Computational Screening of Vitex Negundo Compounds for Potential Arthritis Therapies in India

[{“box”:0,”content”:”[if 992 equals=”Open Access”]n

n

n

n

Open Access

nn

n

n[/if 992]n

n

Year : June 13, 2024 at 4:59 pm | [if 1553 equals=””] Volume :13 [else] Volume :13[/if 1553] | [if 424 equals=”Regular Issue”]Issue[/if 424][if 424 equals=”Special Issue”]Special Issue[/if 424] [if 424 equals=”Conference”][/if 424] : 01 | Page : 01-18

n

n

n

n

n

n

By

n

[foreach 286]n

n

n

Ramayanam Navakanth Raju

n

    n t

  • n

n

n[/foreach]

n

n[if 2099 not_equal=”Yes”]n

    [foreach 286] [if 1175 not_equal=””]n t

  1. Assistant Professor Department of Pharmacy, MB School of Pharmaceutical Sciences, Tirupati Andhra Pradesh India

    2. n[/if 1175][/foreach]

n[/if 2099][if 2099 equals=”Yes”][/if 2099]n

n

Abstract

nObjective: Arthritis, a pervasive medical condition, manifests as inflammation and discomfort within the joints. As of September 2021, arthritis affected an estimated 180 million people in India, making it a substantial public health concern with a considerable impact on individuals’ quality of life and healthcare systems. Therefore, utilizing molecular docking, drug likeness prediction, and ADME analysis, an effort was made to find natural compounds from Vitex negundo, having many medicinal properties in Indian Ayurveda, to avoid the condition. Methodology: The study employed a computational approach to evaluate the inhibitory potential of several phytochemicals on the target proteins 1G0Y (IL-1), 1Alu (IL-6), and 5vqp (TFG B), which were sourced from the PDB database. Docking was carried out systematically using IMPAAT, PubChem, PDB, Open Bable, BIOVIA Discovery Studio Visualizer, PDB sum generate, PyRx, and ADMETlab 2.0 after the removal of the ligands with weak binding and compounds that can disrupt docking. Result: The results of the docking analysis show that the selected ligands possessed improved binding affinities with each of the three target proteins. The statistical distribution of the protein combinations with backbone dihedral angles is shown by a Ramachandran plot. Three compounds from Vitex negundo have been identified through molecular docking studies as having the potential binding affinity to provide anti-inflammatory effect. All three of these compounds were found to be safe and to have drug-like qualities according to the ADMET profile and drug likeness prediction. Conclusion: This computer study examined how Vitex negundo compounds could treat arthritis in India. Our comprehensive molecular docking, drug similarity prediction, and ADME analysis showed that these drugs bound strongly to arthritic target proteins. Lutein and beta-sitosterin showed promise for anti-inflammatory properties, bringing hope for arthritis therapies and enhanced quality of life while relieving India’s healthcare system

n

n

n

Keywords: Arthritis, Vitex negundo, 1G0Y(IL-1), 1Alu (IL-6), and 5vqp (TFG B), luteolin, beta-sitosterin, elixene, molecular docking, ADMET.

n[if 424 equals=”Regular Issue”][This article belongs to Research & Reviews : Journal of Computational Biology(rrjocb)]

n

[/if 424][if 424 equals=”Special Issue”][This article belongs to Special Issue under section in Research & Reviews : Journal of Computational Biology(rrjocb)][/if 424][if 424 equals=”Conference”]This article belongs to Conference [/if 424]

n

n

n

How to cite this article: Ramayanam Navakanth Raju. Computational Screening of Vitex Negundo Compounds for Potential Arthritis Therapies in India. Research & Reviews : Journal of Computational Biology. April 22, 2024; 13(01):01-18.

n

How to cite this URL: Ramayanam Navakanth Raju. Computational Screening of Vitex Negundo Compounds for Potential Arthritis Therapies in India. Research & Reviews : Journal of Computational Biology. April 22, 2024; 13(01):01-18. Available from: https://journals.stmjournals.com/rrjocb/article=April 22, 2024/view=0

nn[if 992 equals=”Open Access”] Full Text PDF Download[/if 992] n[if 992 not_equal=”Open Access”]

[/if 992]n[if 992 not_equal=”Open Access”]

n

nn[/if 992]nn[if 379 not_equal=””]n

Browse Figures

n

n

[foreach 379]n

n[/foreach]n

n

n

n[/if 379]n

n

References

n[if 1104 equals=””]n

  1. Alamanos, Y., & Drosos, A. A. (2005). Epidemiology of adult rheumatoid arthritis. Autoimmunity Reviews, 4(3), 130–136. https://doi.org/10.1016/j.autrev.2004.11.007
  2. Smolen, J. S., Aletaha, D., & McInnes, I. B. (2016). Rheumatoid arthritis. The Lancet, 388(10055), 2023–2038. https://doi.org/10.1016/S0140-6736(16)30173-8
  3. Firestein, G. S. (2003). Evolving concepts of rheumatoid arthritis. Nature, 423(6937), 356-361. https://doi.org/10.1038/nature01661
  4. Cross, M., Smith, E., Hoy, D., Carmona, L., Wolfe, F., Vos, T., … & Williams, B. (2014). The global burden of rheumatoid arthritis: estimates from the Global Burden of Disease 2010 study. Annals of the Rheumatic Diseases, 73(7), 1316–1322. https://doi.org/10.1136/annrheumdis-2013-204627
  5. McInnes, I. B., & Schett, G. (2011). The pathogenesis of rheumatoid arthritis. New England Journal of Medicine, 365(23), 2205–2219. https://doi.org/10.1056/NEJMra1004965
  6. McInnes, I. B., & Schett, G. (2007). Cytokines in the pathogenesis of rheumatoid arthritis. Nature Reviews Immunology, 7(6), 429–442. https://doi.org/10.1038/nri2094
  7. van Vollenhoven, R. F. (2009). Treatment of rheumatoid arthritis: state of the art 2009. Nature Reviews Rheumatology, 5(10), 531–541. https://doi.org/10.1038/nrrheum.2009.182
  8. Choy, E. H., & Panayi, G. S. (2001). Cytokine pathways and joint inflammation in rheumatoid arthritis. New England Journal of Medicine, 344(12), 907–916. https://doi.org/10.1056/NEJM200103223441207
  9. Smolen, J. S., & Maini, R. N. (2010). Interleukin-6: a new therapeutic target. Arthritis Research & Therapy, 12(Suppl 1), S5. https://doi.org/10.1186/ar2881
  10. Scott, D. L., & Kingsley, G. H. (2006). Tumor necrosis factor inhibitors for rheumatoid arthritis. New England Journal of Medicine, 355(7), 704–712. https://doi.org/10.1056/NEJMra052138
  11. Feldmann, M., & Maini, R. N. (2001). Anti-TNF alpha therapy of rheumatoid arthritis: what have we learned? Annual Review of Immunology, 19, 163–196. https://doi.org/10.1146/annurev
    .immunol.19.1.163
  12. Brennan, F. M., & McInnes, I. B. (2008). Evidence that cytokines play a role in rheumatoid arthritis. The Journal of Clinical Investigation, 118(11), 3537–3545. https://doi.org/10.1172/JCI36389
  13. Ruddy, M. J., & Kronenberg, M. (2002). Role of T cells in arthritides associated with immune responses to cartilage proteoglycans. Arthritis Research, 4(Suppl 3), S123–S130. https://doi.org
    /10.1186/ar578
  14. Singh, J. A., Saag, K. G., & Bridges Jr, S. L. (2016). 2015 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis & Rheumatology, 68(1), 1–26. https://doi.org/10.1002/art.39480
  15. Singh, D., & Aggarwal, A. (2019). Role of tumor necrosis factor inhibitors in rheumatoid arthritis. Clinical Medicine Insights: Arthritis and Musculoskeletal Disorders, 12, 1179544119835883. https://doi.org/10.1177/1179544119835883
  16. McInnes, I. B., & Schett, G. (2017). The pathogenesis of rheumatoid arthritis. New England Journal of Medicine, 377(5), 498-511. https://doi.org/10.1056/NEJMra1514284
  17. Burmester, G. R., Pope, J. E., & Emery, P. (2017). The EULAR points to consider for use of antirheumatic drugs before pregnancy, and during pregnancy and lactation. Annals of the Rheumatic Diseases, 76(5), 795–810. https://doi.org/10.1136/annrheumdis-2017-211300
  18. Curtis, J. R., Singh, J. A., & Yun, H. (2017). Necessity of measuring and reporting disease activity in rheumatoid arthritis clinical trials. Arthritis Research & Therapy, 19(1), 205. https://doi.org/
    1186/s13075-017-1405-7
  19. Lin, Y. J., & Anzaghe, M. (2018). Interleukin-1 in osteoarthritis: is it a target for treatment? International Journal of Molecular Sciences, 19(10), 3006. https://doi.org/10.3390/ijms19103006
  20. Scanzello, C. R., & Goldring, S. R. (2012). The role of synovitis in osteoarthritis pathogenesis. Bone, 51(2), 249–257. https://doi.org/10.1016/j.bone.2012.02.012
  21. van Laar, J. M., & van der Woude, D. (2017). Role of TGFβ signaling in control of T-cell–mediated inflammation in rheumatoid arthritis. F1000Research, 6, 625. https://doi.org/10.12688/
    10540.1
  22. Conaghan, P. G., Cook, A. D., Hamilton, J. A., Tak, P. P., & Louis Bridges Jr, S. (2018). Pathogenesis of osteoarthritis. Nature Reviews Rheumatology, 14(10), 627–641. https://doi.org/
    1038/s41584-018-0073-0
  23. Arend, W. P., & Firestein, G. S. (2012). Pre-rheumatoid arthritis: predisposition and transition to clinical synovitis. Nature Reviews Rheumatology, 8(10), 573-586. https://doi.org/10.1038/
    2012.110
  24. Goldring, M. B., & Goldring, S. R. (2007). Osteoarthritis. Journal of Cellular Physiology, 213(3), 626–634. https://doi.org/10.1002/jcp.21258
  25. Inglis, J. J., & McNamee, K. E. (2009). Cytokines in rheumatoid arthritis. Inflammation and Regeneration, 29(6), 250-256. https://doi.org/10.2492/inflammregen.29.250
  26. Li, J., Hsu, H. C., & Mountz, J. D. (2018). Managing macrophages in rheumatoid arthritis by reform or removal. Current Rheumatology Reports, 20(8), 46. https://doi.org/10.1007/s11926-018-0751-9
  27. Kinne, R. W., Stuhlmüller, B., & Burmester, G. R. (2007). Cells of the synovium in rheumatoid arthritis: macrophages. Arthritis Research & Therapy, 9(6), 224. https://doi.org/10.1186/ar2333
  28. Felson, D. T., & Neogi, T. (2014). Osteoarthritis: is it a disease of cartilage or of bone? Arthritis & Rheumatology, 66(7), 1714–1716. https://doi.org/10.1002/art.38633
  29. Perlman, H. (2007). The role of IL-4 and IL-13 in inflammation and tissue destruction. Arthritis Research & Therapy, 9(Suppl 2), S1. https://doi.org/10.1186/ar2199
  30. Trentham, D. E., Townes, A. S., & Kang, A. H. (1977). Autoimmunity to type II collagen an experimental model of arthritis. The Journal of Experimental Medicine, 146(3), 857–868. https://doi.org/10.1084/jem.146.3.857
  31. Klareskog, L., & Catrina, A. I. (2017). Autoimmunity in rheumatoid arthritis: citrulline immunity and beyond. The Lancet, 389(10086), 93-102. https://doi.org/10.1016/S0140-6736(16)31519–4
  32. Kiener, H. P., Niederreiter, B., & Lee, D. M. (2010). Cadherin 11 promotes invasive behavior of fibroblast-like synoviocytes. Arthritis & Rheumatology, 62(6), 1615–1623. https://doi.org/10.1002/art.27473
  33. Katzenballe, M., Terslev, L., & Wang, B. (2019). Ultrasound Doppler in rheumatoid arthritis: do we need additional criteria for remission? Arthritis Research & Therapy, 21(1), 46. https://doi.org/10.1186/s13075-019-1826-0
  34. Zhang, J. M., & An, J. (2007). Cytokines, inflammation, and pain. International Anesthesiology Clinics, 45(2), 27–37. https://doi.org/10.1097/AIA.0b013e318034194e
  35. Schett, G., & Neurath, M. F. (2018). Resolution of chronic inflammatory disease: universal and tissue-specific concepts. Nature Reviews Immunology, 18(6), 319–330. https://doi.org/10.1038/s41577-018-0006-7
  36. Burmester, G. R., & Pope, J. E. (2017). Novel treatment strategies in rheumatoid arthritis. The Lancet, 389(10086), 2338-2348. https://doi.org/10.1016/S0140-6736(17)31491-7

nn[/if 1104][if 1104 not_equal=””]n

    [foreach 1102]n t

  1. [if 1106 equals=””], [/if 1106][if 1106 not_equal=””],[/if 1106]

    2. n[/foreach]

n[/if 1104]

nn

nn[if 1114 equals=”Yes”]n

n[/if 1114]

n

n

[if 424 not_equal=””]Regular Issue[else]Published[/if 424] Subscription Original Research

n

n

[if 2146 equals=”Yes”][/if 2146][if 2146 not_equal=”Yes”][/if 2146]n

n

n

n

n

n

n

n

n

n

n

n

n

n

n

n

n

n

n

n

n[if 1748 not_equal=””]

[else]

[/if 1748]n

n

n

Volume 13
[if 424 equals=”Regular Issue”]Issue[/if 424][if 424 equals=”Special Issue”]Special Issue[/if 424] [if 424 equals=”Conference”][/if 424] 01
Received March 27, 2024
Accepted April 15, 2024
Published April 22, 2024

n

n

Views: 19

n

n

n

n function myFunction2() {n var x = document.getElementById(“browsefigure”);n if (x.style.display === “block”) {n x.style.display = “none”;n }n else { x.style.display = “Block”; }n }n document.querySelector(“.prevBtn”).addEventListener(“click”, () => {n changeSlides(-1);n });n document.querySelector(“.nextBtn”).addEventListener(“click”, () => {n changeSlides(1);n });n var slideIndex = 1;n showSlides(slideIndex);n function changeSlides(n) {n showSlides((slideIndex += n));n }n function currentSlide(n) {n showSlides((slideIndex = n));n }n function showSlides(n) {n var i;n var slides = document.getElementsByClassName(“Slide”);n var dots = document.getElementsByClassName(“Navdot”);n if (n > slides.length) { slideIndex = 1; }n if (n (item.style.display = “none”));n Array.from(dots).forEach(n item => (item.className = item.className.replace(” selected”, “”))n );n slides[slideIndex – 1].style.display = “block”;n dots[slideIndex – 1].className += ” selected”;n }n”}]