rat anti mouse lymphotoxin alpha Search Results


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FIGURE 1 SA inhibited activation of BV2 microglia induced by LPS. (A) Chemical structural formula of sodium aescinate. (B) CCK8 assay was performed to examine the effect of SA to cell viability. BV2 cells were treated by different concentrations of SA (0–200 μM) for 24 h (C) BV2 cells were pretreated with different concentrations of SA (0–20 µM) for 12 h, then add LPS (100 ng/mL) for 12 h. Cell lysates were used to detect the protein levels of iNOS, COX2 and GAPDH by western blot. (D–G) BV2 cells were pretreated with SA (5 μM) for 18 h and treated with LPS (100 ng/mL) for another 6 h. Cell samples were collected, Then RNA was extracted to detect the levels of mRNA of iNOS, COX-2, TNF-α, and IL-6 by qRT-PCR. Date are presented as mean ± SD,**p < 0.01, ***p < 0.001, n = 3 per group. (H–I) BV2 cells were pretreated with SA for 12 h and treated with LPS for another 12 h. The levels of cytokines TNFα and IL-6 in the supernatant were measured by <t>ELISA.</t> Date are presented as mean ± SD, *p < 0.05, **p < 0.01, ***p < 0.001, n = 3 per group. (J) Nitrite concentration was measured by Griess assay, BV2 cells were pretreated with SA (5 μM) for 12 h, and then treated with LPS (100 ng/mL) for 12 h. The supernatant was taken and the corresponding Griess reagent was added, which was detected by a microplate reader. (K) After treatment with SA and LPS 12 h respectively, the cells were rinsed with D-Hank. The cells were incubated with DCFH-DA for 20 min at 37°C and detected by flow cytometry. (L) Statistical map of ROS release. Date are presented as mean ± SD, *p < 0.05, ***p < 0.001, n = 3 per group.
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FIGURE 1 SA inhibited activation of BV2 microglia induced by LPS. (A) Chemical structural formula of sodium aescinate. (B) CCK8 assay was performed to examine the effect of SA to cell viability. BV2 cells were treated by different concentrations of SA (0–200 μM) for 24 h (C) BV2 cells were pretreated with different concentrations of SA (0–20 µM) for 12 h, then add LPS (100 ng/mL) for 12 h. Cell lysates were used to detect the protein levels of iNOS, COX2 and GAPDH by western blot. (D–G) BV2 cells were pretreated with SA (5 μM) for 18 h and treated with LPS (100 ng/mL) for another 6 h. Cell samples were collected, Then RNA was extracted to detect the levels of mRNA of iNOS, COX-2, TNF-α, and IL-6 by qRT-PCR. Date are presented as mean ± SD,**p < 0.01, ***p < 0.001, n = 3 per group. (H–I) BV2 cells were pretreated with SA for 12 h and treated with LPS for another 12 h. The levels of cytokines TNFα and IL-6 in the supernatant were measured by <t>ELISA.</t> Date are presented as mean ± SD, *p < 0.05, **p < 0.01, ***p < 0.001, n = 3 per group. (J) Nitrite concentration was measured by Griess assay, BV2 cells were pretreated with SA (5 μM) for 12 h, and then treated with LPS (100 ng/mL) for 12 h. The supernatant was taken and the corresponding Griess reagent was added, which was detected by a microplate reader. (K) After treatment with SA and LPS 12 h respectively, the cells were rinsed with D-Hank. The cells were incubated with DCFH-DA for 20 min at 37°C and detected by flow cytometry. (L) Statistical map of ROS release. Date are presented as mean ± SD, *p < 0.05, ***p < 0.001, n = 3 per group.
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FIGURE 1 SA inhibited activation of BV2 microglia induced by LPS. (A) Chemical structural formula of sodium aescinate. (B) CCK8 assay was performed to examine the effect of SA to cell viability. BV2 cells were treated by different concentrations of SA (0–200 μM) for 24 h (C) BV2 cells were pretreated with different concentrations of SA (0–20 µM) for 12 h, then add LPS (100 ng/mL) for 12 h. Cell lysates were used to detect the protein levels of iNOS, COX2 and GAPDH by western blot. (D–G) BV2 cells were pretreated with SA (5 μM) for 18 h and treated with LPS (100 ng/mL) for another 6 h. Cell samples were collected, Then RNA was extracted to detect the levels of mRNA of iNOS, COX-2, TNF-α, and IL-6 by qRT-PCR. Date are presented as mean ± SD,**p < 0.01, ***p < 0.001, n = 3 per group. (H–I) BV2 cells were pretreated with SA for 12 h and treated with LPS for another 12 h. The levels of cytokines TNFα and IL-6 in the supernatant were measured by <t>ELISA.</t> Date are presented as mean ± SD, *p < 0.05, **p < 0.01, ***p < 0.001, n = 3 per group. (J) Nitrite concentration was measured by Griess assay, BV2 cells were pretreated with SA (5 μM) for 12 h, and then treated with LPS (100 ng/mL) for 12 h. The supernatant was taken and the corresponding Griess reagent was added, which was detected by a microplate reader. (K) After treatment with SA and LPS 12 h respectively, the cells were rinsed with D-Hank. The cells were incubated with DCFH-DA for 20 min at 37°C and detected by flow cytometry. (L) Statistical map of ROS release. Date are presented as mean ± SD, *p < 0.05, ***p < 0.001, n = 3 per group.
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FIGURE 1 SA inhibited activation of BV2 microglia induced by LPS. (A) Chemical structural formula of sodium aescinate. (B) CCK8 assay was performed to examine the effect of SA to cell viability. BV2 cells were treated by different concentrations of SA (0–200 μM) for 24 h (C) BV2 cells were pretreated with different concentrations of SA (0–20 µM) for 12 h, then add LPS (100 ng/mL) for 12 h. Cell lysates were used to detect the protein levels of iNOS, COX2 and GAPDH by western blot. (D–G) BV2 cells were pretreated with SA (5 μM) for 18 h and treated with LPS (100 ng/mL) for another 6 h. Cell samples were collected, Then RNA was extracted to detect the levels of mRNA of iNOS, COX-2, TNF-α, and IL-6 by qRT-PCR. Date are presented as mean ± SD,**p < 0.01, ***p < 0.001, n = 3 per group. (H–I) BV2 cells were pretreated with SA for 12 h and treated with LPS for another 12 h. The levels of cytokines TNFα and IL-6 in the supernatant were measured by <t>ELISA.</t> Date are presented as mean ± SD, *p < 0.05, **p < 0.01, ***p < 0.001, n = 3 per group. (J) Nitrite concentration was measured by Griess assay, BV2 cells were pretreated with SA (5 μM) for 12 h, and then treated with LPS (100 ng/mL) for 12 h. The supernatant was taken and the corresponding Griess reagent was added, which was detected by a microplate reader. (K) After treatment with SA and LPS 12 h respectively, the cells were rinsed with D-Hank. The cells were incubated with DCFH-DA for 20 min at 37°C and detected by flow cytometry. (L) Statistical map of ROS release. Date are presented as mean ± SD, *p < 0.05, ***p < 0.001, n = 3 per group.
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FIGURE 1 SA inhibited activation of BV2 microglia induced by LPS. (A) Chemical structural formula of sodium aescinate. (B) CCK8 assay was performed to examine the effect of SA to cell viability. BV2 cells were treated by different concentrations of SA (0–200 μM) for 24 h (C) BV2 cells were pretreated with different concentrations of SA (0–20 µM) for 12 h, then add LPS (100 ng/mL) for 12 h. Cell lysates were used to detect the protein levels of iNOS, COX2 and GAPDH by western blot. (D–G) BV2 cells were pretreated with SA (5 μM) for 18 h and treated with LPS (100 ng/mL) for another 6 h. Cell samples were collected, Then RNA was extracted to detect the levels of mRNA of iNOS, COX-2, TNF-α, and IL-6 by qRT-PCR. Date are presented as mean ± SD,**p < 0.01, ***p < 0.001, n = 3 per group. (H–I) BV2 cells were pretreated with SA for 12 h and treated with LPS for another 12 h. The levels of cytokines TNFα and IL-6 in the supernatant were measured by <t>ELISA.</t> Date are presented as mean ± SD, *p < 0.05, **p < 0.01, ***p < 0.001, n = 3 per group. (J) Nitrite concentration was measured by Griess assay, BV2 cells were pretreated with SA (5 μM) for 12 h, and then treated with LPS (100 ng/mL) for 12 h. The supernatant was taken and the corresponding Griess reagent was added, which was detected by a microplate reader. (K) After treatment with SA and LPS 12 h respectively, the cells were rinsed with D-Hank. The cells were incubated with DCFH-DA for 20 min at 37°C and detected by flow cytometry. (L) Statistical map of ROS release. Date are presented as mean ± SD, *p < 0.05, ***p < 0.001, n = 3 per group.
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FIGURE 1 SA inhibited activation of BV2 microglia induced by LPS. (A) Chemical structural formula of sodium aescinate. (B) CCK8 assay was performed to examine the effect of SA to cell viability. BV2 cells were treated by different concentrations of SA (0–200 μM) for 24 h (C) BV2 cells were pretreated with different concentrations of SA (0–20 µM) for 12 h, then add LPS (100 ng/mL) for 12 h. Cell lysates were used to detect the protein levels of iNOS, COX2 and GAPDH by western blot. (D–G) BV2 cells were pretreated with SA (5 μM) for 18 h and treated with LPS (100 ng/mL) for another 6 h. Cell samples were collected, Then RNA was extracted to detect the levels of mRNA of iNOS, COX-2, TNF-α, and IL-6 by qRT-PCR. Date are presented as mean ± SD,**p < 0.01, ***p < 0.001, n = 3 per group. (H–I) BV2 cells were pretreated with SA for 12 h and treated with LPS for another 12 h. The levels of cytokines TNFα and IL-6 in the supernatant were measured by <t>ELISA.</t> Date are presented as mean ± SD, *p < 0.05, **p < 0.01, ***p < 0.001, n = 3 per group. (J) Nitrite concentration was measured by Griess assay, BV2 cells were pretreated with SA (5 μM) for 12 h, and then treated with LPS (100 ng/mL) for 12 h. The supernatant was taken and the corresponding Griess reagent was added, which was detected by a microplate reader. (K) After treatment with SA and LPS 12 h respectively, the cells were rinsed with D-Hank. The cells were incubated with DCFH-DA for 20 min at 37°C and detected by flow cytometry. (L) Statistical map of ROS release. Date are presented as mean ± SD, *p < 0.05, ***p < 0.001, n = 3 per group.
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FIGURE 1 SA inhibited activation of BV2 microglia induced by LPS. (A) Chemical structural formula of sodium aescinate. (B) CCK8 assay was performed to examine the effect of SA to cell viability. BV2 cells were treated by different concentrations of SA (0–200 μM) for 24 h (C) BV2 cells were pretreated with different concentrations of SA (0–20 µM) for 12 h, then add LPS (100 ng/mL) for 12 h. Cell lysates were used to detect the protein levels of iNOS, COX2 and GAPDH by western blot. (D–G) BV2 cells were pretreated with SA (5 μM) for 18 h and treated with LPS (100 ng/mL) for another 6 h. Cell samples were collected, Then RNA was extracted to detect the levels of mRNA of iNOS, COX-2, TNF-α, and IL-6 by qRT-PCR. Date are presented as mean ± SD,**p < 0.01, ***p < 0.001, n = 3 per group. (H–I) BV2 cells were pretreated with SA for 12 h and treated with LPS for another 12 h. The levels of cytokines TNFα and IL-6 in the supernatant were measured by <t>ELISA.</t> Date are presented as mean ± SD, *p < 0.05, **p < 0.01, ***p < 0.001, n = 3 per group. (J) Nitrite concentration was measured by Griess assay, BV2 cells were pretreated with SA (5 μM) for 12 h, and then treated with LPS (100 ng/mL) for 12 h. The supernatant was taken and the corresponding Griess reagent was added, which was detected by a microplate reader. (K) After treatment with SA and LPS 12 h respectively, the cells were rinsed with D-Hank. The cells were incubated with DCFH-DA for 20 min at 37°C and detected by flow cytometry. (L) Statistical map of ROS release. Date are presented as mean ± SD, *p < 0.05, ***p < 0.001, n = 3 per group.
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Effects of NaB and MMF on the integrity and permeability of intestinal barrier. ( A ) The content of DAO in each group was detected by <t>ELISA</t> kits. (n = 5–6). ( B ) The content of D-LA in each group detected by ELISA kits. (n = 7). ( C ) Representative immunoblot for Occludin. ( E ) Representative immunoblot for Claudin-1. Alteration of the colon’s intestinal tight junction. Treatment with NaB and MMF increased the expression of the tight junction proteins ( D ) Occludin and ( F ) Claudin-1, which is measured by Western blotting. (n = 5–6). Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 versus the MPTP + vehicle group.
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Phenotypic changes and inflammation marker expression after HFD-induced obesity. ( A , B ) Body weight gain in WT ( A ) and TLR4 −/− ( B ) mice after 8 weeks of HFD treatment; n = 10 mice/group. ( C – E ) Glucose ( C ), triglycerides ( D ), cholesterol ( E ) plasma levels in WT and TLR4 −/− mice fed with SD or HFD; n = 10 mice/group. ( F , H , J ) Real-time qPCR analysis of TNFα ( F <t>),</t> <t>IL-1β</t> ( H ), and IL-6 ( J ) mRNA levels in ileal tissues from WT and TLR4 −/− mice fed with SD or HFD; n = 5 mice/group. ( G,I,K ) <t>ELISA</t> analysis of TNFα ( G ), IL-1β ( I ), and IL-6 ( K ) protein levels in ileal tissues from WT and TLR4 −/− mice fed with SD or HFD; n = 5 mice/group. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. related SD genotype; °° p < 0.01, °°° p < 0.001 vs. WT SD mice.
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Protein concentration in the serum after lipopolysaccharide (LPS) administration. The bar graphs indicate the serum interleukin (IL)‐1β and tumor necrosis factor (TNF)‐α concentrations of the mice analyzed using <t>enzyme‐linked</t> <t>immunosorbent</t> <t>assays.</t> n.s.: not significant, *** p < 0.001 and **** p < 0.0001 vs. the Air–Veh group using Dunnett's test.
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Protein concentration in the serum after lipopolysaccharide (LPS) administration. The bar graphs indicate the serum interleukin (IL)‐1β and tumor necrosis factor (TNF)‐α concentrations of the mice analyzed using <t>enzyme‐linked</t> <t>immunosorbent</t> <t>assays.</t> n.s.: not significant, *** p < 0.001 and **** p < 0.0001 vs. the Air–Veh group using Dunnett's test.
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Image Search Results


FIGURE 1 SA inhibited activation of BV2 microglia induced by LPS. (A) Chemical structural formula of sodium aescinate. (B) CCK8 assay was performed to examine the effect of SA to cell viability. BV2 cells were treated by different concentrations of SA (0–200 μM) for 24 h (C) BV2 cells were pretreated with different concentrations of SA (0–20 µM) for 12 h, then add LPS (100 ng/mL) for 12 h. Cell lysates were used to detect the protein levels of iNOS, COX2 and GAPDH by western blot. (D–G) BV2 cells were pretreated with SA (5 μM) for 18 h and treated with LPS (100 ng/mL) for another 6 h. Cell samples were collected, Then RNA was extracted to detect the levels of mRNA of iNOS, COX-2, TNF-α, and IL-6 by qRT-PCR. Date are presented as mean ± SD,**p < 0.01, ***p < 0.001, n = 3 per group. (H–I) BV2 cells were pretreated with SA for 12 h and treated with LPS for another 12 h. The levels of cytokines TNFα and IL-6 in the supernatant were measured by ELISA. Date are presented as mean ± SD, *p < 0.05, **p < 0.01, ***p < 0.001, n = 3 per group. (J) Nitrite concentration was measured by Griess assay, BV2 cells were pretreated with SA (5 μM) for 12 h, and then treated with LPS (100 ng/mL) for 12 h. The supernatant was taken and the corresponding Griess reagent was added, which was detected by a microplate reader. (K) After treatment with SA and LPS 12 h respectively, the cells were rinsed with D-Hank. The cells were incubated with DCFH-DA for 20 min at 37°C and detected by flow cytometry. (L) Statistical map of ROS release. Date are presented as mean ± SD, *p < 0.05, ***p < 0.001, n = 3 per group.

Journal: Frontiers in pharmacology

Article Title: Sodium aescinate inhibits microglia activation through NF-κB pathway and exerts neuroprotective effect.

doi: 10.3389/fphar.2023.1086429

Figure Lengend Snippet: FIGURE 1 SA inhibited activation of BV2 microglia induced by LPS. (A) Chemical structural formula of sodium aescinate. (B) CCK8 assay was performed to examine the effect of SA to cell viability. BV2 cells were treated by different concentrations of SA (0–200 μM) for 24 h (C) BV2 cells were pretreated with different concentrations of SA (0–20 µM) for 12 h, then add LPS (100 ng/mL) for 12 h. Cell lysates were used to detect the protein levels of iNOS, COX2 and GAPDH by western blot. (D–G) BV2 cells were pretreated with SA (5 μM) for 18 h and treated with LPS (100 ng/mL) for another 6 h. Cell samples were collected, Then RNA was extracted to detect the levels of mRNA of iNOS, COX-2, TNF-α, and IL-6 by qRT-PCR. Date are presented as mean ± SD,**p < 0.01, ***p < 0.001, n = 3 per group. (H–I) BV2 cells were pretreated with SA for 12 h and treated with LPS for another 12 h. The levels of cytokines TNFα and IL-6 in the supernatant were measured by ELISA. Date are presented as mean ± SD, *p < 0.05, **p < 0.01, ***p < 0.001, n = 3 per group. (J) Nitrite concentration was measured by Griess assay, BV2 cells were pretreated with SA (5 μM) for 12 h, and then treated with LPS (100 ng/mL) for 12 h. The supernatant was taken and the corresponding Griess reagent was added, which was detected by a microplate reader. (K) After treatment with SA and LPS 12 h respectively, the cells were rinsed with D-Hank. The cells were incubated with DCFH-DA for 20 min at 37°C and detected by flow cytometry. (L) Statistical map of ROS release. Date are presented as mean ± SD, *p < 0.05, ***p < 0.001, n = 3 per group.

Article Snippet: BV2 cells were cultivated in 12-well plates at a density of 2 × 105 cells/mL with 1 mL medium per well and treated with LPS and desired concentrations of SA for 24 h. The supernatant of BV2 cells treated by LPS or SA was detected by IL-6 and TNF-α mouse ELISA kit (BOSTER, China) according to the manufacturer’s instructions.

Techniques: Activation Assay, CCK-8 Assay, Western Blot, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Concentration Assay, Griess Assay, Incubation, Cytometry

Effects of NaB and MMF on the integrity and permeability of intestinal barrier. ( A ) The content of DAO in each group was detected by ELISA kits. (n = 5–6). ( B ) The content of D-LA in each group detected by ELISA kits. (n = 7). ( C ) Representative immunoblot for Occludin. ( E ) Representative immunoblot for Claudin-1. Alteration of the colon’s intestinal tight junction. Treatment with NaB and MMF increased the expression of the tight junction proteins ( D ) Occludin and ( F ) Claudin-1, which is measured by Western blotting. (n = 5–6). Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 versus the MPTP + vehicle group.

Journal: Nutrients

Article Title: Neuroprotective Effects of Sodium Butyrate and Monomethyl Fumarate Treatment through GPR109A Modulation and Intestinal Barrier Restoration on PD Mice

doi: 10.3390/nu14194163

Figure Lengend Snippet: Effects of NaB and MMF on the integrity and permeability of intestinal barrier. ( A ) The content of DAO in each group was detected by ELISA kits. (n = 5–6). ( B ) The content of D-LA in each group detected by ELISA kits. (n = 7). ( C ) Representative immunoblot for Occludin. ( E ) Representative immunoblot for Claudin-1. Alteration of the colon’s intestinal tight junction. Treatment with NaB and MMF increased the expression of the tight junction proteins ( D ) Occludin and ( F ) Claudin-1, which is measured by Western blotting. (n = 5–6). Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 versus the MPTP + vehicle group.

Article Snippet: According to the manufacturer’s instructions, IL-6 ELISA Kit (EK0411, BOSTER, Wuhan, China) and TNF-ELISA Kit (EK0527, BOSTER, Wuhan, China) were used to determine the serum concentrations of the inflammatory factor interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α).

Techniques: Permeability, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing

Phenotypic changes and inflammation marker expression after HFD-induced obesity. ( A , B ) Body weight gain in WT ( A ) and TLR4 −/− ( B ) mice after 8 weeks of HFD treatment; n = 10 mice/group. ( C – E ) Glucose ( C ), triglycerides ( D ), cholesterol ( E ) plasma levels in WT and TLR4 −/− mice fed with SD or HFD; n = 10 mice/group. ( F , H , J ) Real-time qPCR analysis of TNFα ( F ), IL-1β ( H ), and IL-6 ( J ) mRNA levels in ileal tissues from WT and TLR4 −/− mice fed with SD or HFD; n = 5 mice/group. ( G,I,K ) ELISA analysis of TNFα ( G ), IL-1β ( I ), and IL-6 ( K ) protein levels in ileal tissues from WT and TLR4 −/− mice fed with SD or HFD; n = 5 mice/group. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. related SD genotype; °° p < 0.01, °°° p < 0.001 vs. WT SD mice.

Journal: International Journal of Molecular Sciences

Article Title: Small Intestine Neuromuscular Dysfunctions and Neurogliopathy in a Mouse Model of High-Fat Diet-Induced Obesity: Involvement of Toll-Like Receptor 4

doi: 10.3390/ijms262110710

Figure Lengend Snippet: Phenotypic changes and inflammation marker expression after HFD-induced obesity. ( A , B ) Body weight gain in WT ( A ) and TLR4 −/− ( B ) mice after 8 weeks of HFD treatment; n = 10 mice/group. ( C – E ) Glucose ( C ), triglycerides ( D ), cholesterol ( E ) plasma levels in WT and TLR4 −/− mice fed with SD or HFD; n = 10 mice/group. ( F , H , J ) Real-time qPCR analysis of TNFα ( F ), IL-1β ( H ), and IL-6 ( J ) mRNA levels in ileal tissues from WT and TLR4 −/− mice fed with SD or HFD; n = 5 mice/group. ( G,I,K ) ELISA analysis of TNFα ( G ), IL-1β ( I ), and IL-6 ( K ) protein levels in ileal tissues from WT and TLR4 −/− mice fed with SD or HFD; n = 5 mice/group. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. related SD genotype; °° p < 0.01, °°° p < 0.001 vs. WT SD mice.

Article Snippet: The concentrations of TNF-α, IL-6, and IL-1β were measured with specific ELISA kits (Mouse TNF-alpha ELISA Kit–Quantikine, cat# MTA00B-1; Mouse IL-6 Quantikine ELISA Kit, cat# M6000B-1; Mouse IL-1 beta/IL-1F2 ELISA Kit–Quantikine Kit, cat# MLB00C-1, R&D System, Bio-Techne SRL, Milan, Italy).

Techniques: Marker, Expressing, Clinical Proteomics, Enzyme-linked Immunosorbent Assay

Protein concentration in the serum after lipopolysaccharide (LPS) administration. The bar graphs indicate the serum interleukin (IL)‐1β and tumor necrosis factor (TNF)‐α concentrations of the mice analyzed using enzyme‐linked immunosorbent assays. n.s.: not significant, *** p < 0.001 and **** p < 0.0001 vs. the Air–Veh group using Dunnett's test.

Journal: PCN Reports: Psychiatry and Clinical Neurosciences

Article Title: Molecular hydrogen supplementation in mice ameliorates lipopolysaccharide‐induced loss of interest

doi: 10.1002/pcn5.70000

Figure Lengend Snippet: Protein concentration in the serum after lipopolysaccharide (LPS) administration. The bar graphs indicate the serum interleukin (IL)‐1β and tumor necrosis factor (TNF)‐α concentrations of the mice analyzed using enzyme‐linked immunosorbent assays. n.s.: not significant, *** p < 0.001 and **** p < 0.0001 vs. the Air–Veh group using Dunnett's test.

Article Snippet: Mouse plasma interleukin (IL)−1β and tumor necrosis factor (TNF)‐α concentrations were determined using a commercially available enzyme‐linked immunosorbent assay (ELISA) kit (Mouse IL‐1 beta/IL‐1F2 Quantikine ELISA Kit, Mouse TNF‐alpha Quantikine ELISA Kit, R&D Systems).

Techniques: Protein Concentration