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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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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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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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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