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P10 rats underwent right carotid artery ligation, followed by 60 min in 8% O 2 (n=12/group). AZ was administered in a 3-injection regimen (45 mg/kg 2 h after HI; 22.5 mg/kg at 24 h and 48 h after HI; AZ*3); controls received saline (NS) injections at the same time-points. Sensorimotor function was evaluated (on P20, P27, P35) with lateral vibrissae-stimulated forepaw placing (10 trials/side, normal score = 10, a ) and bilateral forepaw grip strength (3 trials/side, expressed as left/right (L/R) forepaw ratio, normal = 1, b ). Animals were euthanized on P35. Right hemisphere damage was evaluated in coronal brain sections by digital morphometry (see ). AZ*3 attenuated contralateral deficits (p<0.0001, <t>Repeated-Measures</t> <t>ANOVA;</t> a, b ), and right cerebral hemisphere damage ( c ; *p<0.025, t-test).
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P10 rats underwent right carotid artery ligation, followed by 60 min in 8% O 2 (n=12/group). AZ was administered in a 3-injection regimen (45 mg/kg 2 h after HI; 22.5 mg/kg at 24 h and 48 h after HI; AZ*3); controls received saline (NS) injections at the same time-points. Sensorimotor function was evaluated (on P20, P27, P35) with lateral vibrissae-stimulated forepaw placing (10 trials/side, normal score = 10, a ) and bilateral forepaw grip strength (3 trials/side, expressed as left/right (L/R) forepaw ratio, normal = 1, b ). Animals were euthanized on P35. Right hemisphere damage was evaluated in coronal brain sections by digital morphometry (see ). AZ*3 attenuated contralateral deficits (p<0.0001, <t>Repeated-Measures</t> <t>ANOVA;</t> a, b ), and right cerebral hemisphere damage ( c ; *p<0.025, t-test).
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P10 rats underwent right carotid artery ligation, followed by 60 min in 8% O 2 (n=12/group). AZ was administered in a 3-injection regimen (45 mg/kg 2 h after HI; 22.5 mg/kg at 24 h and 48 h after HI; AZ*3); controls received saline (NS) injections at the same time-points. Sensorimotor function was evaluated (on P20, P27, P35) with lateral vibrissae-stimulated forepaw placing (10 trials/side, normal score = 10, a ) and bilateral forepaw grip strength (3 trials/side, expressed as left/right (L/R) forepaw ratio, normal = 1, b ). Animals were euthanized on P35. Right hemisphere damage was evaluated in coronal brain sections by digital morphometry (see ). AZ*3 attenuated contralateral deficits (p<0.0001, <t>Repeated-Measures</t> <t>ANOVA;</t> a, b ), and right cerebral hemisphere damage ( c ; *p<0.025, t-test).
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P10 rats underwent right carotid artery ligation, followed by 60 min in 8% O 2 (n=12/group). AZ was administered in a 3-injection regimen (45 mg/kg 2 h after HI; 22.5 mg/kg at 24 h and 48 h after HI; AZ*3); controls received saline (NS) injections at the same time-points. Sensorimotor function was evaluated (on P20, P27, P35) with lateral vibrissae-stimulated forepaw placing (10 trials/side, normal score = 10, a ) and bilateral forepaw grip strength (3 trials/side, expressed as left/right (L/R) forepaw ratio, normal = 1, b ). Animals were euthanized on P35. Right hemisphere damage was evaluated in coronal brain sections by digital morphometry (see ). AZ*3 attenuated contralateral deficits (p<0.0001, <t>Repeated-Measures</t> <t>ANOVA;</t> a, b ), and right cerebral hemisphere damage ( c ; *p<0.025, t-test).
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P10 rats underwent right carotid artery ligation, followed by 60 min in 8% O 2 (n=12/group). AZ was administered in a 3-injection regimen (45 mg/kg 2 h after HI; 22.5 mg/kg at 24 h and 48 h after HI; AZ*3); controls received saline (NS) injections at the same time-points. Sensorimotor function was evaluated (on P20, P27, P35) with lateral vibrissae-stimulated forepaw placing (10 trials/side, normal score = 10, a ) and bilateral forepaw grip strength (3 trials/side, expressed as left/right (L/R) forepaw ratio, normal = 1, b ). Animals were euthanized on P35. Right hemisphere damage was evaluated in coronal brain sections by digital morphometry (see ). AZ*3 attenuated contralateral deficits (p<0.0001, <t>Repeated-Measures</t> <t>ANOVA;</t> a, b ), and right cerebral hemisphere damage ( c ; *p<0.025, t-test).
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P10 rats underwent right carotid artery ligation, followed by 60 min in 8% O 2 (n=12/group). AZ was administered in a 3-injection regimen (45 mg/kg 2 h after HI; 22.5 mg/kg at 24 h and 48 h after HI; AZ*3); controls received saline (NS) injections at the same time-points. Sensorimotor function was evaluated (on P20, P27, P35) with lateral vibrissae-stimulated forepaw placing (10 trials/side, normal score = 10, a ) and bilateral forepaw grip strength (3 trials/side, expressed as left/right (L/R) forepaw ratio, normal = 1, b ). Animals were euthanized on P35. Right hemisphere damage was evaluated in coronal brain sections by digital morphometry (see ). AZ*3 attenuated contralateral deficits (p<0.0001, <t>Repeated-Measures</t> <t>ANOVA;</t> a, b ), and right cerebral hemisphere damage ( c ; *p<0.025, t-test).
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P10 rats underwent right carotid artery ligation, followed by 60 min in 8% O 2 (n=12/group). AZ was administered in a 3-injection regimen (45 mg/kg 2 h after HI; 22.5 mg/kg at 24 h and 48 h after HI; AZ*3); controls received saline (NS) injections at the same time-points. Sensorimotor function was evaluated (on P20, P27, P35) with lateral vibrissae-stimulated forepaw placing (10 trials/side, normal score = 10, a ) and bilateral forepaw grip strength (3 trials/side, expressed as left/right (L/R) forepaw ratio, normal = 1, b ). Animals were euthanized on P35. Right hemisphere damage was evaluated in coronal brain sections by digital morphometry (see ). AZ*3 attenuated contralateral deficits (p<0.0001, <t>Repeated-Measures</t> <t>ANOVA;</t> a, b ), and right cerebral hemisphere damage ( c ; *p<0.025, t-test).
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P10 rats underwent right carotid artery ligation, followed by 60 min in 8% O 2 (n=12/group). AZ was administered in a 3-injection regimen (45 mg/kg 2 h after HI; 22.5 mg/kg at 24 h and 48 h after HI; AZ*3); controls received saline (NS) injections at the same time-points. Sensorimotor function was evaluated (on P20, P27, P35) with lateral vibrissae-stimulated forepaw placing (10 trials/side, normal score = 10, a ) and bilateral forepaw grip strength (3 trials/side, expressed as left/right (L/R) forepaw ratio, normal = 1, b ). Animals were euthanized on P35. Right hemisphere damage was evaluated in coronal brain sections by digital morphometry (see ). AZ*3 attenuated contralateral deficits (p<0.0001, Repeated-Measures ANOVA; a, b ), and right cerebral hemisphere damage ( c ; *p<0.025, t-test).

Journal: Pediatric research

Article Title: Repurposing Azithromycin for Neonatal Neuroprotection

doi: 10.1038/s41390-019-0408-6

Figure Lengend Snippet: P10 rats underwent right carotid artery ligation, followed by 60 min in 8% O 2 (n=12/group). AZ was administered in a 3-injection regimen (45 mg/kg 2 h after HI; 22.5 mg/kg at 24 h and 48 h after HI; AZ*3); controls received saline (NS) injections at the same time-points. Sensorimotor function was evaluated (on P20, P27, P35) with lateral vibrissae-stimulated forepaw placing (10 trials/side, normal score = 10, a ) and bilateral forepaw grip strength (3 trials/side, expressed as left/right (L/R) forepaw ratio, normal = 1, b ). Animals were euthanized on P35. Right hemisphere damage was evaluated in coronal brain sections by digital morphometry (see ). AZ*3 attenuated contralateral deficits (p<0.0001, Repeated-Measures ANOVA; a, b ), and right cerebral hemisphere damage ( c ; *p<0.025, t-test).

Article Snippet: Rectal temperatures and body weights over time were compared among groups by repeated measures ANOVA (Prism 7.00, GraphPad Software, San Diego, CA).

Techniques: Ligation, Injection, Saline