i r dmso group Search Results


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ATCC test group bacteria flavone 3 hydroxyflavone 5 hydroxyflavone 6 hydroxyflavone chloramphenicol dmso p aeruginosa atcc 8027 200 200 200
Test Group Bacteria Flavone 3 Hydroxyflavone 5 Hydroxyflavone 6 Hydroxyflavone Chloramphenicol Dmso P Aeruginosa Atcc 8027 200 200 200, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress reperfusion gsk0660
Reperfusion Gsk0660, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Beijing Solarbio Science dimethyl sulfoxide (dmso)
Dimethyl Sulfoxide (Dmso), supplied by Beijing Solarbio Science, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC streptococcus pyogenes
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PanReac AppliChem ethyl acetate
Ethyl Acetate, supplied by PanReac AppliChem, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Sinopharm ltd dimethyl sulfoxide (dmso)
Dimethyl Sulfoxide (Dmso), supplied by Sinopharm ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Scharlau Group dimethyl sulfoxide (dmso)
Dimethyl Sulfoxide (Dmso), supplied by Scharlau Group, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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R&D Systems 1d11
<t>DMSO</t> promotes the migration of diabetic mouse‐derived primary keratinocytes in an indirect manner mediated by fibroblast‐derived TGF‐β1. (a) Migration of the keratinocytes by transwell assays after treatment with or without 5‐mM DMSO or TGF‐β1 for 24 h. Data are presented as the mean ± SEM with n = 5 for all groups, analysed by one‐way ANOVA with Kruskal–Wallis test for multiple comparison. Significance level: *P < 0.05, compared with the control group. NS, not significant. (b) Representative H&E‐stained sections of wound tissue 8 days after injury. The arrow indicates the length of the migrating epithelial tongue. Data are presented as the mean ± SEM with n = 6 for all groups, analysed by Student's t test. Significance level: *P < 0.05, 5‐mM DMSO versus the control group. Scale bars represent 100 μm; original magnification ×100. (c) Immunofluorescence staining of TGF‐β1 in DMSO‐treated and untreated wound tissue (n = 6). Scale bars represent 50 μm; original magnification ×200. (d) Migration of keratinocytes treated as indicated. MF, cocultured with mouse fibroblasts by a transwell assay; <t>1D11,</t> a TGF‐β1 neutralizing antibody. Data are presented as the mean ± SEM with n = 5 for all groups, analysed by one‐way ANOVA with Kruskal–Wallis test for multiple comparison. Significance level: *P < 0.05, compared with the MF group, (e) western blot of migration‐related proteins in the keratinocytes treated as indicated
1d11, 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
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Avantor rapamycin
Central administration of the ROS H 2 O 2 engages mTORC1 signaling to decrease food intake. ( A ) Acute icv co-administration of the mTORC1 inhibitor <t>rapamycin</t> with H 2 O 2 blunts the effect of H 2 O 2 on food intake (Repeated measures ANOVA: treatment effect F (2,15) = 6.39, P < 0.01; time effect F (3,45) = 141.33, P < 0.0001; treatment × time interaction F (6,45) = 4.59, P < 0.01, n = 5–7 mice per group) and ( B ) 24h body weight (BW) change (One-way ANOVA: treatment effect F (2,15) = 9.37, P < 0.005, n = 5–7 mice per group) in C57BL/6J mice. ( C ) Effect of an acute icv administration of H 2 O 2 on food intake (Repeated measures ANOVA: treatment effect F (1,40) = 7.94, P < 0.01; genotype effect F (1,40) = 11.24, P < 0.005; treatment × genotype interaction F (1,40) = 6.18, P < 0.05; time effect F (3,120) = 892.17, P < 0.0001; treatment x genotype × time interaction F (3,120) = 7.58, P < 0.0005, n = 10–12 mice per group) and ( D ) 24h BW change (two-way ANOVA: treatment effect F (1,40) = 5.71, P < 0.05; genotype effect F (1,40) = 4.37, P < 0.05; treatment × genotype interaction F (1,40) = 9.81, P < 0.005, n = 10–12 mice per group) in WT and S6K1 -KO littermates. Data are mean ± SEM. *P < 0.05, **P < 0.005, ***P < 0.0005.
Rapamycin, supplied by Avantor, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
Tocris tnfr1 antagonist r7050
Antagonism of <t>TNFR1</t> and P2X7R rescues RGCs from systemic inflammation. (A) Isodensity maps showing the distribution of Brn3a + RGCs in retinas of intact male mice and mice treated with LPS+vehicle, LPS and TNFR1 antagonist (αTNFR1), LPS and P2X7R antagonist (αP2X7R), and LPS and αP2X7R + αTNFR1. Retinas were analysed 7 days after the injection of LPS. (B) Column graph showing the mean total number ± SD of Brn3a + RGCs the same groups. *Significant vs. intact (*** p <0.001; **** p <0.0001); σ Significant between groups ( σ p <0.05; σσσ p <0.001; σσσσ p <0.0001). One-way ANOVA within sexes, post-hoc Tukey’s test. (C) Column graph showing the averaged percentage ± SD of Brn3a + RGCs in the same groups as before with respect to intact retinas (100%). *Significant differences between females and males (** p <0.01; *** p <0.001; Two-way ANOVA Šidák’s multiple comparison test (treatment p <0.0001; sex p <0.0001). F: females, M: males. I: intact, V: vehicle.
Tnfr1 Antagonist R7050, supplied by Tocris, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Fisher Bioreagents dimethyl sulfoxide (dmso)
Antagonism of <t>TNFR1</t> and P2X7R rescues RGCs from systemic inflammation. (A) Isodensity maps showing the distribution of Brn3a + RGCs in retinas of intact male mice and mice treated with LPS+vehicle, LPS and TNFR1 antagonist (αTNFR1), LPS and P2X7R antagonist (αP2X7R), and LPS and αP2X7R + αTNFR1. Retinas were analysed 7 days after the injection of LPS. (B) Column graph showing the mean total number ± SD of Brn3a + RGCs the same groups. *Significant vs. intact (*** p <0.001; **** p <0.0001); σ Significant between groups ( σ p <0.05; σσσ p <0.001; σσσσ p <0.0001). One-way ANOVA within sexes, post-hoc Tukey’s test. (C) Column graph showing the averaged percentage ± SD of Brn3a + RGCs in the same groups as before with respect to intact retinas (100%). *Significant differences between females and males (** p <0.01; *** p <0.001; Two-way ANOVA Šidák’s multiple comparison test (treatment p <0.0001; sex p <0.0001). F: females, M: males. I: intact, V: vehicle.
Dimethyl Sulfoxide (Dmso), supplied by Fisher Bioreagents, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Merck & Co dimethyl-sulfoxide (dmso
Antagonism of <t>TNFR1</t> and P2X7R rescues RGCs from systemic inflammation. (A) Isodensity maps showing the distribution of Brn3a + RGCs in retinas of intact male mice and mice treated with LPS+vehicle, LPS and TNFR1 antagonist (αTNFR1), LPS and P2X7R antagonist (αP2X7R), and LPS and αP2X7R + αTNFR1. Retinas were analysed 7 days after the injection of LPS. (B) Column graph showing the mean total number ± SD of Brn3a + RGCs the same groups. *Significant vs. intact (*** p <0.001; **** p <0.0001); σ Significant between groups ( σ p <0.05; σσσ p <0.001; σσσσ p <0.0001). One-way ANOVA within sexes, post-hoc Tukey’s test. (C) Column graph showing the averaged percentage ± SD of Brn3a + RGCs in the same groups as before with respect to intact retinas (100%). *Significant differences between females and males (** p <0.01; *** p <0.001; Two-way ANOVA Šidák’s multiple comparison test (treatment p <0.0001; sex p <0.0001). F: females, M: males. I: intact, V: vehicle.
Dimethyl Sulfoxide (Dmso, supplied by Merck & Co, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


DMSO promotes the migration of diabetic mouse‐derived primary keratinocytes in an indirect manner mediated by fibroblast‐derived TGF‐β1. (a) Migration of the keratinocytes by transwell assays after treatment with or without 5‐mM DMSO or TGF‐β1 for 24 h. Data are presented as the mean ± SEM with n = 5 for all groups, analysed by one‐way ANOVA with Kruskal–Wallis test for multiple comparison. Significance level: *P < 0.05, compared with the control group. NS, not significant. (b) Representative H&E‐stained sections of wound tissue 8 days after injury. The arrow indicates the length of the migrating epithelial tongue. Data are presented as the mean ± SEM with n = 6 for all groups, analysed by Student's t test. Significance level: *P < 0.05, 5‐mM DMSO versus the control group. Scale bars represent 100 μm; original magnification ×100. (c) Immunofluorescence staining of TGF‐β1 in DMSO‐treated and untreated wound tissue (n = 6). Scale bars represent 50 μm; original magnification ×200. (d) Migration of keratinocytes treated as indicated. MF, cocultured with mouse fibroblasts by a transwell assay; 1D11, a TGF‐β1 neutralizing antibody. Data are presented as the mean ± SEM with n = 5 for all groups, analysed by one‐way ANOVA with Kruskal–Wallis test for multiple comparison. Significance level: *P < 0.05, compared with the MF group, (e) western blot of migration‐related proteins in the keratinocytes treated as indicated

Journal: British Journal of Pharmacology

Article Title: Low‐concentration DMSO accelerates skin wound healing by Akt / mTOR ‐mediated cell proliferation and migration in diabetic mice

doi: 10.1111/bph.15052

Figure Lengend Snippet: DMSO promotes the migration of diabetic mouse‐derived primary keratinocytes in an indirect manner mediated by fibroblast‐derived TGF‐β1. (a) Migration of the keratinocytes by transwell assays after treatment with or without 5‐mM DMSO or TGF‐β1 for 24 h. Data are presented as the mean ± SEM with n = 5 for all groups, analysed by one‐way ANOVA with Kruskal–Wallis test for multiple comparison. Significance level: *P < 0.05, compared with the control group. NS, not significant. (b) Representative H&E‐stained sections of wound tissue 8 days after injury. The arrow indicates the length of the migrating epithelial tongue. Data are presented as the mean ± SEM with n = 6 for all groups, analysed by Student's t test. Significance level: *P < 0.05, 5‐mM DMSO versus the control group. Scale bars represent 100 μm; original magnification ×100. (c) Immunofluorescence staining of TGF‐β1 in DMSO‐treated and untreated wound tissue (n = 6). Scale bars represent 50 μm; original magnification ×200. (d) Migration of keratinocytes treated as indicated. MF, cocultured with mouse fibroblasts by a transwell assay; 1D11, a TGF‐β1 neutralizing antibody. Data are presented as the mean ± SEM with n = 5 for all groups, analysed by one‐way ANOVA with Kruskal–Wallis test for multiple comparison. Significance level: *P < 0.05, compared with the MF group, (e) western blot of migration‐related proteins in the keratinocytes treated as indicated

Article Snippet: According to the stimulants added to the medium in the bottom chamber, six experimental groups were established: PBS control, DMSO (5 mM), recombinant mouse TGF‐β1 (5 ng·ml −1 , R&D Systems, Minnesota, USA), mouse fibroblasts (MFs, 4 × 10 5 cells), MF + DMSO and MF + DMSO+1D11 (a TGF‐β1 (TGFBR1) neutralizing antibody, 10 g·ml −1 , R&D Systems, Minnesota, USA).

Techniques: Migration, Derivative Assay, Staining, Immunofluorescence, Transwell Assay, Western Blot

Central administration of the ROS H 2 O 2 engages mTORC1 signaling to decrease food intake. ( A ) Acute icv co-administration of the mTORC1 inhibitor rapamycin with H 2 O 2 blunts the effect of H 2 O 2 on food intake (Repeated measures ANOVA: treatment effect F (2,15) = 6.39, P < 0.01; time effect F (3,45) = 141.33, P < 0.0001; treatment × time interaction F (6,45) = 4.59, P < 0.01, n = 5–7 mice per group) and ( B ) 24h body weight (BW) change (One-way ANOVA: treatment effect F (2,15) = 9.37, P < 0.005, n = 5–7 mice per group) in C57BL/6J mice. ( C ) Effect of an acute icv administration of H 2 O 2 on food intake (Repeated measures ANOVA: treatment effect F (1,40) = 7.94, P < 0.01; genotype effect F (1,40) = 11.24, P < 0.005; treatment × genotype interaction F (1,40) = 6.18, P < 0.05; time effect F (3,120) = 892.17, P < 0.0001; treatment x genotype × time interaction F (3,120) = 7.58, P < 0.0005, n = 10–12 mice per group) and ( D ) 24h BW change (two-way ANOVA: treatment effect F (1,40) = 5.71, P < 0.05; genotype effect F (1,40) = 4.37, P < 0.05; treatment × genotype interaction F (1,40) = 9.81, P < 0.005, n = 10–12 mice per group) in WT and S6K1 -KO littermates. Data are mean ± SEM. *P < 0.05, **P < 0.005, ***P < 0.0005.

Journal: Molecular Metabolism

Article Title: mTORC1-dependent increase in oxidative metabolism in POMC neurons regulates food intake and action of leptin

doi: 10.1016/j.molmet.2018.04.002

Figure Lengend Snippet: Central administration of the ROS H 2 O 2 engages mTORC1 signaling to decrease food intake. ( A ) Acute icv co-administration of the mTORC1 inhibitor rapamycin with H 2 O 2 blunts the effect of H 2 O 2 on food intake (Repeated measures ANOVA: treatment effect F (2,15) = 6.39, P < 0.01; time effect F (3,45) = 141.33, P < 0.0001; treatment × time interaction F (6,45) = 4.59, P < 0.01, n = 5–7 mice per group) and ( B ) 24h body weight (BW) change (One-way ANOVA: treatment effect F (2,15) = 9.37, P < 0.005, n = 5–7 mice per group) in C57BL/6J mice. ( C ) Effect of an acute icv administration of H 2 O 2 on food intake (Repeated measures ANOVA: treatment effect F (1,40) = 7.94, P < 0.01; genotype effect F (1,40) = 11.24, P < 0.005; treatment × genotype interaction F (1,40) = 6.18, P < 0.05; time effect F (3,120) = 892.17, P < 0.0001; treatment x genotype × time interaction F (3,120) = 7.58, P < 0.0005, n = 10–12 mice per group) and ( D ) 24h BW change (two-way ANOVA: treatment effect F (1,40) = 5.71, P < 0.05; genotype effect F (1,40) = 4.37, P < 0.05; treatment × genotype interaction F (1,40) = 9.81, P < 0.005, n = 10–12 mice per group) in WT and S6K1 -KO littermates. Data are mean ± SEM. *P < 0.05, **P < 0.005, ***P < 0.0005.

Article Snippet: To study the effect of a central mTORC1 inhibition on the appetite suppressant action of H 2 O 2 , mice received an acute icv injection of rapamycin [VWR International, France; 18 μg in 1 μL dimethyl sulfoxide (DMSO)], an inhibitor of mTORC1 , or its vehicle just before the dark phase, 40 min after an acute icv injection of H 2 O 2 in 24h fasted C57BL/6J mice.

Techniques:

Antagonism of TNFR1 and P2X7R rescues RGCs from systemic inflammation. (A) Isodensity maps showing the distribution of Brn3a + RGCs in retinas of intact male mice and mice treated with LPS+vehicle, LPS and TNFR1 antagonist (αTNFR1), LPS and P2X7R antagonist (αP2X7R), and LPS and αP2X7R + αTNFR1. Retinas were analysed 7 days after the injection of LPS. (B) Column graph showing the mean total number ± SD of Brn3a + RGCs the same groups. *Significant vs. intact (*** p <0.001; **** p <0.0001); σ Significant between groups ( σ p <0.05; σσσ p <0.001; σσσσ p <0.0001). One-way ANOVA within sexes, post-hoc Tukey’s test. (C) Column graph showing the averaged percentage ± SD of Brn3a + RGCs in the same groups as before with respect to intact retinas (100%). *Significant differences between females and males (** p <0.01; *** p <0.001; Two-way ANOVA Šidák’s multiple comparison test (treatment p <0.0001; sex p <0.0001). F: females, M: males. I: intact, V: vehicle.

Journal: Frontiers in Immunology

Article Title: Retinal response to systemic inflammation differs between sexes and neurons

doi: 10.3389/fimmu.2024.1340013

Figure Lengend Snippet: Antagonism of TNFR1 and P2X7R rescues RGCs from systemic inflammation. (A) Isodensity maps showing the distribution of Brn3a + RGCs in retinas of intact male mice and mice treated with LPS+vehicle, LPS and TNFR1 antagonist (αTNFR1), LPS and P2X7R antagonist (αP2X7R), and LPS and αP2X7R + αTNFR1. Retinas were analysed 7 days after the injection of LPS. (B) Column graph showing the mean total number ± SD of Brn3a + RGCs the same groups. *Significant vs. intact (*** p <0.001; **** p <0.0001); σ Significant between groups ( σ p <0.05; σσσ p <0.001; σσσσ p <0.0001). One-way ANOVA within sexes, post-hoc Tukey’s test. (C) Column graph showing the averaged percentage ± SD of Brn3a + RGCs in the same groups as before with respect to intact retinas (100%). *Significant differences between females and males (** p <0.01; *** p <0.001; Two-way ANOVA Šidák’s multiple comparison test (treatment p <0.0001; sex p <0.0001). F: females, M: males. I: intact, V: vehicle.

Article Snippet: Madrid, Spain] and TNFR1 antagonist [12 mg/kg i.p. in 5% of DMSO-saline; R7050, Tocris Bioscience; Bio-Techne R&D Systems, Madrid, Spain], as previously published , were both injected intraperitoneally in a final volume of 200 μL.

Techniques: Injection, Comparison

Transient impairment of retinal functionality after systemic inflammation: effect of TNFR1 and P2X7R antagonism. (A) Electroretinographic waves from female and male mice recorded before (PRE) and 3 and 7 days after being treated with LPS + vehicle, LPS and TNFR1 antagonist (αTNFR1), LPS and P2X7R antagonist (αP2X7R), and LPS and αP2X7R + αTNFR1. (B) ERG quantification bar graphs showing the mean wave amplitude (µV ± SD). Control amplitudes are baseline recordings (pre). * vs. baseline values (* p <0.05; ** p <0.01***; p <0.001; **** p <0.0001); φ 3 rd vs. 7 th day within the same group ( φφφ p <0.001; φφφφ p <0.0001). σ Between different groups ( σ p <0.05; σσ p <0.01; σσσ p <0.001; σσσσ p <0.0001). † p <0.001 females vs. males at the same time point and treatment. Two-way ANOVA Šidák’s multiple comparison test (treatment p <0.0001; sex p >0.05).

Journal: Frontiers in Immunology

Article Title: Retinal response to systemic inflammation differs between sexes and neurons

doi: 10.3389/fimmu.2024.1340013

Figure Lengend Snippet: Transient impairment of retinal functionality after systemic inflammation: effect of TNFR1 and P2X7R antagonism. (A) Electroretinographic waves from female and male mice recorded before (PRE) and 3 and 7 days after being treated with LPS + vehicle, LPS and TNFR1 antagonist (αTNFR1), LPS and P2X7R antagonist (αP2X7R), and LPS and αP2X7R + αTNFR1. (B) ERG quantification bar graphs showing the mean wave amplitude (µV ± SD). Control amplitudes are baseline recordings (pre). * vs. baseline values (* p <0.05; ** p <0.01***; p <0.001; **** p <0.0001); φ 3 rd vs. 7 th day within the same group ( φφφ p <0.001; φφφφ p <0.0001). σ Between different groups ( σ p <0.05; σσ p <0.01; σσσ p <0.001; σσσσ p <0.0001). † p <0.001 females vs. males at the same time point and treatment. Two-way ANOVA Šidák’s multiple comparison test (treatment p <0.0001; sex p >0.05).

Article Snippet: Madrid, Spain] and TNFR1 antagonist [12 mg/kg i.p. in 5% of DMSO-saline; R7050, Tocris Bioscience; Bio-Techne R&D Systems, Madrid, Spain], as previously published , were both injected intraperitoneally in a final volume of 200 μL.

Techniques: Control, Comparison