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atl iii  (MedChemExpress)


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    Structured Review

    MedChemExpress atl iii
    <t>ATL</t> <t>III</t> inhibits the proliferation of cervical carcinoma cells in vitro. (A) The chemical molecular structure of ATL III. (B and C) CCK‐8 assay of ATL III at different concentrations in HeLa and SiHa cells. (D) Apoptosis detection of HeLa and SiHa cells treated with 200 μM ATL III for 24 h. (E) Colony formation assay in HeLa and SiHa cells treated with the concentrations in D for 7 days. Data are presented as the mean ± SEM. N = 3, * p < 0.05, ** p < 0.01, *** p < 0.001. No marker means no significant difference.
    Atl Iii, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/atl+iii/pmc10868144-41-0-5
    Average 86 stars, based on 1 article reviews
    atl iii - by Bioz Stars, 2026-10
    86/100 stars

    Images

    1) Product Images from "Atractylodes macrocephala III suppresses EMT in cervical cancer by regulating IGF2BP3 through ETV5"

    Article Title: Atractylodes macrocephala III suppresses EMT in cervical cancer by regulating IGF2BP3 through ETV5

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.18081

    ATL III inhibits the proliferation of cervical carcinoma cells in vitro. (A) The chemical molecular structure of ATL III. (B and C) CCK‐8 assay of ATL III at different concentrations in HeLa and SiHa cells. (D) Apoptosis detection of HeLa and SiHa cells treated with 200 μM ATL III for 24 h. (E) Colony formation assay in HeLa and SiHa cells treated with the concentrations in D for 7 days. Data are presented as the mean ± SEM. N = 3, * p < 0.05, ** p < 0.01, *** p < 0.001. No marker means no significant difference.
    Figure Legend Snippet: ATL III inhibits the proliferation of cervical carcinoma cells in vitro. (A) The chemical molecular structure of ATL III. (B and C) CCK‐8 assay of ATL III at different concentrations in HeLa and SiHa cells. (D) Apoptosis detection of HeLa and SiHa cells treated with 200 μM ATL III for 24 h. (E) Colony formation assay in HeLa and SiHa cells treated with the concentrations in D for 7 days. Data are presented as the mean ± SEM. N = 3, * p < 0.05, ** p < 0.01, *** p < 0.001. No marker means no significant difference.

    Techniques Used: In Vitro, CCK-8 Assay, Colony Assay, Marker

    ATL III inhibits IGF2BP3 expression in HeLa and SiHa cells. (A) qRT–PCR showed the top 14 gene changes in DEGs after ATL III treatment in HeLa and SiHa cells. (B) IHC showed IGF2BP3 expression in normal cervical tissue, CIN I, CIN III, cervical cancer and paracancerous tissues. (C and D) Western blot showing the protein levels in HeLa and SiHa cells after ATL III treatment at different concentrations and times. (E) IF showing that IGF2BP3 was localized in the cytoplasm and that its expression was decreased after ATL treatment. Data are presented as the mean ± SEM. N = 3. * p < 0.05, ** p < 0.01, *** p < 0.001. No marker means no significant difference.
    Figure Legend Snippet: ATL III inhibits IGF2BP3 expression in HeLa and SiHa cells. (A) qRT–PCR showed the top 14 gene changes in DEGs after ATL III treatment in HeLa and SiHa cells. (B) IHC showed IGF2BP3 expression in normal cervical tissue, CIN I, CIN III, cervical cancer and paracancerous tissues. (C and D) Western blot showing the protein levels in HeLa and SiHa cells after ATL III treatment at different concentrations and times. (E) IF showing that IGF2BP3 was localized in the cytoplasm and that its expression was decreased after ATL treatment. Data are presented as the mean ± SEM. N = 3. * p < 0.05, ** p < 0.01, *** p < 0.001. No marker means no significant difference.

    Techniques Used: Expressing, Quantitative RT-PCR, Western Blot, Marker

    ATL III inhibits the metastasis of HeLa and SiHa cells. (A) Wound‐healing assay showing the effect of ATL III on HeLa and SiHa cell migration. (B) Transwell assays showed that ATL III inhibited the invasion of cervical cancer cells. (C) Western blot showing the protein levels of E‐cadherin, N‐cadherin, vimentin, Snail and Slug; β‐Actin was used as the loading control. Data are presented as the mean ± SEM. N = 3. * p < 0.05, ** p < 0.01, *** p < 0.001. No marker means no significant difference.
    Figure Legend Snippet: ATL III inhibits the metastasis of HeLa and SiHa cells. (A) Wound‐healing assay showing the effect of ATL III on HeLa and SiHa cell migration. (B) Transwell assays showed that ATL III inhibited the invasion of cervical cancer cells. (C) Western blot showing the protein levels of E‐cadherin, N‐cadherin, vimentin, Snail and Slug; β‐Actin was used as the loading control. Data are presented as the mean ± SEM. N = 3. * p < 0.05, ** p < 0.01, *** p < 0.001. No marker means no significant difference.

    Techniques Used: Wound Healing Assay, Migration, Western Blot, Marker

    ATL III regulates EMT through IGF2BP3 in cervical cancer cells. (A, B) WB assay showing the level of EMT proteins in HeLa and SiHa cells overexpressing IGF2BP3 after ATL treatment. Data are presented as the mean ± SEM. N = 3. *Compared with NC p < 0.05, **compared with NC p < 0.01, ***compared with NC p < 0.001. #compared with ALT III p < 0.05, ## compared with ALT III p < 0.01, ### compared with ALT III p < 0.001. No marker means no significant difference.
    Figure Legend Snippet: ATL III regulates EMT through IGF2BP3 in cervical cancer cells. (A, B) WB assay showing the level of EMT proteins in HeLa and SiHa cells overexpressing IGF2BP3 after ATL treatment. Data are presented as the mean ± SEM. N = 3. *Compared with NC p < 0.05, **compared with NC p < 0.01, ***compared with NC p < 0.001. #compared with ALT III p < 0.05, ## compared with ALT III p < 0.01, ### compared with ALT III p < 0.001. No marker means no significant difference.

    Techniques Used: Marker

    ATL III inhibits the binding of ETV5 to the transcription start site of IGF2BP3. (A) JASPAR was used to predict the potential transcription factor of IGF2BP3, which intersected with the upregulated gene in RNA‐Seq. (B) The protein expression of ETV in ALT III‐treated cells was detected. (C) Protein expression levels of IGF2BP3 and ETV5 were detected after the use of ETV5 siRNA. (D) Possible binding sites and motifs of the ETV and IGF2BP3 transcription initiation regions. (E) HEK 293 T cells were cotransfected with IGF2BP3 promoter plasmids (−1000/+100 bp, −700/+100 bp, and − 300/+100 bp) and ETV5 plasmids. Then, luciferase activity was measured. Data are presented as the mean ± SEM. N = 3. *Compared with NC p < 0.05, **compared with NC p < 0.01.
    Figure Legend Snippet: ATL III inhibits the binding of ETV5 to the transcription start site of IGF2BP3. (A) JASPAR was used to predict the potential transcription factor of IGF2BP3, which intersected with the upregulated gene in RNA‐Seq. (B) The protein expression of ETV in ALT III‐treated cells was detected. (C) Protein expression levels of IGF2BP3 and ETV5 were detected after the use of ETV5 siRNA. (D) Possible binding sites and motifs of the ETV and IGF2BP3 transcription initiation regions. (E) HEK 293 T cells were cotransfected with IGF2BP3 promoter plasmids (−1000/+100 bp, −700/+100 bp, and − 300/+100 bp) and ETV5 plasmids. Then, luciferase activity was measured. Data are presented as the mean ± SEM. N = 3. *Compared with NC p < 0.05, **compared with NC p < 0.01.

    Techniques Used: Binding Assay, RNA Sequencing Assay, Expressing, Luciferase, Activity Assay

    Related Articles

    Concentration Assay:

    Article Title: Atractylenolide III Promotes Astrocyte Aβ Clearance by Up-regulating AQP4 to Improve Alzheimer's Disease.
    Article Snippet: C8-D1A astrocytes (CL-0506, Procell, Wuhan, China) were cultured in dedicated medium (CM-0506, Procell) and maintained in a 37 °C incubator with 5 % CO2. .. To identify the optimal concentration of ATL-III, C8-D1A cells were treated with various concentrations of ATL-III (HY-N0203, MCE; 1, 10, 50, 100, 200 μM) for 48 hours (Jeong et al., 2019). ..

    Injection:

    Article Title: Atractylenolide-III restrains cardiac fibrosis after myocardial infarction via suppression of the RhoA/ROCK1 and ERK1/2 pathway.
    Article Snippet: Background: Cardiac fibrosis, a critical factor in myocardial remodeling post-myocardial infarction (MI), can advance heart failure progression.. Atractylenolide III (ATL-III), derived from Atractylodes lancea, has recognized antioxidant and anti-inflammatory effects; however, its influence on cardiac fibrosis remains unclear.. Methods: MI was induced in mice by permanent ligation of the left anterior descending (LAD) coronary artery, followed by 2 weeks of ATL-III or dimethyl sulfoxide (DMSO) treatment.



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    Image Search Results


    ATL III inhibits the proliferation of cervical carcinoma cells in vitro. (A) The chemical molecular structure of ATL III. (B and C) CCK‐8 assay of ATL III at different concentrations in HeLa and SiHa cells. (D) Apoptosis detection of HeLa and SiHa cells treated with 200 μM ATL III for 24 h. (E) Colony formation assay in HeLa and SiHa cells treated with the concentrations in D for 7 days. Data are presented as the mean ± SEM. N = 3, * p < 0.05, ** p < 0.01, *** p < 0.001. No marker means no significant difference.

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Atractylodes macrocephala III suppresses EMT in cervical cancer by regulating IGF2BP3 through ETV5

    doi: 10.1111/jcmm.18081

    Figure Lengend Snippet: ATL III inhibits the proliferation of cervical carcinoma cells in vitro. (A) The chemical molecular structure of ATL III. (B and C) CCK‐8 assay of ATL III at different concentrations in HeLa and SiHa cells. (D) Apoptosis detection of HeLa and SiHa cells treated with 200 μM ATL III for 24 h. (E) Colony formation assay in HeLa and SiHa cells treated with the concentrations in D for 7 days. Data are presented as the mean ± SEM. N = 3, * p < 0.05, ** p < 0.01, *** p < 0.001. No marker means no significant difference.

    Article Snippet: ATL III was purchased from MedChemExpress (purity ≥99%).

    Techniques: In Vitro, CCK-8 Assay, Colony Assay, Marker

    ATL III inhibits IGF2BP3 expression in HeLa and SiHa cells. (A) qRT–PCR showed the top 14 gene changes in DEGs after ATL III treatment in HeLa and SiHa cells. (B) IHC showed IGF2BP3 expression in normal cervical tissue, CIN I, CIN III, cervical cancer and paracancerous tissues. (C and D) Western blot showing the protein levels in HeLa and SiHa cells after ATL III treatment at different concentrations and times. (E) IF showing that IGF2BP3 was localized in the cytoplasm and that its expression was decreased after ATL treatment. Data are presented as the mean ± SEM. N = 3. * p < 0.05, ** p < 0.01, *** p < 0.001. No marker means no significant difference.

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Atractylodes macrocephala III suppresses EMT in cervical cancer by regulating IGF2BP3 through ETV5

    doi: 10.1111/jcmm.18081

    Figure Lengend Snippet: ATL III inhibits IGF2BP3 expression in HeLa and SiHa cells. (A) qRT–PCR showed the top 14 gene changes in DEGs after ATL III treatment in HeLa and SiHa cells. (B) IHC showed IGF2BP3 expression in normal cervical tissue, CIN I, CIN III, cervical cancer and paracancerous tissues. (C and D) Western blot showing the protein levels in HeLa and SiHa cells after ATL III treatment at different concentrations and times. (E) IF showing that IGF2BP3 was localized in the cytoplasm and that its expression was decreased after ATL treatment. Data are presented as the mean ± SEM. N = 3. * p < 0.05, ** p < 0.01, *** p < 0.001. No marker means no significant difference.

    Article Snippet: ATL III was purchased from MedChemExpress (purity ≥99%).

    Techniques: Expressing, Quantitative RT-PCR, Western Blot, Marker

    ATL III inhibits the metastasis of HeLa and SiHa cells. (A) Wound‐healing assay showing the effect of ATL III on HeLa and SiHa cell migration. (B) Transwell assays showed that ATL III inhibited the invasion of cervical cancer cells. (C) Western blot showing the protein levels of E‐cadherin, N‐cadherin, vimentin, Snail and Slug; β‐Actin was used as the loading control. Data are presented as the mean ± SEM. N = 3. * p < 0.05, ** p < 0.01, *** p < 0.001. No marker means no significant difference.

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Atractylodes macrocephala III suppresses EMT in cervical cancer by regulating IGF2BP3 through ETV5

    doi: 10.1111/jcmm.18081

    Figure Lengend Snippet: ATL III inhibits the metastasis of HeLa and SiHa cells. (A) Wound‐healing assay showing the effect of ATL III on HeLa and SiHa cell migration. (B) Transwell assays showed that ATL III inhibited the invasion of cervical cancer cells. (C) Western blot showing the protein levels of E‐cadherin, N‐cadherin, vimentin, Snail and Slug; β‐Actin was used as the loading control. Data are presented as the mean ± SEM. N = 3. * p < 0.05, ** p < 0.01, *** p < 0.001. No marker means no significant difference.

    Article Snippet: ATL III was purchased from MedChemExpress (purity ≥99%).

    Techniques: Wound Healing Assay, Migration, Western Blot, Marker

    ATL III regulates EMT through IGF2BP3 in cervical cancer cells. (A, B) WB assay showing the level of EMT proteins in HeLa and SiHa cells overexpressing IGF2BP3 after ATL treatment. Data are presented as the mean ± SEM. N = 3. *Compared with NC p < 0.05, **compared with NC p < 0.01, ***compared with NC p < 0.001. #compared with ALT III p < 0.05, ## compared with ALT III p < 0.01, ### compared with ALT III p < 0.001. No marker means no significant difference.

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Atractylodes macrocephala III suppresses EMT in cervical cancer by regulating IGF2BP3 through ETV5

    doi: 10.1111/jcmm.18081

    Figure Lengend Snippet: ATL III regulates EMT through IGF2BP3 in cervical cancer cells. (A, B) WB assay showing the level of EMT proteins in HeLa and SiHa cells overexpressing IGF2BP3 after ATL treatment. Data are presented as the mean ± SEM. N = 3. *Compared with NC p < 0.05, **compared with NC p < 0.01, ***compared with NC p < 0.001. #compared with ALT III p < 0.05, ## compared with ALT III p < 0.01, ### compared with ALT III p < 0.001. No marker means no significant difference.

    Article Snippet: ATL III was purchased from MedChemExpress (purity ≥99%).

    Techniques: Marker

    ATL III inhibits the binding of ETV5 to the transcription start site of IGF2BP3. (A) JASPAR was used to predict the potential transcription factor of IGF2BP3, which intersected with the upregulated gene in RNA‐Seq. (B) The protein expression of ETV in ALT III‐treated cells was detected. (C) Protein expression levels of IGF2BP3 and ETV5 were detected after the use of ETV5 siRNA. (D) Possible binding sites and motifs of the ETV and IGF2BP3 transcription initiation regions. (E) HEK 293 T cells were cotransfected with IGF2BP3 promoter plasmids (−1000/+100 bp, −700/+100 bp, and − 300/+100 bp) and ETV5 plasmids. Then, luciferase activity was measured. Data are presented as the mean ± SEM. N = 3. *Compared with NC p < 0.05, **compared with NC p < 0.01.

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Atractylodes macrocephala III suppresses EMT in cervical cancer by regulating IGF2BP3 through ETV5

    doi: 10.1111/jcmm.18081

    Figure Lengend Snippet: ATL III inhibits the binding of ETV5 to the transcription start site of IGF2BP3. (A) JASPAR was used to predict the potential transcription factor of IGF2BP3, which intersected with the upregulated gene in RNA‐Seq. (B) The protein expression of ETV in ALT III‐treated cells was detected. (C) Protein expression levels of IGF2BP3 and ETV5 were detected after the use of ETV5 siRNA. (D) Possible binding sites and motifs of the ETV and IGF2BP3 transcription initiation regions. (E) HEK 293 T cells were cotransfected with IGF2BP3 promoter plasmids (−1000/+100 bp, −700/+100 bp, and − 300/+100 bp) and ETV5 plasmids. Then, luciferase activity was measured. Data are presented as the mean ± SEM. N = 3. *Compared with NC p < 0.05, **compared with NC p < 0.01.

    Article Snippet: ATL III was purchased from MedChemExpress (purity ≥99%).

    Techniques: Binding Assay, RNA Sequencing Assay, Expressing, Luciferase, Activity Assay

    ATL III attenuates esophageal injury in RE rats A) Images show the esophagus of rats after RE establishment and ATL III treatment in samples of a) sham group, b) RE group, c) ATL III (0.6 mg/kg), d) ATL-III 1.2 mg/kg, and e) ATL III 2.4 mg/kg treated groups. B) H&E stained images of the sectioned esophagus tissues of rats after RE establishment and ATL III treatment. a) sham group, b) RE group, c) ATL III (0.6 mg/kg) d) ATL-III 1.2 mg/kg, and e) ATL III 2.4 mg/kg treated groups. Arrow marker: lymphocyte infiltration. C) The graph represents the esophageal mucosal injury score after RE establishment and ATL III treatment. D) The graph indicates the gastric pH changes after RE establishment and ATL III treatment. *** indicates P < 0.001 vs. RE group. E) The graphs present the ROS and F) TBARS levels after various treatments of ATL-III group. *** indicates P < 0.001 vs. RE group .

    Journal: Heliyon

    Article Title: Atractylenolide III ameliorated reflux esophagitis via PI3K/AKT/NF-κB/iNOS pathway in rats

    doi: 10.1016/j.heliyon.2023.e21224

    Figure Lengend Snippet: ATL III attenuates esophageal injury in RE rats A) Images show the esophagus of rats after RE establishment and ATL III treatment in samples of a) sham group, b) RE group, c) ATL III (0.6 mg/kg), d) ATL-III 1.2 mg/kg, and e) ATL III 2.4 mg/kg treated groups. B) H&E stained images of the sectioned esophagus tissues of rats after RE establishment and ATL III treatment. a) sham group, b) RE group, c) ATL III (0.6 mg/kg) d) ATL-III 1.2 mg/kg, and e) ATL III 2.4 mg/kg treated groups. Arrow marker: lymphocyte infiltration. C) The graph represents the esophageal mucosal injury score after RE establishment and ATL III treatment. D) The graph indicates the gastric pH changes after RE establishment and ATL III treatment. *** indicates P < 0.001 vs. RE group. E) The graphs present the ROS and F) TBARS levels after various treatments of ATL-III group. *** indicates P < 0.001 vs. RE group .

    Article Snippet: ATL III and 740 Y–P were obtained from Abmole Bioscience Inc. (Shanghai, China).

    Techniques: Staining, Marker

    ATL III attenuates esophageal inflammation in RE rats. The graphs show the levels of various inflammatory indicators, A) IL-1β, B) IL-6, C) IL-8, and D) TNF-α. E) The Western blot analysis indicates the expression levels of various IL-1β, IL-6, IL-8, and TNF-α proteins against β-Actin as internal standard at the 2.4 mg/kg dose of ATL III. * indicates P < 0.05 vs. RE group, and *** represents P < 0.001.

    Journal: Heliyon

    Article Title: Atractylenolide III ameliorated reflux esophagitis via PI3K/AKT/NF-κB/iNOS pathway in rats

    doi: 10.1016/j.heliyon.2023.e21224

    Figure Lengend Snippet: ATL III attenuates esophageal inflammation in RE rats. The graphs show the levels of various inflammatory indicators, A) IL-1β, B) IL-6, C) IL-8, and D) TNF-α. E) The Western blot analysis indicates the expression levels of various IL-1β, IL-6, IL-8, and TNF-α proteins against β-Actin as internal standard at the 2.4 mg/kg dose of ATL III. * indicates P < 0.05 vs. RE group, and *** represents P < 0.001.

    Article Snippet: ATL III and 740 Y–P were obtained from Abmole Bioscience Inc. (Shanghai, China).

    Techniques: Western Blot, Expressing

    ATL III inhibits PI3K/AKT/NF-κB/iNOS pathway. A) Images show the esophagus of rats after treatment with a) sham group, b) RE group, c) RE+2.4 mg/kg of ATL III, d) RE+2.4 mg/kg of ATL III +10 mg/kg of 740 Y–P. B) H&E stained images of the sectioned esophagus tissues of rats after treatment with a) sham group, b) RE group, c) RE+2.4 mg/kg ATL III, d) RE+2.4 mg/kg of ATL III +10 mg/kg of 740 Y–P. Arrow marker: lymphocyte infiltration. C) The graph represents the esophageal mucosal injury score after treatment with ATL III +10 mg/kg of 740 Y–P in RE rats. D) The graph signifies the gastric content pH after treatment with ATL III +10 mg/kg of 740 Y–P in RE rats. E) The image shows the ROS levels after treatment with ATL III +10 mg/kg of 740 Y–P in RE rats. F) The image shows the TBARS levels after treatment with ATL III +10 mg/kg of 740 Y–P in RE rats. G) The image shows the expression levels of various inflammatory indicators (TNF-α, IL-8, IL-6, and IL-1β) after treatment with ATL III + 10 mg/kg of 740 Y–P in RE rats. ** indicates P < 0.01 and *** represents P < 0.001 vs. RE. & presents P < 0.05 and &&& signifies P < 0.001 vs. RE + 2.4 mg/kg ATL III.

    Journal: Heliyon

    Article Title: Atractylenolide III ameliorated reflux esophagitis via PI3K/AKT/NF-κB/iNOS pathway in rats

    doi: 10.1016/j.heliyon.2023.e21224

    Figure Lengend Snippet: ATL III inhibits PI3K/AKT/NF-κB/iNOS pathway. A) Images show the esophagus of rats after treatment with a) sham group, b) RE group, c) RE+2.4 mg/kg of ATL III, d) RE+2.4 mg/kg of ATL III +10 mg/kg of 740 Y–P. B) H&E stained images of the sectioned esophagus tissues of rats after treatment with a) sham group, b) RE group, c) RE+2.4 mg/kg ATL III, d) RE+2.4 mg/kg of ATL III +10 mg/kg of 740 Y–P. Arrow marker: lymphocyte infiltration. C) The graph represents the esophageal mucosal injury score after treatment with ATL III +10 mg/kg of 740 Y–P in RE rats. D) The graph signifies the gastric content pH after treatment with ATL III +10 mg/kg of 740 Y–P in RE rats. E) The image shows the ROS levels after treatment with ATL III +10 mg/kg of 740 Y–P in RE rats. F) The image shows the TBARS levels after treatment with ATL III +10 mg/kg of 740 Y–P in RE rats. G) The image shows the expression levels of various inflammatory indicators (TNF-α, IL-8, IL-6, and IL-1β) after treatment with ATL III + 10 mg/kg of 740 Y–P in RE rats. ** indicates P < 0.01 and *** represents P < 0.001 vs. RE. & presents P < 0.05 and &&& signifies P < 0.001 vs. RE + 2.4 mg/kg ATL III.

    Article Snippet: ATL III and 740 Y–P were obtained from Abmole Bioscience Inc. (Shanghai, China).

    Techniques: Staining, Marker, Expressing

    A)ATL III inhibits PI3K/AKT/NF-κB in the esophageal tissues of RE rats. The Western blot analysis indicates the expression levels of various p-PI3K, p -AKT, iNOS, and nuclear NF-κB and Laminin B1 proteins against β-Actin as internal standard at the 2.4 mg/kg dose of ATL III. B) The Western blot analysis indicates the expression levels of various p-PI3K, p -AKT, iNOS, and nuclear NF-κB and Laminin B1 proteins against β-Actin as internal standard after treated with the ATL III +740 Y–P.

    Journal: Heliyon

    Article Title: Atractylenolide III ameliorated reflux esophagitis via PI3K/AKT/NF-κB/iNOS pathway in rats

    doi: 10.1016/j.heliyon.2023.e21224

    Figure Lengend Snippet: A)ATL III inhibits PI3K/AKT/NF-κB in the esophageal tissues of RE rats. The Western blot analysis indicates the expression levels of various p-PI3K, p -AKT, iNOS, and nuclear NF-κB and Laminin B1 proteins against β-Actin as internal standard at the 2.4 mg/kg dose of ATL III. B) The Western blot analysis indicates the expression levels of various p-PI3K, p -AKT, iNOS, and nuclear NF-κB and Laminin B1 proteins against β-Actin as internal standard after treated with the ATL III +740 Y–P.

    Article Snippet: ATL III and 740 Y–P were obtained from Abmole Bioscience Inc. (Shanghai, China).

    Techniques: Western Blot, Expressing