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LF-PVA@Pro NPs alleviate CRS-induced neuropathological damage and restore neuronal activity and neurotransmitter-related signaling in the VTA and NAc. ( A ) Representative H&E staining images of the ventral tegmental area and nucleus accumbens from the control, CRS, free-propofol, PVA@Pro NPs and LF-PVA@Pro NPs groups. Boxed regions are shown at higher magnification. ( B ) Quantification of histopathological injury scores in the VTA and NAc. ( C ) Representative Nissl-staining images of the VTA and NAc in the indicated groups, with enlarged views of the selected regions. ( D) Quantification of morphologically normal Nissl-positive neurons in the VTA and NAc. ( E ) Representative immunofluorescence images of c-Fos&GABA and c-Fos&DAT staining in the VTA. Nuclei were <t>counterstained</t> with <t>DAPI.</t> ( F ) Quantification of c-Fos and GABA fluorescence intensities in the VTA. ( G ) Quantification of c-Fos and DAT fluorescence intensities in the VTA. ( H ) Representative immunofluorescence images of c-Fos&GABA and c-Fos&DAT staining in the NAc. ( I ) Quantification of c-Fos and GABA fluorescence intensities in the NAc. ( J ) Quantification of c-Fos and DAT fluorescence intensities in the NAc. CRS exposure caused marked histopathological injury, loss of Nissl-positive neurons, and reductions in c-Fos-, GABA-, and DAT-associated fluorescence signals in the VTA and NAc. LF-PVA@Pro NPs treatment attenuated tissue injury and produced greater recovery of neuronal integrity and functional marker expression than free propofol. Data are presented as the mean ± SD (n=3). *p <0.05, p <0.01, ***p <0.001 , and ****p <0.0001 ; ns, not significant.
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LF-PVA@Pro NPs alleviate CRS-induced neuropathological damage and restore neuronal activity and neurotransmitter-related signaling in the VTA and NAc. ( A ) Representative H&E staining images of the ventral tegmental area and nucleus accumbens from the control, CRS, free-propofol, PVA@Pro NPs and LF-PVA@Pro NPs groups. Boxed regions are shown at higher magnification. ( B ) Quantification of histopathological injury scores in the VTA and NAc. ( C ) Representative Nissl-staining images of the VTA and NAc in the indicated groups, with enlarged views of the selected regions. ( D) Quantification of morphologically normal Nissl-positive neurons in the VTA and NAc. ( E ) Representative immunofluorescence images of c-Fos&GABA and c-Fos&DAT staining in the VTA. Nuclei were <t>counterstained</t> with <t>DAPI.</t> ( F ) Quantification of c-Fos and GABA fluorescence intensities in the VTA. ( G ) Quantification of c-Fos and DAT fluorescence intensities in the VTA. ( H ) Representative immunofluorescence images of c-Fos&GABA and c-Fos&DAT staining in the NAc. ( I ) Quantification of c-Fos and GABA fluorescence intensities in the NAc. ( J ) Quantification of c-Fos and DAT fluorescence intensities in the NAc. CRS exposure caused marked histopathological injury, loss of Nissl-positive neurons, and reductions in c-Fos-, GABA-, and DAT-associated fluorescence signals in the VTA and NAc. LF-PVA@Pro NPs treatment attenuated tissue injury and produced greater recovery of neuronal integrity and functional marker expression than free propofol. Data are presented as the mean ± SD (n=3). *p <0.05, p <0.01, ***p <0.001 , and ****p <0.0001 ; ns, not significant.
Sybr Green Nucleic Acid Gel Stain Tsingke Biotech N A One Step Tunel Apoptosis Assay Kit Beyotime C1086 Dapi, supplied by Beyotime, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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LF-PVA@Pro NPs alleviate CRS-induced neuropathological damage and restore neuronal activity and neurotransmitter-related signaling in the VTA and NAc. ( A ) Representative H&E staining images of the ventral tegmental area and nucleus accumbens from the control, CRS, free-propofol, PVA@Pro NPs and LF-PVA@Pro NPs groups. Boxed regions are shown at higher magnification. ( B ) Quantification of histopathological injury scores in the VTA and NAc. ( C ) Representative Nissl-staining images of the VTA and NAc in the indicated groups, with enlarged views of the selected regions. ( D) Quantification of morphologically normal Nissl-positive neurons in the VTA and NAc. ( E ) Representative immunofluorescence images of c-Fos&GABA and c-Fos&DAT staining in the VTA. Nuclei were <t>counterstained</t> with <t>DAPI.</t> ( F ) Quantification of c-Fos and GABA fluorescence intensities in the VTA. ( G ) Quantification of c-Fos and DAT fluorescence intensities in the VTA. ( H ) Representative immunofluorescence images of c-Fos&GABA and c-Fos&DAT staining in the NAc. ( I ) Quantification of c-Fos and GABA fluorescence intensities in the NAc. ( J ) Quantification of c-Fos and DAT fluorescence intensities in the NAc. CRS exposure caused marked histopathological injury, loss of Nissl-positive neurons, and reductions in c-Fos-, GABA-, and DAT-associated fluorescence signals in the VTA and NAc. LF-PVA@Pro NPs treatment attenuated tissue injury and produced greater recovery of neuronal integrity and functional marker expression than free propofol. Data are presented as the mean ± SD (n=3). *p <0.05, p <0.01, ***p <0.001 , and ****p <0.0001 ; ns, not significant.
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LF-PVA@Pro NPs alleviate CRS-induced neuropathological damage and restore neuronal activity and neurotransmitter-related signaling in the VTA and NAc. ( A ) Representative H&E staining images of the ventral tegmental area and nucleus accumbens from the control, CRS, free-propofol, PVA@Pro NPs and LF-PVA@Pro NPs groups. Boxed regions are shown at higher magnification. ( B ) Quantification of histopathological injury scores in the VTA and NAc. ( C ) Representative Nissl-staining images of the VTA and NAc in the indicated groups, with enlarged views of the selected regions. ( D) Quantification of morphologically normal Nissl-positive neurons in the VTA and NAc. ( E ) Representative immunofluorescence images of c-Fos&GABA and c-Fos&DAT staining in the VTA. Nuclei were <t>counterstained</t> with <t>DAPI.</t> ( F ) Quantification of c-Fos and GABA fluorescence intensities in the VTA. ( G ) Quantification of c-Fos and DAT fluorescence intensities in the VTA. ( H ) Representative immunofluorescence images of c-Fos&GABA and c-Fos&DAT staining in the NAc. ( I ) Quantification of c-Fos and GABA fluorescence intensities in the NAc. ( J ) Quantification of c-Fos and DAT fluorescence intensities in the NAc. CRS exposure caused marked histopathological injury, loss of Nissl-positive neurons, and reductions in c-Fos-, GABA-, and DAT-associated fluorescence signals in the VTA and NAc. LF-PVA@Pro NPs treatment attenuated tissue injury and produced greater recovery of neuronal integrity and functional marker expression than free propofol. Data are presented as the mean ± SD (n=3). *p <0.05, p <0.01, ***p <0.001 , and ****p <0.0001 ; ns, not significant.
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Effects of GSK’872 on pain behaviours and spinal neuroinflammation in LRP rats. (A, B) GSK’872 significantly improved MWT and TWL in LRP rats (n = 9 rats/group). Data are presented as mean ± SEM. Two-way repeated-measures ANOVA was performed, followed by Tukey’s post hoc test (* p < 0.05 vs. sham group; # p < 0.05 vs. vehicle group). (C) Representative western blots showing the protein expression of RIP3 and MLKL (n = 4 rats/group). (F) Representative Western blots showing protein expression of IL-1β, IL-6, AND TNF-α (n = 3 rats/group). (J) Representative images of PI staining for necrotic cells (red) (n = 3 rats/group); scale bars: 100 µm. (D, E, G-I, K) Quantitative analyses of protein levels of RIP3 (D) , MLKL (E) , IL-1β (G) , IL-6 (H) , and TNF-α (I) , as well as PI-positive cell number (K) . Data are presented as mean ± SEM. Statistical comparisons were performed using one-way ANOVA followed by Tukey’s post hoc test (* p < 0.05 vs. sham group; # p < 0.05 vs. vehicle group). Abbreviations: IL-1β, interleukin-1β; IL-6, interleukin-6; LRP, lumbar radicular pain; MLKL, mixed lineage kinase domain-like protein; MWT, mechanical withdrawal threshold; PI, propidium iodide; RIP3, receptor-interacting protein kinase 3; DAPI, <t>4’,6-Diamidino-2-phenylindole;</t> TNF-α, tumor necrosis factor-α; TWL, thermal withdrawal latency.
4 6 Diamidino 2 Phenylindole, supplied by Boster Bio, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Effects of GSK’872 on pain behaviours and spinal neuroinflammation in LRP rats. (A, B) GSK’872 significantly improved MWT and TWL in LRP rats (n = 9 rats/group). Data are presented as mean ± SEM. Two-way repeated-measures ANOVA was performed, followed by Tukey’s post hoc test (* p < 0.05 vs. sham group; # p < 0.05 vs. vehicle group). (C) Representative western blots showing the protein expression of RIP3 and MLKL (n = 4 rats/group). (F) Representative Western blots showing protein expression of IL-1β, IL-6, AND TNF-α (n = 3 rats/group). (J) Representative images of PI staining for necrotic cells (red) (n = 3 rats/group); scale bars: 100 µm. (D, E, G-I, K) Quantitative analyses of protein levels of RIP3 (D) , MLKL (E) , IL-1β (G) , IL-6 (H) , and TNF-α (I) , as well as PI-positive cell number (K) . Data are presented as mean ± SEM. Statistical comparisons were performed using one-way ANOVA followed by Tukey’s post hoc test (* p < 0.05 vs. sham group; # p < 0.05 vs. vehicle group). Abbreviations: IL-1β, interleukin-1β; IL-6, interleukin-6; LRP, lumbar radicular pain; MLKL, mixed lineage kinase domain-like protein; MWT, mechanical withdrawal threshold; PI, propidium iodide; RIP3, receptor-interacting protein kinase 3; DAPI, <t>4’,6-Diamidino-2-phenylindole;</t> TNF-α, tumor necrosis factor-α; TWL, thermal withdrawal latency.
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Effects of GSK’872 on pain behaviours and spinal neuroinflammation in LRP rats. (A, B) GSK’872 significantly improved MWT and TWL in LRP rats (n = 9 rats/group). Data are presented as mean ± SEM. Two-way repeated-measures ANOVA was performed, followed by Tukey’s post hoc test (* p < 0.05 vs. sham group; # p < 0.05 vs. vehicle group). (C) Representative western blots showing the protein expression of RIP3 and MLKL (n = 4 rats/group). (F) Representative Western blots showing protein expression of IL-1β, IL-6, AND TNF-α (n = 3 rats/group). (J) Representative images of PI staining for necrotic cells (red) (n = 3 rats/group); scale bars: 100 µm. (D, E, G-I, K) Quantitative analyses of protein levels of RIP3 (D) , MLKL (E) , IL-1β (G) , IL-6 (H) , and TNF-α (I) , as well as PI-positive cell number (K) . Data are presented as mean ± SEM. Statistical comparisons were performed using one-way ANOVA followed by Tukey’s post hoc test (* p < 0.05 vs. sham group; # p < 0.05 vs. vehicle group). Abbreviations: IL-1β, interleukin-1β; IL-6, interleukin-6; LRP, lumbar radicular pain; MLKL, mixed lineage kinase domain-like protein; MWT, mechanical withdrawal threshold; PI, propidium iodide; RIP3, receptor-interacting protein kinase 3; DAPI, <t>4’,6-Diamidino-2-phenylindole;</t> TNF-α, tumor necrosis factor-α; TWL, thermal withdrawal latency.
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Effects of GSK’872 on pain behaviours and spinal neuroinflammation in LRP rats. (A, B) GSK’872 significantly improved MWT and TWL in LRP rats (n = 9 rats/group). Data are presented as mean ± SEM. Two-way repeated-measures ANOVA was performed, followed by Tukey’s post hoc test (* p < 0.05 vs. sham group; # p < 0.05 vs. vehicle group). (C) Representative western blots showing the protein expression of RIP3 and MLKL (n = 4 rats/group). (F) Representative Western blots showing protein expression of IL-1β, IL-6, AND TNF-α (n = 3 rats/group). (J) Representative images of PI staining for necrotic cells (red) (n = 3 rats/group); scale bars: 100 µm. (D, E, G-I, K) Quantitative analyses of protein levels of RIP3 (D) , MLKL (E) , IL-1β (G) , IL-6 (H) , and TNF-α (I) , as well as PI-positive cell number (K) . Data are presented as mean ± SEM. Statistical comparisons were performed using one-way ANOVA followed by Tukey’s post hoc test (* p < 0.05 vs. sham group; # p < 0.05 vs. vehicle group). Abbreviations: IL-1β, interleukin-1β; IL-6, interleukin-6; LRP, lumbar radicular pain; MLKL, mixed lineage kinase domain-like protein; MWT, mechanical withdrawal threshold; PI, propidium iodide; RIP3, receptor-interacting protein kinase 3; DAPI, <t>4’,6-Diamidino-2-phenylindole;</t> TNF-α, tumor necrosis factor-α; TWL, thermal withdrawal latency.
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Image Search Results


LF-PVA@Pro NPs alleviate CRS-induced neuropathological damage and restore neuronal activity and neurotransmitter-related signaling in the VTA and NAc. ( A ) Representative H&E staining images of the ventral tegmental area and nucleus accumbens from the control, CRS, free-propofol, PVA@Pro NPs and LF-PVA@Pro NPs groups. Boxed regions are shown at higher magnification. ( B ) Quantification of histopathological injury scores in the VTA and NAc. ( C ) Representative Nissl-staining images of the VTA and NAc in the indicated groups, with enlarged views of the selected regions. ( D) Quantification of morphologically normal Nissl-positive neurons in the VTA and NAc. ( E ) Representative immunofluorescence images of c-Fos&GABA and c-Fos&DAT staining in the VTA. Nuclei were counterstained with DAPI. ( F ) Quantification of c-Fos and GABA fluorescence intensities in the VTA. ( G ) Quantification of c-Fos and DAT fluorescence intensities in the VTA. ( H ) Representative immunofluorescence images of c-Fos&GABA and c-Fos&DAT staining in the NAc. ( I ) Quantification of c-Fos and GABA fluorescence intensities in the NAc. ( J ) Quantification of c-Fos and DAT fluorescence intensities in the NAc. CRS exposure caused marked histopathological injury, loss of Nissl-positive neurons, and reductions in c-Fos-, GABA-, and DAT-associated fluorescence signals in the VTA and NAc. LF-PVA@Pro NPs treatment attenuated tissue injury and produced greater recovery of neuronal integrity and functional marker expression than free propofol. Data are presented as the mean ± SD (n=3). *p <0.05, p <0.01, ***p <0.001 , and ****p <0.0001 ; ns, not significant.

Journal: International Journal of Nanomedicine

Article Title: Lactoferrin-Modified Ultra-Sustained Release Propofol Nanoparticles for Multi-Pathway Therapy of Depression via Intraperitoneal Injection

doi: 10.2147/IJN.S645818

Figure Lengend Snippet: LF-PVA@Pro NPs alleviate CRS-induced neuropathological damage and restore neuronal activity and neurotransmitter-related signaling in the VTA and NAc. ( A ) Representative H&E staining images of the ventral tegmental area and nucleus accumbens from the control, CRS, free-propofol, PVA@Pro NPs and LF-PVA@Pro NPs groups. Boxed regions are shown at higher magnification. ( B ) Quantification of histopathological injury scores in the VTA and NAc. ( C ) Representative Nissl-staining images of the VTA and NAc in the indicated groups, with enlarged views of the selected regions. ( D) Quantification of morphologically normal Nissl-positive neurons in the VTA and NAc. ( E ) Representative immunofluorescence images of c-Fos&GABA and c-Fos&DAT staining in the VTA. Nuclei were counterstained with DAPI. ( F ) Quantification of c-Fos and GABA fluorescence intensities in the VTA. ( G ) Quantification of c-Fos and DAT fluorescence intensities in the VTA. ( H ) Representative immunofluorescence images of c-Fos&GABA and c-Fos&DAT staining in the NAc. ( I ) Quantification of c-Fos and GABA fluorescence intensities in the NAc. ( J ) Quantification of c-Fos and DAT fluorescence intensities in the NAc. CRS exposure caused marked histopathological injury, loss of Nissl-positive neurons, and reductions in c-Fos-, GABA-, and DAT-associated fluorescence signals in the VTA and NAc. LF-PVA@Pro NPs treatment attenuated tissue injury and produced greater recovery of neuronal integrity and functional marker expression than free propofol. Data are presented as the mean ± SD (n=3). *p <0.05, p <0.01, ***p <0.001 , and ****p <0.0001 ; ns, not significant.

Article Snippet: The sections were subsequently counterstained with DAPI staining solution (Boster Biological Technology Co., Ltd.) for 15 min.

Techniques: Activity Assay, Staining, Control, Immunofluorescence, Fluorescence, Tissue, Produced, Functional Assay, Marker, Expressing

Effects of GSK’872 on pain behaviours and spinal neuroinflammation in LRP rats. (A, B) GSK’872 significantly improved MWT and TWL in LRP rats (n = 9 rats/group). Data are presented as mean ± SEM. Two-way repeated-measures ANOVA was performed, followed by Tukey’s post hoc test (* p < 0.05 vs. sham group; # p < 0.05 vs. vehicle group). (C) Representative western blots showing the protein expression of RIP3 and MLKL (n = 4 rats/group). (F) Representative Western blots showing protein expression of IL-1β, IL-6, AND TNF-α (n = 3 rats/group). (J) Representative images of PI staining for necrotic cells (red) (n = 3 rats/group); scale bars: 100 µm. (D, E, G-I, K) Quantitative analyses of protein levels of RIP3 (D) , MLKL (E) , IL-1β (G) , IL-6 (H) , and TNF-α (I) , as well as PI-positive cell number (K) . Data are presented as mean ± SEM. Statistical comparisons were performed using one-way ANOVA followed by Tukey’s post hoc test (* p < 0.05 vs. sham group; # p < 0.05 vs. vehicle group). Abbreviations: IL-1β, interleukin-1β; IL-6, interleukin-6; LRP, lumbar radicular pain; MLKL, mixed lineage kinase domain-like protein; MWT, mechanical withdrawal threshold; PI, propidium iodide; RIP3, receptor-interacting protein kinase 3; DAPI, 4’,6-Diamidino-2-phenylindole; TNF-α, tumor necrosis factor-α; TWL, thermal withdrawal latency.

Journal: Frontiers in Pharmacology

Article Title: Protectin DX alleviates lumbar radicular pain in rats by suppressing RIP3/MLKL-associated necroinflammation through restoration of autophagic function

doi: 10.3389/fphar.2026.1957244

Figure Lengend Snippet: Effects of GSK’872 on pain behaviours and spinal neuroinflammation in LRP rats. (A, B) GSK’872 significantly improved MWT and TWL in LRP rats (n = 9 rats/group). Data are presented as mean ± SEM. Two-way repeated-measures ANOVA was performed, followed by Tukey’s post hoc test (* p < 0.05 vs. sham group; # p < 0.05 vs. vehicle group). (C) Representative western blots showing the protein expression of RIP3 and MLKL (n = 4 rats/group). (F) Representative Western blots showing protein expression of IL-1β, IL-6, AND TNF-α (n = 3 rats/group). (J) Representative images of PI staining for necrotic cells (red) (n = 3 rats/group); scale bars: 100 µm. (D, E, G-I, K) Quantitative analyses of protein levels of RIP3 (D) , MLKL (E) , IL-1β (G) , IL-6 (H) , and TNF-α (I) , as well as PI-positive cell number (K) . Data are presented as mean ± SEM. Statistical comparisons were performed using one-way ANOVA followed by Tukey’s post hoc test (* p < 0.05 vs. sham group; # p < 0.05 vs. vehicle group). Abbreviations: IL-1β, interleukin-1β; IL-6, interleukin-6; LRP, lumbar radicular pain; MLKL, mixed lineage kinase domain-like protein; MWT, mechanical withdrawal threshold; PI, propidium iodide; RIP3, receptor-interacting protein kinase 3; DAPI, 4’,6-Diamidino-2-phenylindole; TNF-α, tumor necrosis factor-α; TWL, thermal withdrawal latency.

Article Snippet: Cryosections (10 μm) were prepared, washed with phosphate-buffered saline (PBS), and counterstained with 4′,6-diamidino-2-phenylindole (DAPI; Boster, China) for 5 min at room temperature.

Techniques: Western Blot, Expressing, Staining

Effects of Protectin DX on pain behaviors and spinal necroinflammation in LRP rats. (A, B) PDX (10ng, 100ng or 200ng) treatment prominently meliorated the 50% MWT and prolonged TWL of LRP rat models (n = 9 rats/group). Data are presented as the mean ± SEM; Two-way ANOVA was used for comparisons among groups followed by Turkey’s multiple comparisons test (*P < 0.05 versus sham group; #P < 0.05 versus vehicle group; & P < 0.05 versus 10ng group). (C, F) Representative western blots showing protein expression of RIP3, MLKL, IL-1β, IL-6, and TNF-α (n = 4 rats/group). (J) Double immunofluorescence staining for MLKL (green) and PI (red) in the lumbar spinal cord on postoperative day 7 ((n = 3 rats/group). scale bars: 100µm. (D, E, G-I, K) Quantitative analyses of protein levels of RIP3 (D) , MLKL (E) , IL-1β (G) , IL-6 (H) , and TNF-α (I) , as well as MLKL/PI double-positive cell numbers (K) . Data are presented as mean ± SEM. Statistical comparisons were performed using one-way ANOVA followed by Tukey’s post hoc test (* p < 0.05 versus sham group; # p < 0.05 versus vehicle group; & p < 0.05 versus 10ng group). Abbreviations: IL-1β, interleukin-1β; IL-6, interleukin-6; LRP, lumbar radicular pain; MLKL, mixed lineage kinase domain-like protein; MWT, mechanical withdrawal threshold; PI, propidium iodide; RIP3, receptor-intracting protein kinase 3; DAPI, 4’ 6-Diamidino-2-phenylindole; TNF-α, tumor necrosis factor-α; TWL, thermal withdrawal latency; Protectin DX, PDX.

Journal: Frontiers in Pharmacology

Article Title: Protectin DX alleviates lumbar radicular pain in rats by suppressing RIP3/MLKL-associated necroinflammation through restoration of autophagic function

doi: 10.3389/fphar.2026.1957244

Figure Lengend Snippet: Effects of Protectin DX on pain behaviors and spinal necroinflammation in LRP rats. (A, B) PDX (10ng, 100ng or 200ng) treatment prominently meliorated the 50% MWT and prolonged TWL of LRP rat models (n = 9 rats/group). Data are presented as the mean ± SEM; Two-way ANOVA was used for comparisons among groups followed by Turkey’s multiple comparisons test (*P < 0.05 versus sham group; #P < 0.05 versus vehicle group; & P < 0.05 versus 10ng group). (C, F) Representative western blots showing protein expression of RIP3, MLKL, IL-1β, IL-6, and TNF-α (n = 4 rats/group). (J) Double immunofluorescence staining for MLKL (green) and PI (red) in the lumbar spinal cord on postoperative day 7 ((n = 3 rats/group). scale bars: 100µm. (D, E, G-I, K) Quantitative analyses of protein levels of RIP3 (D) , MLKL (E) , IL-1β (G) , IL-6 (H) , and TNF-α (I) , as well as MLKL/PI double-positive cell numbers (K) . Data are presented as mean ± SEM. Statistical comparisons were performed using one-way ANOVA followed by Tukey’s post hoc test (* p < 0.05 versus sham group; # p < 0.05 versus vehicle group; & p < 0.05 versus 10ng group). Abbreviations: IL-1β, interleukin-1β; IL-6, interleukin-6; LRP, lumbar radicular pain; MLKL, mixed lineage kinase domain-like protein; MWT, mechanical withdrawal threshold; PI, propidium iodide; RIP3, receptor-intracting protein kinase 3; DAPI, 4’ 6-Diamidino-2-phenylindole; TNF-α, tumor necrosis factor-α; TWL, thermal withdrawal latency; Protectin DX, PDX.

Article Snippet: Cryosections (10 μm) were prepared, washed with phosphate-buffered saline (PBS), and counterstained with 4′,6-diamidino-2-phenylindole (DAPI; Boster, China) for 5 min at room temperature.

Techniques: Western Blot, Expressing, Double Immunofluorescence Staining