding ELISA kits (Elabscience Biotechnology Co., Ltd.) in peripheral blood samples of rats and cell culture medium of NHBE cells.

    Techniques: Over Expression, Transfection, Enzyme-linked Immunosorbent Assay, Expressing, Real-time Polymerase Chain Reaction, Negative Control

    TLR4 knockdown alleviates LPS-induced inflammatory factors secretion from NHBE cells. (A) Western blot analysis for TLR4 protein expression after transfection with si-TLR4. The secretion levels of (B) TNF-α, (C) IL-1β and (D) IL-6 were measured by ELISA following transfection of NHBE cells with si-TLR4 or si-NC for 48 h. * P<0.05. LPS, lipopolysaccharide; TNF-α, tumor necrosis factor α; IL, interleukin; si, small interfering; NC, negative control; TLR4, toll-like receptor 4; NHBE, normal human bronchial epithelial.

    Journal: Experimental and Therapeutic Medicine

    Article Title: MicroRNA-16 regulates lipopolysaccharide-induced inflammatory factor expression by targeting TLR4 in normal human bronchial epithelial cells

    doi: 10.3892/etm.2021.10414

    Figure Lengend Snippet: TLR4 knockdown alleviates LPS-induced inflammatory factors secretion from NHBE cells. (A) Western blot analysis for TLR4 protein expression after transfection with si-TLR4. The secretion levels of (B) TNF-α, (C) IL-1β and (D) IL-6 were measured by ELISA following transfection of NHBE cells with si-TLR4 or si-NC for 48 h. * P<0.05. LPS, lipopolysaccharide; TNF-α, tumor necrosis factor α; IL, interleukin; si, small interfering; NC, negative control; TLR4, toll-like receptor 4; NHBE, normal human bronchial epithelial.

    Article Snippet: The secretion levels of TNF-α (cat. no. E-EL-R0019c), IL-1β (cat. no. E-EL-H0149c) and IL-6 (cat. no. E-EL-H0102c) were determined using the corresponding ELISA kits (Elabscience Biotechnology Co., Ltd.) in peripheral blood samples of rats and cell culture medium of NHBE cells.

    Techniques: Western Blot, Expressing, Transfection, Enzyme-linked Immunosorbent Assay, Negative Control

    miR-16 exerts protective effects against ALI-induced inflammatory responses by modulating TLR4 expression. Secretion levels of (A) TNF-α, (B) IL-1β and (C) IL-6 were assessed by ELISA after co-transfection and LPS treatment. * P<0.05. ALI, acute lung injury; TNF-α, tumor necrosis factor α; IL-1β, interleukin 1β.

    Journal: Experimental and Therapeutic Medicine

    Article Title: MicroRNA-16 regulates lipopolysaccharide-induced inflammatory factor expression by targeting TLR4 in normal human bronchial epithelial cells

    doi: 10.3892/etm.2021.10414

    Figure Lengend Snippet: miR-16 exerts protective effects against ALI-induced inflammatory responses by modulating TLR4 expression. Secretion levels of (A) TNF-α, (B) IL-1β and (C) IL-6 were assessed by ELISA after co-transfection and LPS treatment. * P<0.05. ALI, acute lung injury; TNF-α, tumor necrosis factor α; IL-1β, interleukin 1β.

    Article Snippet: The secretion levels of TNF-α (cat. no. E-EL-R0019c), IL-1β (cat. no. E-EL-H0149c) and IL-6 (cat. no. E-EL-H0102c) were determined using the corresponding ELISA kits (Elabscience Biotechnology Co., Ltd.) in peripheral blood samples of rats and cell culture medium of NHBE cells.

    Techniques: Expressing, Enzyme-linked Immunosorbent Assay, Cotransfection

    miR-149-5p mimics inhibited TNF-α-induced growth inhibition and inflammation. After transfection with miR-149-5p mimics or miR-149-5p mimics combined with TRADD vector into chondrocytes with or without TNF-α treatment, cell viability was measured by CCK8 assays ( A ); the production of inflammatory cytokines, including IL-1β, IL-6 and IL-18, was detected by ELISA assays ( B–D ). n = 3 in each group, * p < 0.05

    Journal: Archives of Medical Science : AMS

    Article Title: miR-149-5p mitigates tumor necrosis factor-α-induced chondrocyte apoptosis by inhibiting TRADD

    doi: 10.5114/aoms.2020.92324

    Figure Lengend Snippet: miR-149-5p mimics inhibited TNF-α-induced growth inhibition and inflammation. After transfection with miR-149-5p mimics or miR-149-5p mimics combined with TRADD vector into chondrocytes with or without TNF-α treatment, cell viability was measured by CCK8 assays ( A ); the production of inflammatory cytokines, including IL-1β, IL-6 and IL-18, was detected by ELISA assays ( B–D ). n = 3 in each group, * p < 0.05

    Article Snippet: The levels of IL-1β (Cat. no: E-EL-H0149c), IL-6 (Cat. no: E-EL-H0102c) and IL-18 (Cat. no: E-EL-H0253c) in the supernatant of cultured chondrocytes were measured using ELISA kits (Elabscience Biotechnology Co., Ltd, Wuhan, China) as described previously [ ].

    Techniques: Inhibition, Transfection, Plasmid Preparation, Enzyme-linked Immunosorbent Assay