Journal: Cell & Bioscience

Article Title: Gut microbial metabolite deoxycholic acid facilitates Th17 differentiation through modulating cholesterol biosynthesis and participates in high-fat diet-associated colonic inflammation

doi: 10.1186/s13578-023-01109-0

Figure Lengend Snippet: DCA increases CYP51 expression by targeting transcriptional factor SREBP2. a EL4 cells were stimulated with DCA (100 µM) in the presence or absence of Triamterene (10 μM, TGR5 inhibitor), Z-Guggulsterone (20 μM, FXR inhibitor), JTE-013 (10 μM, S1PR2 inhibitor) or methoctramine (5 µM, M2-mAchR inhibitor). The mRNA expression levels of CYP51 were determined by real-time PCR (n = 3). b EL4 cells were stimulated with DCA (100 µM) in the presence or absence of KG-501 (10 µM) or fatostatin (10 µM). The mRNA expression levels of CYP51 were determined by real-time PCR (n = 3). c Predicted SREBP2 binding site on Cyp51 promoter. Colorful letters were the motif of SREBF2 binding site cited from JASPAR. d EL4 cells were stimulated with or without DCA (100 µM) for 24 h and then ChIP assay was performed. Anti-SREBP2 antibody or isotype-matched IgG control antibody were used. PCR was applied to quantify the precipitated DNA with primers flanking the SREBP2 binding region of the CYP51 promoter. e Representative SREBP2 (red) and DAPI (blue) immunofluorescence staining of EL4 cells untreated or treated with DCA (n = 3). Data are pooled from three independent experiments. Each dot represents one microscopic high power field (HPF); four to five HPFs were scored per experiment and totally at least 300 cells were evaluated. *p < 0.05; **p < 0.01; ****p < 0.0001. n.s.: no statistically significant difference ( p > 0.05). One-way ANOVA with Tukey's multiple comparisons tests (a, b) or two-tailed Student’s t -test with Welch's correction (e: right panel) was used. Data are expressed as mean ± SEM from at least three independent experiments or representative data (d, e: left panel)

Article Snippet: Triamterene, 4-DAMP, ketoconazole, lovastatin, KG-501 and fatostatin were purchased from MedChemexpress (Monmouth Junction, NJ, USA).

Techniques: Expressing, Real-time Polymerase Chain Reaction, Binding Assay, Control, Immunofluorescence, Staining, Two Tailed Test

Journal: Molecular metabolism

Article Title: PACAP attenuates hepatic lipid accumulation through the FAIM/AMPK/IRβ axis during overnutrition.

doi: 10.1016/j.molmet.2022.101584

Figure Lengend Snippet: Figure 4: FAIM deficiency suppressed the effects of PACAP on alleviating hepatic lipid accumulation in HFD-fed mice. (A) FAIM protein level of mice liver was subjected to western blot. Statistical analysis of FAIM/b-actin was shown in a bar chart (right) (*P < 0.05, **P < 0.01, ***P < 0.001 vs. CD group; #P < 0.05, ##P < 0.01, ###P < 0.001 vs. HFD group). (B) Schematic diagram of HFD mouse model with PACAP treatment (0.4 mg/kg) or control saline solution and lentivirus mediated Faim knockdown. (C) Hepatic Faim mRNA level was determined by qRT-PCR, n ¼ 3. (DeH) Modulation of Faim level in the liver influenced HFD-induced hepatic steatosis, (D) bodyweight, liver weight, and WAT weight; (E) liver TG and TC contents; (F) plasma TG, TC, HDL-c, and LDL-c levels; (G) fasting blood glucose level; blood glucose concentrations were measured on day 12 after lentivirus injection; (H) representative photomicrographs of Oil Red O and H&E staining of liver tissues in different groups (scale bars: 50 or 200 mM). (I and J) Ablation of Faim impaired glucose tolerance and insulin sensitivity in mice. IPGTT (I) and IPITT (J), blood glucose was measured at different time points after glucose or insulin injection (left), and quantification of the AUC (right). Data are presented as mean SEM, n ¼ 5 (*P < 0.05, **P < 0.01, ***P < 0.001).

Article Snippet: In CREB inhibitor experiment, AML12 were transfected with FAIM reporter plasmids for 24 h and treated with 1 mM PACAP for an additional 24 h in the presence or absence of the CREB inhibitor KG-501 (S8409, 18228-17- 6, Selleck Chemicals, USA).

Techniques: Western Blot, Control, Saline, Knockdown, Quantitative RT-PCR, Clinical Proteomics, Injection, Staining

Journal: Molecular metabolism

Article Title: PACAP attenuates hepatic lipid accumulation through the FAIM/AMPK/IRβ axis during overnutrition.

doi: 10.1016/j.molmet.2022.101584

Figure Lengend Snippet: Figure 5: PACAP activates the FAIM-AMPK-IRb axis to govern the SREBP and lipid synthetic gene program. (A and B) PACAP activated AMPK-IRb signaling pathway and down- regulated the expression of lipogenesis genes in HFD-fed mice, such effects were suppressed following knockdown of Faim. Western blot analysis were used to detect the protein level of indicated antibodies. (C and D) The overexpression of FAIM activated AMPK-IRb signaling pathway, the protein levels of FAIM, p-AMPK, AMPK, p-IRb, IRb, and lipid synthesis genes SREBP1, SREBP2, FAS, SCD1, HMGCR were determined by western blot with quantifications. Data are presented as mean SEM, n ¼ 3 (*P < 0.05, **P < 0.01, ***P < 0.001).

Article Snippet: In CREB inhibitor experiment, AML12 were transfected with FAIM reporter plasmids for 24 h and treated with 1 mM PACAP for an additional 24 h in the presence or absence of the CREB inhibitor KG-501 (S8409, 18228-17- 6, Selleck Chemicals, USA).

Techniques: Expressing, Knockdown, Western Blot, Over Expression

Journal: Molecular metabolism

Article Title: PACAP attenuates hepatic lipid accumulation through the FAIM/AMPK/IRβ axis during overnutrition.

doi: 10.1016/j.molmet.2022.101584

Figure Lengend Snippet: Figure 6: Knockdown of Faim inhibited the effects of PACAP on decreasing lipid accumulation and activating AMPK-IRb signaling pathway. AML12 cells were transiently transfected with Faim siRNA or scramble siRNA in cell culture medium containing 200 mM PA or 10% BSA (as control of PA solution) for 24 h, then the cells were treated with PACAP (1 mM) and Max.D.4 (10 mM) for another 24 h as indicated. (A) Representative for Oil Red O staining of AML12 (Scale bars, 50 mM). (B and C) Impacts of Faim knockdown on cellular TG and TC level (B), glucose uptake and glycogen content (C) of AML12. (D and E) Faim knockdown impaired the activation of AMPK-IRb pathway in AML12 treated with PACAP, the protein levels were analyzed by western blot and quantitative measurements (right). (F and G) AML12 were exposed to PA for 24 h, then treated with PACAP (1 mM), Max.D.4 (10 mM) and Compound C (10 mM) (F) or AICAR (0.5 mM) (G) for another 24 h. The protein level of FAIM was detected by western blot analysis and quantitative measurements (down). Data are presented as mean SEM. n ¼ 3 (&P < 0.05, &&P < 0.01, &&&P < 0.001 vs. control group; *P < 0.05, **P < 0.01, ***P < 0.001 vs. PA group; #P < 0.05, ##P < 0.01, ###P < 0.001 vs. PA þ PACAP group, OP < 0.05, OOP < 0.01, OOOP < 0.001 vs. PA þ PACAP þ Max.D.4 group).

Article Snippet: In CREB inhibitor experiment, AML12 were transfected with FAIM reporter plasmids for 24 h and treated with 1 mM PACAP for an additional 24 h in the presence or absence of the CREB inhibitor KG-501 (S8409, 18228-17- 6, Selleck Chemicals, USA).

Techniques: Knockdown, Transfection, Cell Culture, Control, Staining, Activation Assay, Western Blot

Journal: Molecular metabolism

Article Title: PACAP attenuates hepatic lipid accumulation through the FAIM/AMPK/IRβ axis during overnutrition.

doi: 10.1016/j.molmet.2022.101584

Figure Lengend Snippet: Figure 7: PACAP activates the PAC1-PKA-CREB signaling pathway to stimulate FAIM expression. (A) mRNA level of Faim in PA-induced AML12 treated with PACAP, determined by qRT-PCR (n ¼ 3). (B) The effect of PACAP on the activation of PKA and CREB in PA induced AML12 cells, the protein levels of PKA, CREB and FAIM, and phosphorylation of PKA and CREB were determined by western blot. (*P < 0.05, **P < 0.01, ***P < 0.001 vs. PA group; #P < 0.05, ##P < 0.01, ###P < 0.001 vs. PACAP (1 mM) group). (C) Schematic of the sequence of two CRE binding sites that CREB targets the WT or mutated promoter region of Faim mRNA. (DeF) Luciferase activities in AML12 transiently transfected with either wild type (WT), truncated, or mutant Faim promoter-luciferase reporter constructs. Then the cells were treated with PACAP (1 mM), or co- transfected with CREB cDNA or empty vectors. (G) Luciferase activities of FAIM WT reporter plasmids in AML12 cells with the treatment of KG-501 (a specific CREB inhibitor) and PACAP (1 mM) as indicated. Data are shown as mean SEM, n ¼ 3 or 5 (*P < 0.05, **P < 0.01, ***P < 0.001).

Article Snippet: In CREB inhibitor experiment, AML12 were transfected with FAIM reporter plasmids for 24 h and treated with 1 mM PACAP for an additional 24 h in the presence or absence of the CREB inhibitor KG-501 (S8409, 18228-17- 6, Selleck Chemicals, USA).

Techniques: Expressing, Quantitative RT-PCR, Activation Assay, Phospho-proteomics, Western Blot, Sequencing, Binding Assay, Luciferase, Transfection, Mutagenesis, Construct

Journal: Heliyon

Article Title: Therapeutic Effects of Intranasal Administration of Resveratrol on the Rat Model of Brain Ischemia

doi: 10.1016/j.heliyon.2024.e32592

Figure Lengend Snippet: Schematic diagram of the experimental design to evaluate the therapeutic effects of intranasal administration of resveratrol on the rat model of brain ischemia. Rats were subjected to 1 h of ischemia followed by 7 days of reperfusion with neurological evaluations including the wire hanging test (1 day prior to MCAO induction, 3 h after MCAO induction, and day 7) and mNSS (2 h, 72 h, and 7 days after MCAO induction). Intranasal administration of resveratrol or vehicle was applied from day 1 to day 7. On day 7, after body weight monitoring and behavioral tests, all rats were euthanized for BBB permeability, infarct volume, brain water content evaluations, and real-time PCR analysis (MMP-9, NF-KB, Bax, and Bcl2 mRNA expression levels) MCAO, middle cerebral artery occlusion; mNSS, modified neurologic severity score; BBB, blood-brain barrier; MMP-9, Matrix metalloproteinase-9; NF-KB, nuclear factor-kappa B; Bcl2, B-cell lymphoma protein 2; Bax, B-cell lymphoma protein 2-associated X.

Article Snippet: After MCAO, in the vehicle control and resveratrol groups, vehicle (0.05 percent dimethyl sulfoxide (DMSO) in phosphate-buffered saline, Sigma-Aldrich, St. Louis, MO, USA) or 100 μl of a 135 mg/ml (13.5 mg/rat) resveratrol solution (∼50 mg/kg body weight, Sigma-Aldrich, St. Louis, MO, USA) [ ] in 0.05 percent DMSO were inoculated through drip with a micropipette into each nostril of the rat for intranasal administration once a day for 7 consecutive days, while the rat was in the head-back supine position with a 70°–90° tilt to enhance drug absorption from the nasal cavity and facilitate uptake into the brain, while minimizing drainage into the esophagus and trachea ( ) [ ].

Techniques: Permeability, Real-time Polymerase Chain Reaction, Expressing, Modification

Journal: Heliyon

Article Title: Therapeutic Effects of Intranasal Administration of Resveratrol on the Rat Model of Brain Ischemia

doi: 10.1016/j.heliyon.2024.e32592

Figure Lengend Snippet: - A, Body weight in intranasal resveratrol-treated and vehicle-treated MCAO rats, as well as the sham group, on days 0 (before MCAO) and 7 post-ischemia-reperfusion injuries. Data is expressed as mean ± SE.M (n = 15 rats per group); B, significant neurobehavioral improvement in mNSS in the MCAO intranasal resveratrol treatment group compared to the MCAO vehicle group on days 3 and 7 post-ischemia–reperfusion injury. Data is expressed as mean ± S.E.M (n = 15 rats per group); C, fall latency from wire hanging tests of the sham-operated, intranasal resveratrol, and vehicle-treated MCAO rats at baseline (before surgery), 3 h (day 0), and 7 days after MCAO. Data is expressed as mean ± S.E.M (n = 7 rats per group); Statistical analysis was performed with one-way ANOVA and post-hoc Tukey's test. * P<0.05, **P< 0.01, ***P<0.001 MCAO, middle cerebral artery occlusion; mNSS, modified neurologic severity score.

Article Snippet: After MCAO, in the vehicle control and resveratrol groups, vehicle (0.05 percent dimethyl sulfoxide (DMSO) in phosphate-buffered saline, Sigma-Aldrich, St. Louis, MO, USA) or 100 μl of a 135 mg/ml (13.5 mg/rat) resveratrol solution (∼50 mg/kg body weight, Sigma-Aldrich, St. Louis, MO, USA) [ ] in 0.05 percent DMSO were inoculated through drip with a micropipette into each nostril of the rat for intranasal administration once a day for 7 consecutive days, while the rat was in the head-back supine position with a 70°–90° tilt to enhance drug absorption from the nasal cavity and facilitate uptake into the brain, while minimizing drainage into the esophagus and trachea ( ) [ ].

Techniques: Modification

Journal: Heliyon

Article Title: Therapeutic Effects of Intranasal Administration of Resveratrol on the Rat Model of Brain Ischemia

doi: 10.1016/j.heliyon.2024.e32592

Figure Lengend Snippet: A, Representative images of rats after administration of EB 2 % at doses of 4 ml/kg by I.V. bolus into the femoral vein. B, Photographs of EB-stained brains from the rats sacrificed 7 days after sham surgery or MCAO treated intranasally with vehicle and resveratrol. Bar = 5 mm. C, Quantitative analysis of the permeability of the blood-brain barrier or EB content (μg/g) from rat brain extracts from the sham-operated, vehicle, and resveratrol-treated MCAO groups 7 days after MCAO (n = 5 rats/group). Data is expressed as mean ± S.E.M (n = 5 rats per group); Statistical analysis was performed with one-way ANOVA and post-hoc Tukey's test. * P<0.05, ***P<0.001. EB, Evans blue; I.V, intravenous; MCAO, middle cerebral artery occlusion.

Article Snippet: After MCAO, in the vehicle control and resveratrol groups, vehicle (0.05 percent dimethyl sulfoxide (DMSO) in phosphate-buffered saline, Sigma-Aldrich, St. Louis, MO, USA) or 100 μl of a 135 mg/ml (13.5 mg/rat) resveratrol solution (∼50 mg/kg body weight, Sigma-Aldrich, St. Louis, MO, USA) [ ] in 0.05 percent DMSO were inoculated through drip with a micropipette into each nostril of the rat for intranasal administration once a day for 7 consecutive days, while the rat was in the head-back supine position with a 70°–90° tilt to enhance drug absorption from the nasal cavity and facilitate uptake into the brain, while minimizing drainage into the esophagus and trachea ( ) [ ].

Techniques: Staining, Permeability

Journal: Heliyon

Article Title: Therapeutic Effects of Intranasal Administration of Resveratrol on the Rat Model of Brain Ischemia

doi: 10.1016/j.heliyon.2024.e32592

Figure Lengend Snippet: Quantification of edema or BWC% in the sham-operated, vehicle, and resveratrol-treated MCAO groups 7 days after MCAO using the wet/dry weight technique. Valueswere shown as the mean ± SEM (n = 5 rats/group). Statistical analysis was performed with one-way ANOVA and post-hoc Tukey's test. * P<0.05, ** *P<0.001 . BWC, brain water content; MCAO, middle cerebral artery occlusion.

Article Snippet: After MCAO, in the vehicle control and resveratrol groups, vehicle (0.05 percent dimethyl sulfoxide (DMSO) in phosphate-buffered saline, Sigma-Aldrich, St. Louis, MO, USA) or 100 μl of a 135 mg/ml (13.5 mg/rat) resveratrol solution (∼50 mg/kg body weight, Sigma-Aldrich, St. Louis, MO, USA) [ ] in 0.05 percent DMSO were inoculated through drip with a micropipette into each nostril of the rat for intranasal administration once a day for 7 consecutive days, while the rat was in the head-back supine position with a 70°–90° tilt to enhance drug absorption from the nasal cavity and facilitate uptake into the brain, while minimizing drainage into the esophagus and trachea ( ) [ ].

Techniques:

Journal: Heliyon

Article Title: Therapeutic Effects of Intranasal Administration of Resveratrol on the Rat Model of Brain Ischemia

doi: 10.1016/j.heliyon.2024.e32592

Figure Lengend Snippet: - A, Representative photographs of TTC-stained brain sections of sham, vehicle, and resveratrol-treated MCAO rats. The non-ischemia regions were stained red, while the ischemic tissue area remained white. Bar = 5 mm B, Percentage of cerebral infarct volume in the MCAO vehicle-treated, and MCAO resveratrol-treated rats 7 days after MCAO. Valuesare expressed in percentage as mean ± SEM (resveratrol (n = 7), and vehicle MCAO groups (n = 7). Statistical analysis was performed with one-way ANOVA and post-hoc Tukey's test. * *P<0.01. TTC, 2,3,5-triphenyltetrazolium chloride; MCAO, middle cerebral artery occlusion.

Article Snippet: After MCAO, in the vehicle control and resveratrol groups, vehicle (0.05 percent dimethyl sulfoxide (DMSO) in phosphate-buffered saline, Sigma-Aldrich, St. Louis, MO, USA) or 100 μl of a 135 mg/ml (13.5 mg/rat) resveratrol solution (∼50 mg/kg body weight, Sigma-Aldrich, St. Louis, MO, USA) [ ] in 0.05 percent DMSO were inoculated through drip with a micropipette into each nostril of the rat for intranasal administration once a day for 7 consecutive days, while the rat was in the head-back supine position with a 70°–90° tilt to enhance drug absorption from the nasal cavity and facilitate uptake into the brain, while minimizing drainage into the esophagus and trachea ( ) [ ].

Techniques: Staining

Journal: Heliyon

Article Title: Therapeutic Effects of Intranasal Administration of Resveratrol on the Rat Model of Brain Ischemia

doi: 10.1016/j.heliyon.2024.e32592

Figure Lengend Snippet: Quantitative real-time PCR for the mRNA expression of (A) MMP-9 and (B) NF-κB in the ipsilateral ischemic cortex 7 days after cerebral ischemia in sham, vehicle, and resveratrol-treated rats, the results were expressed as fold change over GAPDH. Data are presented as mean ± SEM (n = 6 rats/group). Statistical analysis was performed with one-way ANOVA and post-hoc Tukey's test. * P<0.05, ** P < 0.01, *** *P< 0.0001. MMP-9, Matrix metalloproteinase-9; NF-KB, nuclear factor-kappa B; GAPDH, Glyceraldehyde 3-phosphate dehydrogenase.

Article Snippet: After MCAO, in the vehicle control and resveratrol groups, vehicle (0.05 percent dimethyl sulfoxide (DMSO) in phosphate-buffered saline, Sigma-Aldrich, St. Louis, MO, USA) or 100 μl of a 135 mg/ml (13.5 mg/rat) resveratrol solution (∼50 mg/kg body weight, Sigma-Aldrich, St. Louis, MO, USA) [ ] in 0.05 percent DMSO were inoculated through drip with a micropipette into each nostril of the rat for intranasal administration once a day for 7 consecutive days, while the rat was in the head-back supine position with a 70°–90° tilt to enhance drug absorption from the nasal cavity and facilitate uptake into the brain, while minimizing drainage into the esophagus and trachea ( ) [ ].

Techniques: Real-time Polymerase Chain Reaction, Expressing

Journal: Heliyon

Article Title: Therapeutic Effects of Intranasal Administration of Resveratrol on the Rat Model of Brain Ischemia

doi: 10.1016/j.heliyon.2024.e32592

Figure Lengend Snippet: - Quantitative real-time PCR for mRNA expression of apoptosis-associated genes (A) Bax and (B) Bcl-2 in the ipsilateral ischemic brain cortex 7 days after cerebral ischemia in sham, vehicle-, and resveratrol-treated rats. The results were expressed as fold changes over GAPDH. Data are presented as mean ± SEM (n = 6 rats/group). Statistical analysis was performed with one-way ANOVA and post-hoc Tukey's test. ** P < 0.001 Bcl2, B-cell lymphoma protein 2; Bax, B-cell lymphoma protein 2-associated X; GAPDH, Glyceraldehyde 3-phosphate dehydrogenase.

Article Snippet: After MCAO, in the vehicle control and resveratrol groups, vehicle (0.05 percent dimethyl sulfoxide (DMSO) in phosphate-buffered saline, Sigma-Aldrich, St. Louis, MO, USA) or 100 μl of a 135 mg/ml (13.5 mg/rat) resveratrol solution (∼50 mg/kg body weight, Sigma-Aldrich, St. Louis, MO, USA) [ ] in 0.05 percent DMSO were inoculated through drip with a micropipette into each nostril of the rat for intranasal administration once a day for 7 consecutive days, while the rat was in the head-back supine position with a 70°–90° tilt to enhance drug absorption from the nasal cavity and facilitate uptake into the brain, while minimizing drainage into the esophagus and trachea ( ) [ ].

Techniques: Real-time Polymerase Chain Reaction, Expressing

Journal: Physiological Research

Article Title: Protective Effects of Resveratrol Against Airway Hyperreactivity, Oxidative Stress, and Lung Inflammation in a Rat Pup Model of Bronchopulmonary Dysplasia

doi: 10.33549/physiolres.935239

Figure Lengend Snippet: The effect of in vitro and in vivo resveratrol supplementation on the methacholine-induced contraction of TSM of rat pups. A: TSM contractile responses in hyperoxic and ambient air control groups (*** p<0.001; n=10). B: TSM contractile responses in hyperoxic and ambient air groups in the absence or presence of resveratrol supplemented in vitro (n=7). C: TSM contractile responses in hyperoxic and ambient air groups in the absence or presence of resveratrol supplemented in vivo (n=7). (***P<0.001 – H-res vs. H-veh; †††P<0.001 – AA-res vs. H-veh; ###P<0.001 – AA-veh vs. H-veh). H-veh: hyperoxia-vehicle; AA-veh: ambient air-vehicle; H-res: hyperoxia+resveratrol; AA-res: ambient air+resveratrol. Data are reported as means±SEM.

Article Snippet: Subsets from each group were supplemented intraperitoneally (i.p.) with resveratrol (30 mg·kg −1 ·day −1 ; Sigma, Germany) (25μl) during the exposure time (H-res group, n=19 ; AA-res group, n=19 ).

Techniques: In Vitro, In Vivo

Journal: Physiological Research

Article Title: Protective Effects of Resveratrol Against Airway Hyperreactivity, Oxidative Stress, and Lung Inflammation in a Rat Pup Model of Bronchopulmonary Dysplasia

doi: 10.33549/physiolres.935239

Figure Lengend Snippet: Effect of L-NAME on MCh-induced airway hyperreactivity. A: TSM contractile responses in hyperoxia-exposed rat pups in absence or presence of L-NAME and/or resveratrol (n=8; **P<0.001 – H-res vs. H+L-NAME / H-veh; †P<0.05 – H-res+L-NAME vs. H-res; §P<0.05 – H-veh vs. H-res+L-NAME; #P<0.05 – H+L-NAME vs. H-res+L-NAME). B: TSM contractile responses in ambient air-exposed rat pups in the absence or presence of L-NAME and/or resveratrol (n=6; **P<0.01 - AA+L-NAME vs. AA-veh; †P<0.05 –AA-res+L-NAME vs. AA+L-NAME; ###P<0.001 – AA-res vs. AA+L-NAME). H-veh: hyperoxia-vehicle; AA-veh: ambient air-vehicle; H-res: hyperoxia+resveratrol; AA-res: ambient air+resveratrol. Data are reported as means ± SEM.

Article Snippet: Subsets from each group were supplemented intraperitoneally (i.p.) with resveratrol (30 mg·kg −1 ·day −1 ; Sigma, Germany) (25μl) during the exposure time (H-res group, n=19 ; AA-res group, n=19 ).

Techniques:

Journal: Physiological Research

Article Title: Protective Effects of Resveratrol Against Airway Hyperreactivity, Oxidative Stress, and Lung Inflammation in a Rat Pup Model of Bronchopulmonary Dysplasia

doi: 10.33549/physiolres.935239

Figure Lengend Snippet: Effect of in vitro resveratrol supplementation on TSM relaxation of rat pups. A: TSM relaxation in hyperoxic and ambient air control groups (***P<0.001; n=8). B: TSM relaxation in hyperoxia-exposed rat pups in the absence or presence of resveratrol and/or L-NAME (n=8; ***P<0.001 – H-res vs. H-veh/H+L-NAME; †P<0.05 – H-res+L-NAME vs. H-res; §§§P<0.001 – H-veh vs. H-res+L-NAME; ###P<0.001 – H+L-NAME vs. H-res+L-NAME). C: TSM relaxation in ambient air groups in the absence or presence of resveratrol and/or L-NAME (n=8; ***P<0.001 – AA+L-NAME vs. AA-veh; ##P<0.01 – AA-res+L-NAME vs. AA+L-NAME; §P<0.05 – AA-res+L-NAME vs. AA-res; †P<0.05 – AA-res+L-NAME vs. AA-veh. H-veh: hyperoxia-vehicle; AA-veh: ambient air-vehicle; H-res: hyperoxia+resveratrol; AA-res: ambient air+resveratrol. Data are reported as means ± SEM.

Article Snippet: Subsets from each group were supplemented intraperitoneally (i.p.) with resveratrol (30 mg·kg −1 ·day −1 ; Sigma, Germany) (25μl) during the exposure time (H-res group, n=19 ; AA-res group, n=19 ).

Techniques: In Vitro

Journal: Physiological Research

Article Title: Protective Effects of Resveratrol Against Airway Hyperreactivity, Oxidative Stress, and Lung Inflammation in a Rat Pup Model of Bronchopulmonary Dysplasia

doi: 10.33549/physiolres.935239

Figure Lengend Snippet: Effect of resveratrol on SOD and GPx activity in lung tissue of rat pups. A: SOD activity in lung tissue of rat pups exposed to hyperoxia or ambient air in the absence (n=10) or presence of resveratrol (n=8). B: GPx activity in lung tissue of rat pups exposed to hyperoxia or ambient air in the absence (n=7) or presence of resveratrol (n=8). **P<0.01; H-veh vs. AA-veh/ H-res/ AA-res. H-veh: hyperoxia-vehicle; AA-veh: ambient air-vehicle; H-res: hyperoxia+resveratrol; AA-res: ambient air+resveratrol. Data are presented as means ± SEM.

Article Snippet: Subsets from each group were supplemented intraperitoneally (i.p.) with resveratrol (30 mg·kg −1 ·day −1 ; Sigma, Germany) (25μl) during the exposure time (H-res group, n=19 ; AA-res group, n=19 ).

Techniques: Activity Assay

Journal: Physiological Research

Article Title: Protective Effects of Resveratrol Against Airway Hyperreactivity, Oxidative Stress, and Lung Inflammation in a Rat Pup Model of Bronchopulmonary Dysplasia

doi: 10.33549/physiolres.935239

Figure Lengend Snippet: Effect of resveratrol on proinflammatory cytokines in the lung tissue of rat pups. A: TNF-α level in lung tissue of rat pups exposed to hyperoxia or ambient air (n=6). B: IL-1β level in lung tissue of rat pups exposed to hyperoxia or ambient air (n=6). (**P<0.01; ***P<0.001, H-veh vs. other groups). H-veh: hyperoxia-vehicle; AA-veh: ambient air-vehicle; H-res: hyperoxia+resveratrol; AA-res: ambient air+resveratrol. Data are presented as means ± SEM.

Article Snippet: Subsets from each group were supplemented intraperitoneally (i.p.) with resveratrol (30 mg·kg −1 ·day −1 ; Sigma, Germany) (25μl) during the exposure time (H-res group, n=19 ; AA-res group, n=19 ).

Techniques:

Journal: Physiological Research

Article Title: Protective Effects of Resveratrol Against Airway Hyperreactivity, Oxidative Stress, and Lung Inflammation in a Rat Pup Model of Bronchopulmonary Dysplasia

doi: 10.33549/physiolres.935239

Figure Lengend Snippet: Representative photomicrographs of histological sections of the lungs of neonatal rats showing normalization of alveolar spaces and interalveolar fibroelastic septas by resveratrol. A: AA-veh group; B: AA-res group; C: H-veh group (the arrow is pointing to the thickening of the interalveolar septa with interstitial proliferative changes); D: H-res group, (10x; n=4 / per group).

Article Snippet: Subsets from each group were supplemented intraperitoneally (i.p.) with resveratrol (30 mg·kg −1 ·day −1 ; Sigma, Germany) (25μl) during the exposure time (H-res group, n=19 ; AA-res group, n=19 ).

Techniques: