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The glial cell inhibitor <t>minocycline</t> and LPA1R antagonist Ki16425 reversed pain behaviors. ( A – C ), ( D – F ) Mechanical allodynia, thermal hyperalgesia, and spontaneous pain behaviors in CVI rats after minocycline administration on Days 7 and 14 post-CVI, respectively. ( G – I ), ( J – L ) Mechanical allodynia, thermal hyperalgesia, and spontaneous pain behaviors in CVI rats after Ki16425 administration on Days 7 and 11 post-CVI, respectively. Drugs were administered via intraganglionic injection into the L4 DRG (i.drg.). * P < 0.05, ** P < 0.01 versus the vehicle group, two-way ANOVA with Bonferroni’s post hoc test. n = 6/group
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The glial cell inhibitor <t>minocycline</t> and LPA1R antagonist Ki16425 reversed pain behaviors. ( A – C ), ( D – F ) Mechanical allodynia, thermal hyperalgesia, and spontaneous pain behaviors in CVI rats after minocycline administration on Days 7 and 14 post-CVI, respectively. ( G – I ), ( J – L ) Mechanical allodynia, thermal hyperalgesia, and spontaneous pain behaviors in CVI rats after Ki16425 administration on Days 7 and 11 post-CVI, respectively. Drugs were administered via intraganglionic injection into the L4 DRG (i.drg.). * P < 0.05, ** P < 0.01 versus the vehicle group, two-way ANOVA with Bonferroni’s post hoc test. n = 6/group
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Average 96 stars, based on 1 article reviews
glial cell line svgp12 - by Bioz Stars, 2026-02
96/100 stars
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The glial cell inhibitor minocycline and LPA1R antagonist Ki16425 reversed pain behaviors. ( A – C ), ( D – F ) Mechanical allodynia, thermal hyperalgesia, and spontaneous pain behaviors in CVI rats after minocycline administration on Days 7 and 14 post-CVI, respectively. ( G – I ), ( J – L ) Mechanical allodynia, thermal hyperalgesia, and spontaneous pain behaviors in CVI rats after Ki16425 administration on Days 7 and 11 post-CVI, respectively. Drugs were administered via intraganglionic injection into the L4 DRG (i.drg.). * P < 0.05, ** P < 0.01 versus the vehicle group, two-way ANOVA with Bonferroni’s post hoc test. n = 6/group

Journal: Journal of Translational Medicine

Article Title: Demyelination-related pain: role of lysophosphatidic acid in satellite glial cell–neuron crosstalk

doi: 10.1186/s12967-025-07568-y

Figure Lengend Snippet: The glial cell inhibitor minocycline and LPA1R antagonist Ki16425 reversed pain behaviors. ( A – C ), ( D – F ) Mechanical allodynia, thermal hyperalgesia, and spontaneous pain behaviors in CVI rats after minocycline administration on Days 7 and 14 post-CVI, respectively. ( G – I ), ( J – L ) Mechanical allodynia, thermal hyperalgesia, and spontaneous pain behaviors in CVI rats after Ki16425 administration on Days 7 and 11 post-CVI, respectively. Drugs were administered via intraganglionic injection into the L4 DRG (i.drg.). * P < 0.05, ** P < 0.01 versus the vehicle group, two-way ANOVA with Bonferroni’s post hoc test. n = 6/group

Article Snippet: The LPA1/3 inhibitor Ki16425, the glial cell inhibitor minocycline, and the gap junction decoupler carbenoxolone (CBX) were purchased from MCE.

Techniques: Injection

The LPA/LPA1R signaling pathway mediated the release of TNF-α and IL-6 from activated SGCs after demyelination. ( A – C ) Protein levels of TNF-α, IL-6, and IL-1β in the DRG of sham, CVI (at day 7), and CVI rats treated with minocycline or Ki16425, respectively. n = 5/group. ( D – F ) mRNA levels of Tnf -α, Il -6, and Il -1β in the DRG of rats from different groups. Results were normalized to those of the sham group. n = 3/group. * P < 0.05, ** P < 0.01, *** P < 0.001 versus the sham group, and # P < 0.05, ## P < 0.01 versus the 7-day demyelination group, one-way ANOVA with Tukey’s post hoc test

Journal: Journal of Translational Medicine

Article Title: Demyelination-related pain: role of lysophosphatidic acid in satellite glial cell–neuron crosstalk

doi: 10.1186/s12967-025-07568-y

Figure Lengend Snippet: The LPA/LPA1R signaling pathway mediated the release of TNF-α and IL-6 from activated SGCs after demyelination. ( A – C ) Protein levels of TNF-α, IL-6, and IL-1β in the DRG of sham, CVI (at day 7), and CVI rats treated with minocycline or Ki16425, respectively. n = 5/group. ( D – F ) mRNA levels of Tnf -α, Il -6, and Il -1β in the DRG of rats from different groups. Results were normalized to those of the sham group. n = 3/group. * P < 0.05, ** P < 0.01, *** P < 0.001 versus the sham group, and # P < 0.05, ## P < 0.01 versus the 7-day demyelination group, one-way ANOVA with Tukey’s post hoc test

Article Snippet: The LPA1/3 inhibitor Ki16425, the glial cell inhibitor minocycline, and the gap junction decoupler carbenoxolone (CBX) were purchased from MCE.

Techniques:

The glial cell inhibitor minocycline reduced C-fiber excitability in the DRG following demyelination. ( A ) Representative responses of C-neurons to mechanical stimulation of their peripheral receptive field with von Frey filaments following ganglionic administration of minocycline at day 7 after CVI. ( B ) Quantification of action potentials (APs) evoked by mechanical stimulation of C-neurons. Data are mean ± S. E. M. ( n = 10/group). * p < 0.05, ** p < 0.01 versus vehicle group, two-way RM ANOVA with Bonferroni’s post hoc test

Journal: Journal of Translational Medicine

Article Title: Demyelination-related pain: role of lysophosphatidic acid in satellite glial cell–neuron crosstalk

doi: 10.1186/s12967-025-07568-y

Figure Lengend Snippet: The glial cell inhibitor minocycline reduced C-fiber excitability in the DRG following demyelination. ( A ) Representative responses of C-neurons to mechanical stimulation of their peripheral receptive field with von Frey filaments following ganglionic administration of minocycline at day 7 after CVI. ( B ) Quantification of action potentials (APs) evoked by mechanical stimulation of C-neurons. Data are mean ± S. E. M. ( n = 10/group). * p < 0.05, ** p < 0.01 versus vehicle group, two-way RM ANOVA with Bonferroni’s post hoc test

Article Snippet: The LPA1/3 inhibitor Ki16425, the glial cell inhibitor minocycline, and the gap junction decoupler carbenoxolone (CBX) were purchased from MCE.

Techniques:

WDR neuronal responses decreased following ganglionic administration of minocycline. ( A ) Experimental setup for in vivo extracellular recording of WDR neurons and drug application to L4-DRG. ( B ) Representative recordings showing WDR neuron responses to high-threshold electrical stimulation (3.0 mA, 2 ms) of the tibial nerve in sham, CVI (at day 7), and minocycline groups. A- and C-fiber components (number of action potentials) were separated based on latency. ( C ) Quantification of C-component responses to electrical stimulation in different groups. Data are mean ± S. E. M. *** p < 0.001 versus sham group; ## p < 0.01 versus 7d group, one-way ANOVA with Dunnett’s post hoc test

Journal: Journal of Translational Medicine

Article Title: Demyelination-related pain: role of lysophosphatidic acid in satellite glial cell–neuron crosstalk

doi: 10.1186/s12967-025-07568-y

Figure Lengend Snippet: WDR neuronal responses decreased following ganglionic administration of minocycline. ( A ) Experimental setup for in vivo extracellular recording of WDR neurons and drug application to L4-DRG. ( B ) Representative recordings showing WDR neuron responses to high-threshold electrical stimulation (3.0 mA, 2 ms) of the tibial nerve in sham, CVI (at day 7), and minocycline groups. A- and C-fiber components (number of action potentials) were separated based on latency. ( C ) Quantification of C-component responses to electrical stimulation in different groups. Data are mean ± S. E. M. *** p < 0.001 versus sham group; ## p < 0.01 versus 7d group, one-way ANOVA with Dunnett’s post hoc test

Article Snippet: The LPA1/3 inhibitor Ki16425, the glial cell inhibitor minocycline, and the gap junction decoupler carbenoxolone (CBX) were purchased from MCE.

Techniques: In Vivo