Journal of Traditional Chinese Medicine ›› 2024, Vol. 44 ›› Issue (1): 35-43.DOI: 10.19852/j.cnki.jtcm.2024.01.004
• Original articles • Previous Articles Next Articles
Identifying Qingkailing (清开灵) ingredients-dependent mesenchymal-epithelial transition factor-axiation “π” structuring module with angiogenesis and neurogenesis effects
CHENG Kunming1, YUAN Jianan1, LIU Jun2, ZHANG Shengpeng1, XU Qixiang1, XIE Yong3, ZHAO Jingfeng3, ZHANG Xiaoxu2, TANG Xudong4, ZHENG Yongqiu1(
), WANG Zhong2()
- 1 Provincial Engineering Laboratory for Screening and Re-evaluation of Active Compounds of Herbal Medicines in Southern Anhui, Teaching and Research Section of Traditional Chinese Medicine, School of Pharmacy, Wannan Medical College, Wuhu 241000, China
2 Institute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Sciences, Beijing 100700, China
3 Key Laboratory of Bioactive Substances and Resources Utilization of Chinese Herbal Medicine, Ministry of Education, Department of Medicinal Plant Development, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100193, China
4 Department of Gastroenterology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091, China
-
Received:2023-02-19Accepted:2023-05-22Online:2024-02-15Published:2023-12-28 -
Contact:WANG Zhong, Institute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Sciences, Beijing 100700, China. zhonw@vip.sina.com;ZHENG Yongqiu, Provincial Engineering Laboratory for Screening and Re-evaluation of Active Compounds of Herbal Medicines in Southern Anhui, Teaching and Research Section of Traditional Chinese Medicine, School of Pharmacy, Wannan Medical College, Wuhu 241000, China. yongqiuzheng@sina.com -
Supported by:National Major Scientific and Technological Special Project for “Significant New Drugs Development”: Clinical Value Prescription Discovery and Evaluation Technology Based on Modular Pharmacology(2017ZX09301059);Joint Innovation Project of China Academy of Chinese Medical Sciences: Study on the Mechanism of Action of Neuronal Regenerative Function Module Activated by Qingkailing Components(ZZ11-026);University Collaborative Innovation Project of Anhui: Creation of a Combined Animal Model of Coronary Heart Disease Based on the Theory of Xin'an Medicine(GXXT-2020-024);University Natural Science Research Project of Anhui Province :Molecular Mechanism of the Anti-hepatic Fibrosis Effect of Wickerwork Amide Based on the Regulation of Intercellular Communication by PTRF(2023AH051752)
Cite this article
CHENG Kunming, YUAN Jianan, LIU Jun, ZHANG Shengpeng, XU Qixiang, XIE Yong, ZHAO Jingfeng, ZHANG Xiaoxu, TANG Xudong, ZHENG Yongqiu, WANG Zhong. Identifying Qingkailing (清开灵) ingredients-dependent mesenchymal-epithelial transition factor-axiation “π” structuring module with angiogenesis and neurogenesis effects[J]. Journal of Traditional Chinese Medicine, 2024, 44(1): 35-43.
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Figure 1 Effects of Met, Inppl1 and Dapk3 interaction models A: results of GST-pull down assays for GST-PSI domain of Met binding to the SH2 domain of Inppl1. The eluted and input proteins were subjected to SDS-PAGE and stained with Coomassie Brilliant Blue (CBB); B: ITC experiments with met and Dapk3; B1: results of ITC experiments of PKC domain of Dapk3 were titrated into PKC domain of Met; B2: C-terminal domain of Dapk3 was titrated into PKC domain of Met; Top panel: raw data obtained for a representative experiment from 19 injections. Bottom panel: the integrated data with a best-fit curve for the representative experiment generated using the Origin software package for a single-site binding model; C: interaction model among Met, Inppl1, and Dapk3. Inppl1: inositol polyphosphate phosphatase like 1; SH2: src homology; EEP: endonuclease-exonuclease-phosphatase; SAM: sterile alpha motif; Met: mesenchymal-epithelial transition; SEMA: semaphorins; PSI: plexin-semaphorin-integrindomain; IPT: immunoglobulin-plexins-transcription; Dapk3: death associated protein kinase 3; PKC: protein kinase c; Met: mesenchymal-epithelial transition; N-ter: N-terminus; C-ter: C-terminus; GST: glutathione-s-transferase; SDS-PAGE: sodium dodecyl sulfate-polyacrylamide gel electrophoresis; ITC: isothermal titration calorimetry.
Figure 1 Effects of Met, Inppl1 and Dapk3 interaction models A: results of GST-pull down assays for GST-PSI domain of Met binding to the SH2 domain of Inppl1. The eluted and input proteins were subjected to SDS-PAGE and stained with Coomassie Brilliant Blue (CBB); B: ITC experiments with met and Dapk3; B1: results of ITC experiments of PKC domain of Dapk3 were titrated into PKC domain of Met; B2: C-terminal domain of Dapk3 was titrated into PKC domain of Met; Top panel: raw data obtained for a representative experiment from 19 injections. Bottom panel: the integrated data with a best-fit curve for the representative experiment generated using the Origin software package for a single-site binding model; C: interaction model among Met, Inppl1, and Dapk3. Inppl1: inositol polyphosphate phosphatase like 1; SH2: src homology; EEP: endonuclease-exonuclease-phosphatase; SAM: sterile alpha motif; Met: mesenchymal-epithelial transition; SEMA: semaphorins; PSI: plexin-semaphorin-integrindomain; IPT: immunoglobulin-plexins-transcription; Dapk3: death associated protein kinase 3; PKC: protein kinase c; Met: mesenchymal-epithelial transition; N-ter: N-terminus; C-ter: C-terminus; GST: glutathione-s-transferase; SDS-PAGE: sodium dodecyl sulfate-polyacrylamide gel electrophoresis; ITC: isothermal titration calorimetry.
Figure 2 Crispr/cas9 Met inhibits Dapk3, Inppl1 and Met expression in brain homogenates A: immunoblots of Dapk3, Inppl1, and Met expressions in cerebral homogenates showed that treatments of Crispr Met can sufficiently block the effects of BA + JA + CA on Inppl1, but not Dapk3; B: immunoblots of Dapk3, Inppl1, and Met expressions showed that BA + JA + CA could increase Dapk3 and Inppl1 expressions blocked by Met crispr, while BA, JA, CA had no effects; C: bar graphs showed quantitative evaluation of A; D: bar graphs showed quantitative evaluation of B; E: bar graphs showed quantitative evaluation of B. BA: 750 mg JA/kg body weight, 210 mg CA/kg body weight, or 50 mg BA + 250 mg JA + 70 mg CA /kg body weight (BA+JA+CA group) during treatment. AS1949490 was used at a 300 mg/kg dose. BA: baicalin; CA: cholic acid; JA: jasminoidin; I/R: ischemia-reperfusion; Crispr: crispr/cas9; Met: mesenchymal-epithelial transition; Inppl1: inositol polyphosphate phosphatase like 1 ; Dapk3: death associated protein kinase 3. All data are expressed as mean ± standard deviation (n = 3). Statistical significance between multiple groups was determined in this study primarily using one-way or two-way analysis of variance. aP < 0.05, compared to the Sham group.
Figure 2 Crispr/cas9 Met inhibits Dapk3, Inppl1 and Met expression in brain homogenates A: immunoblots of Dapk3, Inppl1, and Met expressions in cerebral homogenates showed that treatments of Crispr Met can sufficiently block the effects of BA + JA + CA on Inppl1, but not Dapk3; B: immunoblots of Dapk3, Inppl1, and Met expressions showed that BA + JA + CA could increase Dapk3 and Inppl1 expressions blocked by Met crispr, while BA, JA, CA had no effects; C: bar graphs showed quantitative evaluation of A; D: bar graphs showed quantitative evaluation of B; E: bar graphs showed quantitative evaluation of B. BA: 750 mg JA/kg body weight, 210 mg CA/kg body weight, or 50 mg BA + 250 mg JA + 70 mg CA /kg body weight (BA+JA+CA group) during treatment. AS1949490 was used at a 300 mg/kg dose. BA: baicalin; CA: cholic acid; JA: jasminoidin; I/R: ischemia-reperfusion; Crispr: crispr/cas9; Met: mesenchymal-epithelial transition; Inppl1: inositol polyphosphate phosphatase like 1 ; Dapk3: death associated protein kinase 3. All data are expressed as mean ± standard deviation (n = 3). Statistical significance between multiple groups was determined in this study primarily using one-way or two-way analysis of variance. aP < 0.05, compared to the Sham group.
Figure 3 Inhibition of biological effects of the modules of neurons generation composed of Met, Inppl1, and Dapk3 impaired BA + JA + CA-induced angiogenesis and neurogenesis A: co-treatment with SHIP2 inhibitors AS1949490 and/or Crispr-Met impaired BA + JA + CA-induced angiogenesis as demonstrated by CD31 and BrdU immunostaining (× 40 magnification, each sample was repeated three times, use of immunofluorescence staining). A1: Sham Group; A2: I/R group; A3: I/R + BA + JA + CA group; A4: I/R + BA + JA + CA + AS group; A5: I/R + BA + JA + CA + CrisprMet group; A6: I/R + BA + JA + CA + CrisprMet + AS group; Arrows point to co-localisation of CD31 and BrdU indicate angiogenesis. B: co-treatment with SHIP2 inhibitors AS1949490 and/or Crispr-Met impaired BA + JA + CA-induced neurogenesis as demonstrated by NeuN and BrdU immunostaining (× 40 magnification, each sample was repeated three times, use of immunofluorescence staining); B1: Sham Group; B2: I/R group; B3: I/R + BA + JA + CA group; B4: I/R + BA + JA + CA + AS group; B5: I/R + BA + JA + CA + CrisprMet group; B6: I/R + BA + JA + CA + CrisprMet + AS group. The arrows point to the co-localisation of NeuN and BrdU, suggesting that neuronal biogenesis. C: contents of BDNF in brain tissues; D: contents of VEGF in brain tissues; E: bar graphs showed quantitative evaluation of A; F: bar graphs showed quantitative evaluation of B. 750 mg JA/kg body weight, 210 mg CA/kg body weight, or 50 mg BA + 250 mg JA + 70 mg CA /kg body weight (BA + JA + CA group) during treatment. AS1949490 was used at a 300 mg/kg dose. BA: baicalin; CA: cholic acid; JA: jasminoidin; I/R: ischemia-reperfusion; Crispr: Crispr/cas9; Met: mesenchymal-epithelial transition; Inppl1: inositol polyphosphate phosphatase like 1; Dapk3: death associated protein kinase 3; SHIP2: src homology 2 domain-containing inositol 5'-phosphatase 2; BrdU: bromodeoxyuridine; AS: Clustered Regularly Interspaced Short Palindromic Repeats; BDNF: brain-derived neurotrophic factor; VEGF: vascular endothelial growth factor. Statistical significance between multiple groups was determined in this study primarily using one-way or two-way analysis of variance. All data are expressed as mean ± standard deviation (n = 5). aP < 0.05, compared with sham + empty vector group; bP < 0.05, compared with I/R group; cP < 0.05, compared with I/R + BA + JA + CA group; dP < 0.05, compared with sham + I/R + BA + JA + CA + Crispr Met + AS group.
Figure 3 Inhibition of biological effects of the modules of neurons generation composed of Met, Inppl1, and Dapk3 impaired BA + JA + CA-induced angiogenesis and neurogenesis A: co-treatment with SHIP2 inhibitors AS1949490 and/or Crispr-Met impaired BA + JA + CA-induced angiogenesis as demonstrated by CD31 and BrdU immunostaining (× 40 magnification, each sample was repeated three times, use of immunofluorescence staining). A1: Sham Group; A2: I/R group; A3: I/R + BA + JA + CA group; A4: I/R + BA + JA + CA + AS group; A5: I/R + BA + JA + CA + CrisprMet group; A6: I/R + BA + JA + CA + CrisprMet + AS group; Arrows point to co-localisation of CD31 and BrdU indicate angiogenesis. B: co-treatment with SHIP2 inhibitors AS1949490 and/or Crispr-Met impaired BA + JA + CA-induced neurogenesis as demonstrated by NeuN and BrdU immunostaining (× 40 magnification, each sample was repeated three times, use of immunofluorescence staining); B1: Sham Group; B2: I/R group; B3: I/R + BA + JA + CA group; B4: I/R + BA + JA + CA + AS group; B5: I/R + BA + JA + CA + CrisprMet group; B6: I/R + BA + JA + CA + CrisprMet + AS group. The arrows point to the co-localisation of NeuN and BrdU, suggesting that neuronal biogenesis. C: contents of BDNF in brain tissues; D: contents of VEGF in brain tissues; E: bar graphs showed quantitative evaluation of A; F: bar graphs showed quantitative evaluation of B. 750 mg JA/kg body weight, 210 mg CA/kg body weight, or 50 mg BA + 250 mg JA + 70 mg CA /kg body weight (BA + JA + CA group) during treatment. AS1949490 was used at a 300 mg/kg dose. BA: baicalin; CA: cholic acid; JA: jasminoidin; I/R: ischemia-reperfusion; Crispr: Crispr/cas9; Met: mesenchymal-epithelial transition; Inppl1: inositol polyphosphate phosphatase like 1; Dapk3: death associated protein kinase 3; SHIP2: src homology 2 domain-containing inositol 5'-phosphatase 2; BrdU: bromodeoxyuridine; AS: Clustered Regularly Interspaced Short Palindromic Repeats; BDNF: brain-derived neurotrophic factor; VEGF: vascular endothelial growth factor. Statistical significance between multiple groups was determined in this study primarily using one-way or two-way analysis of variance. All data are expressed as mean ± standard deviation (n = 5). aP < 0.05, compared with sham + empty vector group; bP < 0.05, compared with I/R group; cP < 0.05, compared with I/R + BA + JA + CA group; dP < 0.05, compared with sham + I/R + BA + JA + CA + Crispr Met + AS group.
Figure 4 Effects of Crispr-Met on BA + JA + CA-induced apoptosis of neurons as demonstrated by PI and Annexin-FITC V staining A: neuronal apoptosis in Met Crispr animals; A1: Sham group; A2: I/R group; A3: I/R + BA group; A4: I/R + CA group; A5: I/R + JA group; A6: I/R + BA + CA + JA group; B: neuroapoptosis in non-Met Crispr animals; B1: Sham group; B2: I/R group; B3: I/R + BA group; B4: I/R + CA group; B5: I/R + JA group; B6: I/R + BA + CA + JA group; C: percentages of apoptotic cells are indicated; D: percentages of apoptotic cells are indicated; E: percentages of apoptotic cells are indicated. 750 mg JA/kg body weight, 210 mg CA/kg body weight, or 50 mg BA + 250 mg JA + 70 mg CA /kg body weight (BA + JA + CA group) during treatment. AS1949490 was used at a 300 mg/kg dose; Met: mesenchymal-epithelial transition; PI: propidine iodide; FITC: fluorescein isothiocyanate; BA: baicalin; CA: cholic acid; JA: jasminoidin; I/R: ischemia-reperfusion. All data are expressed as mean ± standard deviation (n = 3). Statistical significance between multiple groups was determined in this study primarily using one-way or two-way analysis of variance. aP < 0.05, compared with I/R.
Figure 4 Effects of Crispr-Met on BA + JA + CA-induced apoptosis of neurons as demonstrated by PI and Annexin-FITC V staining A: neuronal apoptosis in Met Crispr animals; A1: Sham group; A2: I/R group; A3: I/R + BA group; A4: I/R + CA group; A5: I/R + JA group; A6: I/R + BA + CA + JA group; B: neuroapoptosis in non-Met Crispr animals; B1: Sham group; B2: I/R group; B3: I/R + BA group; B4: I/R + CA group; B5: I/R + JA group; B6: I/R + BA + CA + JA group; C: percentages of apoptotic cells are indicated; D: percentages of apoptotic cells are indicated; E: percentages of apoptotic cells are indicated. 750 mg JA/kg body weight, 210 mg CA/kg body weight, or 50 mg BA + 250 mg JA + 70 mg CA /kg body weight (BA + JA + CA group) during treatment. AS1949490 was used at a 300 mg/kg dose; Met: mesenchymal-epithelial transition; PI: propidine iodide; FITC: fluorescein isothiocyanate; BA: baicalin; CA: cholic acid; JA: jasminoidin; I/R: ischemia-reperfusion. All data are expressed as mean ± standard deviation (n = 3). Statistical significance between multiple groups was determined in this study primarily using one-way or two-way analysis of variance. aP < 0.05, compared with I/R.
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