The pharmacological network of Tinospora cordifolia: Its role in regulating ınflammation and cathelicidin production

Ahmad Shobrun Jamil

Article Details

The pharmacological network of Tinospora cordifolia: Its role in regulating ınflammation and cathelicidin production

Authors:

Ahmad Shobrun Jamil

Publisher:

Marmara University

Main Topics:

Pharmacology and Pharmaceutical Sciences (Other)

Journal:

Journal of Research in Pharmacy Vol.29 Issue 3, pp.903-917

Document Type:

Article

Publication Date:

4/2025

Document Language:

English

Document ID (Org No.):

2001344595

pISSN:

2630-6344

Keywords:

Abstract:

 This study aims to promote a pharmacological network strategy to investigate the potential antiinflammatory activity and molecular mechanisms of the bioactive compounds in Tinospora cordifolia TC for controlling inflammation and regulating the production of the antimicrobial peptide cathelicidin. Using the Knapsack database and several recent research findings, SwissADME, PubChem, and PASS Online, we screened the drug-likeness of various TC compounds. Utilizing the SwissTargetPrediction, String-DB, GeneCards, and Venny Diagram, we identified 468 potential targets related to inflammation target protein and cathelicidin production. Further refinement using Cytoscape with CytoHubba highlighted 15 core targets, including BCL2, JUN, STAT3, HSP90AA1, MTOR, AKT1, ESR1, SRC, BCL2L1, TNF, MDM2, PTGS2, HSP90AB1, MMP9, and MMP2. GO and KEGG pathway analysis revealed that the core targets for inflammation control and cathelicidin production are predominantly enriched in TLR, NOD, MAPK, and NFKB inflammatory pathways. Molecular docking conducted with Autodock confirmed strong binding between TC ligands and several proteins in these pathways, such as JAK1, AKT1, IKBKB, and IRAK4. Overall, these findings suggest that TC is predicted to inhibit inflammation by inhibiting the activity of these four target proteins in the inflammatory pathways. This research provides a theoretical basis for understanding the molecular mechanisms of TC in inhibiting inflammation and controlling the production of the antimicrobial peptide cathelicidin.

 This study aims to promote a pharmacological network strategy to investigate the potential antiinflammatory activity and molecular mechanisms of the bioactive compounds in Tinospora cordifolia TC for controlling inflammation and regulating the production of the antimicrobial peptide cathelicidin. Using the Knapsack database and several recent research findings, SwissADME, PubChem, and PASS Online, we screened the drug-likeness of various TC compounds. Utilizing the SwissTargetPrediction, String-DB, GeneCards, and Venny Diagram, we identified 468 potential targets related to inflammation target protein and cathelicidin production. Further refinement using Cytoscape with CytoHubba highlighted 15 core targets, including BCL2, JUN, STAT3, HSP90AA1, MTOR, AKT1, ESR1, SRC, BCL2L1, TNF, MDM2, PTGS2, HSP90AB1, MMP9, and MMP2. GO and KEGG pathway analysis revealed that the core targets for inflammation control and cathelicidin production are predominantly enriched in TLR, NOD, MAPK, and NFKB inflammatory pathways. Molecular docking conducted with Autodock confirmed strong binding between TC ligands and several proteins in these pathways, such as JAK1, AKT1, IKBKB, and IRAK4. Overall, these findings suggest that TC is predicted to inhibit inflammation by inhibiting the activity of these four target proteins in the inflammatory pathways. This research provides a theoretical basis for understanding the molecular mechanisms of TC in inhibiting inflammation and controlling the production of the antimicrobial peptide cathelicidin.

 This study aims to promote a pharmacological network strategy to investigate the potential antiinflammatory activity and molecular mechanisms of the bioactive compounds in Tinospora cordifolia TC for controlling inflammation and regulating the production of the antimicrobial peptide cathelicidin. Using the Knapsack database and several recent research findings, SwissADME, PubChem, and PASS Online, we screened the drug-likeness of various TC compounds. Utilizing the SwissTargetPrediction, String-DB, GeneCards, and Venny Diagram, we identified 468 potential targets related to inflammation target protein and cathelicidin production. Further refinement using Cytoscape with CytoHubba highlighted 15 core targets, including BCL2, JUN, STAT3, HSP90AA1, MTOR, AKT1, ESR1, SRC, BCL2L1, TNF, MDM2, PTGS2, HSP90AB1, MMP9, and MMP2. GO and KEGG pathway analysis revealed that the core targets for inflammation control and cathelicidin production are predominantly enriched in TLR, NOD, MAPK, and NFKB inflammatory pathways. Molecular docking conducted with Autodock confirmed strong binding between TC ligands and several proteins in these pathways, such as JAK1, AKT1, IKBKB, and IRAK4. Overall, these findings suggest that TC is predicted to inhibit inflammation by inhibiting the activity of these four target proteins in the inflammatory pathways. This research provides a theoretical basis for understanding the molecular mechanisms of TC in inhibiting inflammation and controlling the production of the antimicrobial peptide cathelicidin.

 This study aims to promote a pharmacological network strategy to investigate the potential antiinflammatory activity and molecular mechanisms of the bioactive compounds in Tinospora cordifolia TC for controlling inflammation and regulating the production of the antimicrobial peptide cathelicidin. Using the Knapsack database and several recent research findings, SwissADME, PubChem, and PASS Online, we screened the drug-likeness of various TC compounds. Utilizing the SwissTargetPrediction, String-DB, GeneCards, and Venny Diagram, we identified 468 potential targets related to inflammation target protein and cathelicidin production. Further refinement using Cytoscape with CytoHubba highlighted 15 core targets, including BCL2, JUN, STAT3, HSP90AA1, MTOR, AKT1, ESR1, SRC, BCL2L1, TNF, MDM2, PTGS2, HSP90AB1, MMP9, and MMP2. GO and KEGG pathway analysis revealed that the core targets for inflammation control and cathelicidin production are predominantly enriched in TLR, NOD, MAPK, and NFKB inflammatory pathways. Molecular docking conducted with Autodock confirmed strong binding between TC ligands and several proteins in these pathways, such as JAK1, AKT1, IKBKB, and IRAK4. Overall, these findings suggest that TC is predicted to inhibit inflammation by inhibiting the activity of these four target proteins in the inflammatory pathways. This research provides a theoretical basis for understanding the molecular mechanisms of TC in inhibiting inflammation and controlling the production of the antimicrobial peptide cathelicidin.

Article Details

The pharmacological network of Tinospora cordifolia: Its role in regulating ınflammation and cathelicidin production

Authors:

Ahmad Shobrun Jamil

Publisher:

Marmara University

Main Topics:

Pharmacology and Pharmaceutical Sciences (Other)

Journal:

Journal of Research in Pharmacy Vol.29 Issue 3, pp.903-917

Document Type:

Article

Publication Date:

4/2025

Document Language:

English

Document ID (Org No.):

2001344595

pISSN:

2630-6344

Cathelicidin

inflammation

network pharmacology

Tinospora cordifolia

Issues

Article Details

The pharmacological network of Tinospora cordifolia: Its role in regulating ınflammation and cathelicidin production

Authors: Ahmad Shobrun Jamil

Publisher: Marmara University

Main Topics: Pharmacology and Pharmaceutical Sciences (Other)

Journal: Journal of Research in Pharmacy Vol.29 Issue 3, pp.903-917

Document Type: Article

Publication Date: 4/2025

Document Language: English

Document ID (Org No.): 2001344595

pISSN: 2630-6344

Cathelicidin

inflammation

network pharmacology

Tinospora cordifolia

Issues

Authors:

Ahmad Shobrun Jamil

Publisher:

Marmara University

Main Topics:

Pharmacology and Pharmaceutical Sciences (Other)

Journal:

Journal of Research in Pharmacy Vol.29 Issue 3, pp.903-917

Document Type:

Article

Publication Date:

4/2025

Document Language:

English

Document ID (Org No.):

2001344595

pISSN:

2630-6344