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5 mm par1 inhibitor sch79797 (R&D Systems)

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R&D Systems 5 mm par1 inhibitor sch79797

Determination of thrombin, PARs, and MIF expression at lesion sites following rat SCI. a ELISA measurement of thrombin protein levels at lesion sites following SCI at 0, 1, 4, and 7d. b Western blot analysis of MIF following SCI at 0, 1, 4, and 7d. Quantities were normalized to endogenous β-actin. c PCR assay for determining the expression abundance of <t>par1</t> , par3, and par4 in the intact spinal cord. Quantities were normalized to endogenous gapdh . d–f RT-PCR assays of par1 ( d ), par3 ( e ), and par4 ( f ) transcriptional changes following SCI at 0, 1, 4, and 7d, respectively. Quantities were normalized to endogenous gapdh . Experiments were performed at least in technical triplicates. The values shown in the figures were the average of each technical replicate. Error bars represent the SEM (* P < 0.05). g Colocalization of PAR1 with GFAP-positive astrocytes before and after SCI. The sections were prepared using a cryostat from 0.25 cm length to the lesion epicenter. Rectangle indicates region magnified. Arrowheads indicate the positive signals. Scale bars, 500 μm, and 50 μm in magnification

5 Mm Par1 Inhibitor Sch79797, supplied by R&D Systems, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/5+mm+par1+inhibitor+sch79797/anti+par1/pmc09137112-62-11-14
Average 90 stars, based on 1 article reviews

5 mm par1 inhibitor sch79797 - by Bioz Stars, 2026-10

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1) Product Images from "Thrombin acts as inducer of proinflammatory macrophage migration inhibitory factor in astrocytes following rat spinal cord injury"

Article Title: Thrombin acts as inducer of proinflammatory macrophage migration inhibitory factor in astrocytes following rat spinal cord injury

Journal: Journal of Neuroinflammation

doi: 10.1186/s12974-022-02488-w

Figure Legend Snippet: Determination of thrombin, PARs, and MIF expression at lesion sites following rat SCI. a ELISA measurement of thrombin protein levels at lesion sites following SCI at 0, 1, 4, and 7d. b Western blot analysis of MIF following SCI at 0, 1, 4, and 7d. Quantities were normalized to endogenous β-actin. c PCR assay for determining the expression abundance of par1 , par3, and par4 in the intact spinal cord. Quantities were normalized to endogenous gapdh . d–f RT-PCR assays of par1 ( d ), par3 ( e ), and par4 ( f ) transcriptional changes following SCI at 0, 1, 4, and 7d, respectively. Quantities were normalized to endogenous gapdh . Experiments were performed at least in technical triplicates. The values shown in the figures were the average of each technical replicate. Error bars represent the SEM (* P < 0.05). g Colocalization of PAR1 with GFAP-positive astrocytes before and after SCI. The sections were prepared using a cryostat from 0.25 cm length to the lesion epicenter. Rectangle indicates region magnified. Arrowheads indicate the positive signals. Scale bars, 500 μm, and 50 μm in magnification

Techniques Used: Expressing, Enzyme-linked Immunosorbent Assay, Western Blot, Reverse Transcription Polymerase Chain Reaction

Functional annotation of DEGs following astrocyte stimulation with thrombin. a Primary cultured rat spinal cord astrocytes stained with GFAP and Hoechst 33,342 with purity over 95%. b PCR assay for determining the abundance of par1 , par3, and par4 at transcriptional levels in the primary astrocytes. Quantities were normalized to endogenous gapdh . c Bar graphs of DEGs following astrocyte stimulation with 100 nM thrombin for 6, 12, and 24 h, respectively. d Integration of DEGs at 6, 12, and 24 h. e GO analysis of the DEGs relating to biological processes. Scale bar, 50 μm in a

Figure Legend Snippet: Functional annotation of DEGs following astrocyte stimulation with thrombin. a Primary cultured rat spinal cord astrocytes stained with GFAP and Hoechst 33,342 with purity over 95%. b PCR assay for determining the abundance of par1 , par3, and par4 at transcriptional levels in the primary astrocytes. Quantities were normalized to endogenous gapdh . c Bar graphs of DEGs following astrocyte stimulation with 100 nM thrombin for 6, 12, and 24 h, respectively. d Integration of DEGs at 6, 12, and 24 h. e GO analysis of the DEGs relating to biological processes. Scale bar, 50 μm in a

Techniques Used: Functional Assay, Cell Culture, Staining

Effects of interfering PAR1, PAR3, or PAR4 expression on the thrombin-induced MIF production of astrocytes. a Western blot analysis of MIF protein levels in the astrocytes treated by 0–5 μM PAR1 inhibitor SCH79797 for 24 h in the presence of 100 nM thrombin. b Quantification data as shown in a . Quantities were normalized to endogenous β-actin. c MTT assay of SCH79797 effects on the cell viability of the astrocytes. d Interference efficiency of siRNA oligonucleotide for PAR3 was measured by RT-PCR, and siRNA1 was used for the knockdown experiments. e Western blot analysis of MIF in the astrocytes following PAR3 knockdown for 24 h, prior to stimulation with 100 nM thrombin for 24 h. Scrambles were used as control. f Quantification data as shown in e . Quantities were normalized to endogenous β-actin. (g) Western blot analysis of MIF protein levels in the astrocytes treated by 0–100 μM PAR4 inhibitor tcy-NH 2 for 24 h in the presence of 100 nM thrombin. h Quantification data as shown in g . Quantities were normalized to endogenous β-actin. i MTT assay of tcy-NH 2 effects on the cell viability of the astrocytes. Experiments were performed in triplicates. Error bars represent the SEM (* P < 0.05)

Figure Legend Snippet: Effects of interfering PAR1, PAR3, or PAR4 expression on the thrombin-induced MIF production of astrocytes. a Western blot analysis of MIF protein levels in the astrocytes treated by 0–5 μM PAR1 inhibitor SCH79797 for 24 h in the presence of 100 nM thrombin. b Quantification data as shown in a . Quantities were normalized to endogenous β-actin. c MTT assay of SCH79797 effects on the cell viability of the astrocytes. d Interference efficiency of siRNA oligonucleotide for PAR3 was measured by RT-PCR, and siRNA1 was used for the knockdown experiments. e Western blot analysis of MIF in the astrocytes following PAR3 knockdown for 24 h, prior to stimulation with 100 nM thrombin for 24 h. Scrambles were used as control. f Quantification data as shown in e . Quantities were normalized to endogenous β-actin. (g) Western blot analysis of MIF protein levels in the astrocytes treated by 0–100 μM PAR4 inhibitor tcy-NH 2 for 24 h in the presence of 100 nM thrombin. h Quantification data as shown in g . Quantities were normalized to endogenous β-actin. i MTT assay of tcy-NH 2 effects on the cell viability of the astrocytes. Experiments were performed in triplicates. Error bars represent the SEM (* P < 0.05)

Techniques Used: Expressing, Western Blot, MTT Assay, Reverse Transcription Polymerase Chain Reaction

Determination of the phosphorylated activation of the MAPKs/NFκB signals in the astrocytes following stimulation with thrombin. a Western blot analysis of phosphorylation of ERK, P38, JNK kinase, and p65NFκB protein after astrocyte stimulation with 0–200 nM thrombin for 24 h. b–e Quantification data as shown in a . Quantities were normalized to endogenous β-actin. f Western blot analysis of phosphorylation of ERK, P38, JNK kinase, and p65NFκB protein after astrocyte treatment with 0–5 μM SCH79797 for 24 h in the presence of 100 nM thrombin. g–j Quantification data as shown in f . Quantities were normalized to endogenous β-actin. Experiments were performed in triplicates. Error bars represent the SEM (* P < 0.05)

Figure Legend Snippet: Determination of the phosphorylated activation of the MAPKs/NFκB signals in the astrocytes following stimulation with thrombin. a Western blot analysis of phosphorylation of ERK, P38, JNK kinase, and p65NFκB protein after astrocyte stimulation with 0–200 nM thrombin for 24 h. b–e Quantification data as shown in a . Quantities were normalized to endogenous β-actin. f Western blot analysis of phosphorylation of ERK, P38, JNK kinase, and p65NFκB protein after astrocyte treatment with 0–5 μM SCH79797 for 24 h in the presence of 100 nM thrombin. g–j Quantification data as shown in f . Quantities were normalized to endogenous β-actin. Experiments were performed in triplicates. Error bars represent the SEM (* P < 0.05)

Techniques Used: Activation Assay, Western Blot

Effects of PAR1 inhibition on the production of MIF following rat SCI. a Western blot analysis of MIF from 1 cm cord segments following injection of 4.5 μl of 5 mM PAR1 inhibitor SCH79797 or vehicle at lesion sites of the contused cord at 0, 1, 4, and 7d, respectively. b Quantification data as shown in a . Quantities were normalized to endogenous β-actin. Experiments were performed in triplicates. Error bars represent the SEM, * P < 0.05, # P < 0.05, two-way ANOVA with Tukey’s test. c–h Immunostaining for MIF expressed in S100β-positive astrocytes at 4d following SCH79797 treatment on the injured cord. Arrowheads indicate the positive signals. Scale bars, 500 μm in c , e , and g ; 50 μm in d , f , and h

Figure Legend Snippet: Effects of PAR1 inhibition on the production of MIF following rat SCI. a Western blot analysis of MIF from 1 cm cord segments following injection of 4.5 μl of 5 mM PAR1 inhibitor SCH79797 or vehicle at lesion sites of the contused cord at 0, 1, 4, and 7d, respectively. b Quantification data as shown in a . Quantities were normalized to endogenous β-actin. Experiments were performed in triplicates. Error bars represent the SEM, * P < 0.05, # P < 0.05, two-way ANOVA with Tukey’s test. c–h Immunostaining for MIF expressed in S100β-positive astrocytes at 4d following SCH79797 treatment on the injured cord. Arrowheads indicate the positive signals. Scale bars, 500 μm in c , e , and g ; 50 μm in d , f , and h

Techniques Used: Inhibition, Western Blot, Injection, Immunostaining

Effects of PAR1 inhibition on the recovery of motor function following rat SCI. a HE staining of the injured spinal cord at 21 d after injection of 4.5 μl of 5 mM PAR1 inhibitor SCH79797 or vehicle at lesion sites. b Quantification data as shown in a from eight animals each 3 sections. Lesion area was analyzed within 2000 μm either side of the lesion center based on the HE-negative proportion. c BBB score of hindlimbs analyzed two-way repeated measures ANOVA followed by Sidak's post hoc test at 0d, 7d, 14d, and 21d following intrathecal injection of 4.5 μl of 5 mM PAR1 inhibitor SCH79797 or vehicle at lesion sites. Error bars represent the SEM (* P < 0.05). Scale bars 1000 μm

Figure Legend Snippet: Effects of PAR1 inhibition on the recovery of motor function following rat SCI. a HE staining of the injured spinal cord at 21 d after injection of 4.5 μl of 5 mM PAR1 inhibitor SCH79797 or vehicle at lesion sites. b Quantification data as shown in a from eight animals each 3 sections. Lesion area was analyzed within 2000 μm either side of the lesion center based on the HE-negative proportion. c BBB score of hindlimbs analyzed two-way repeated measures ANOVA followed by Sidak's post hoc test at 0d, 7d, 14d, and 21d following intrathecal injection of 4.5 μl of 5 mM PAR1 inhibitor SCH79797 or vehicle at lesion sites. Error bars represent the SEM (* P < 0.05). Scale bars 1000 μm

Techniques Used: Inhibition, Staining, Injection

Injection:

Article Title: Thrombin acts as inducer of proinflammatory macrophage migration inhibitory factor in astrocytes following rat spinal cord injury
Article Snippet: .. For drug delivery, a total of 4.5 μl of 5 mM PAR1 inhibitor SCH79797 (R&D systems) was slowly injected intrathecally, prior to the incision suture. ..

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Journal: Journal of Neuroinflammation

Article Title: Thrombin acts as inducer of proinflammatory macrophage migration inhibitory factor in astrocytes following rat spinal cord injury

doi: 10.1186/s12974-022-02488-w

Figure Lengend Snippet: Determination of thrombin, PARs, and MIF expression at lesion sites following rat SCI. a ELISA measurement of thrombin protein levels at lesion sites following SCI at 0, 1, 4, and 7d. b Western blot analysis of MIF following SCI at 0, 1, 4, and 7d. Quantities were normalized to endogenous β-actin. c PCR assay for determining the expression abundance of par1 , par3, and par4 in the intact spinal cord. Quantities were normalized to endogenous gapdh . d–f RT-PCR assays of par1 ( d ), par3 ( e ), and par4 ( f ) transcriptional changes following SCI at 0, 1, 4, and 7d, respectively. Quantities were normalized to endogenous gapdh . Experiments were performed at least in technical triplicates. The values shown in the figures were the average of each technical replicate. Error bars represent the SEM (* P < 0.05). g Colocalization of PAR1 with GFAP-positive astrocytes before and after SCI. The sections were prepared using a cryostat from 0.25 cm length to the lesion epicenter. Rectangle indicates region magnified. Arrowheads indicate the positive signals. Scale bars, 500 μm, and 50 μm in magnification

Article Snippet: For drug delivery, a total of 4.5 μl of 5 mM PAR1 inhibitor SCH79797 (R&D systems) was slowly injected intrathecally, prior to the incision suture.

Techniques: Expressing, Enzyme-linked Immunosorbent Assay, Western Blot, Reverse Transcription Polymerase Chain Reaction

Journal: Journal of Neuroinflammation

Article Title: Thrombin acts as inducer of proinflammatory macrophage migration inhibitory factor in astrocytes following rat spinal cord injury

doi: 10.1186/s12974-022-02488-w

Figure Lengend Snippet: Functional annotation of DEGs following astrocyte stimulation with thrombin. a Primary cultured rat spinal cord astrocytes stained with GFAP and Hoechst 33,342 with purity over 95%. b PCR assay for determining the abundance of par1 , par3, and par4 at transcriptional levels in the primary astrocytes. Quantities were normalized to endogenous gapdh . c Bar graphs of DEGs following astrocyte stimulation with 100 nM thrombin for 6, 12, and 24 h, respectively. d Integration of DEGs at 6, 12, and 24 h. e GO analysis of the DEGs relating to biological processes. Scale bar, 50 μm in a

Article Snippet: For drug delivery, a total of 4.5 μl of 5 mM PAR1 inhibitor SCH79797 (R&D systems) was slowly injected intrathecally, prior to the incision suture.

Techniques: Functional Assay, Cell Culture, Staining

Journal: Journal of Neuroinflammation

Article Title: Thrombin acts as inducer of proinflammatory macrophage migration inhibitory factor in astrocytes following rat spinal cord injury

doi: 10.1186/s12974-022-02488-w

Figure Lengend Snippet: Effects of interfering PAR1, PAR3, or PAR4 expression on the thrombin-induced MIF production of astrocytes. a Western blot analysis of MIF protein levels in the astrocytes treated by 0–5 μM PAR1 inhibitor SCH79797 for 24 h in the presence of 100 nM thrombin. b Quantification data as shown in a . Quantities were normalized to endogenous β-actin. c MTT assay of SCH79797 effects on the cell viability of the astrocytes. d Interference efficiency of siRNA oligonucleotide for PAR3 was measured by RT-PCR, and siRNA1 was used for the knockdown experiments. e Western blot analysis of MIF in the astrocytes following PAR3 knockdown for 24 h, prior to stimulation with 100 nM thrombin for 24 h. Scrambles were used as control. f Quantification data as shown in e . Quantities were normalized to endogenous β-actin. (g) Western blot analysis of MIF protein levels in the astrocytes treated by 0–100 μM PAR4 inhibitor tcy-NH 2 for 24 h in the presence of 100 nM thrombin. h Quantification data as shown in g . Quantities were normalized to endogenous β-actin. i MTT assay of tcy-NH 2 effects on the cell viability of the astrocytes. Experiments were performed in triplicates. Error bars represent the SEM (* P < 0.05)

Article Snippet: For drug delivery, a total of 4.5 μl of 5 mM PAR1 inhibitor SCH79797 (R&D systems) was slowly injected intrathecally, prior to the incision suture.

Techniques: Expressing, Western Blot, MTT Assay, Reverse Transcription Polymerase Chain Reaction

Journal: Journal of Neuroinflammation

Article Title: Thrombin acts as inducer of proinflammatory macrophage migration inhibitory factor in astrocytes following rat spinal cord injury

doi: 10.1186/s12974-022-02488-w

Figure Lengend Snippet: Determination of the phosphorylated activation of the MAPKs/NFκB signals in the astrocytes following stimulation with thrombin. a Western blot analysis of phosphorylation of ERK, P38, JNK kinase, and p65NFκB protein after astrocyte stimulation with 0–200 nM thrombin for 24 h. b–e Quantification data as shown in a . Quantities were normalized to endogenous β-actin. f Western blot analysis of phosphorylation of ERK, P38, JNK kinase, and p65NFκB protein after astrocyte treatment with 0–5 μM SCH79797 for 24 h in the presence of 100 nM thrombin. g–j Quantification data as shown in f . Quantities were normalized to endogenous β-actin. Experiments were performed in triplicates. Error bars represent the SEM (* P < 0.05)

Article Snippet: For drug delivery, a total of 4.5 μl of 5 mM PAR1 inhibitor SCH79797 (R&D systems) was slowly injected intrathecally, prior to the incision suture.

Techniques: Activation Assay, Western Blot

Journal: Journal of Neuroinflammation

Article Title: Thrombin acts as inducer of proinflammatory macrophage migration inhibitory factor in astrocytes following rat spinal cord injury

doi: 10.1186/s12974-022-02488-w

Figure Lengend Snippet: Effects of PAR1 inhibition on the production of MIF following rat SCI. a Western blot analysis of MIF from 1 cm cord segments following injection of 4.5 μl of 5 mM PAR1 inhibitor SCH79797 or vehicle at lesion sites of the contused cord at 0, 1, 4, and 7d, respectively. b Quantification data as shown in a . Quantities were normalized to endogenous β-actin. Experiments were performed in triplicates. Error bars represent the SEM, * P < 0.05, # P < 0.05, two-way ANOVA with Tukey’s test. c–h Immunostaining for MIF expressed in S100β-positive astrocytes at 4d following SCH79797 treatment on the injured cord. Arrowheads indicate the positive signals. Scale bars, 500 μm in c , e , and g ; 50 μm in d , f , and h

Article Snippet: For drug delivery, a total of 4.5 μl of 5 mM PAR1 inhibitor SCH79797 (R&D systems) was slowly injected intrathecally, prior to the incision suture.

Techniques: Inhibition, Western Blot, Injection, Immunostaining

Journal: Journal of Neuroinflammation

Article Title: Thrombin acts as inducer of proinflammatory macrophage migration inhibitory factor in astrocytes following rat spinal cord injury

doi: 10.1186/s12974-022-02488-w

Figure Lengend Snippet: Effects of PAR1 inhibition on the recovery of motor function following rat SCI. a HE staining of the injured spinal cord at 21 d after injection of 4.5 μl of 5 mM PAR1 inhibitor SCH79797 or vehicle at lesion sites. b Quantification data as shown in a from eight animals each 3 sections. Lesion area was analyzed within 2000 μm either side of the lesion center based on the HE-negative proportion. c BBB score of hindlimbs analyzed two-way repeated measures ANOVA followed by Sidak's post hoc test at 0d, 7d, 14d, and 21d following intrathecal injection of 4.5 μl of 5 mM PAR1 inhibitor SCH79797 or vehicle at lesion sites. Error bars represent the SEM (* P < 0.05). Scale bars 1000 μm

Article Snippet: For drug delivery, a total of 4.5 μl of 5 mM PAR1 inhibitor SCH79797 (R&D systems) was slowly injected intrathecally, prior to the incision suture.

Techniques: Inhibition, Staining, Injection

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5 mm par1 inhibitor sch79797 (R&D Systems)

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