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Introduction <p>Avipattikar Churna is prescribed for gastric conditions in Ayurveda. The herbs present in churna have anti-inflammatory, antioxidant, and cytoprotective activities and the sugar part of churna is responsible for acid neutralization. We investigated the mechanism of action of Avipattikar churna against peptic ulcer using network pharmacology, in-vitro, ex-vivo and in vivo studies<b>.</b></p> Methods <p>Network pharmacology of churna was performed to identify the protein and pathways targeted by phytoconstituents of churna. In the phytochemical analysis the quantification of phenols, flavonoids, tannins, in vitro studies including acid neutralizing capacity, ex-vivo studies including proton pump inhibition and antioxidant activities of three extracts of churna (aqueous, alcoholic and hydro-alcoholic) and in vivo studies were performed.</p> Results <p>Network analysis revealed Quercetin, Ellagic acid, Turpetholic acid, Copaene, and Eugenol having activity in peptic ulcer. The quantitative estimation of total phenols, flavonoids and tannins were found to be 12.467 ± 0.273%&#xa0;w/w, 4.734 ± 0.091%&#xa0;w/w, and 8.0368 ± 0.138%&#xa0;w/w respectively. The proton pump inhibition activity of all three extracts was concentration-dependent, with the hydroalcohol extract being the most effective at 250&#xa0;ug/mL. Aqueous and hydroalcoholic extracts were found to improve levels of SOD, catalase and glutathione. Additionally, <i>in-vivo</i> studies revealed decrease in NFκB, TNF-α, and IL-6 post treatment. The ulcer protective effect was supported by histopathology results.</p> Conclusion <p>From the experimental data we conclude that Avipattikar churna may act via various mechanisms including acid neutralization, proton pump inhibition and antioxidant activity. Further in vivo studies suggest that churna may suppress the NF-κB signaling pathway, which is associated with significant reductions in TNF-α and IL-6 levels, decreased inflammatory cell infiltration, promotion of ulcer healing, and induction of apoptosis.</p>

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Mechanistic insights into the anti-ulcerative effects of Avipattikar churna: a network pharmacology and experimental approach

  • 期刊论文

  • 发表日期：

    2025年3月30日

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  • Priya Shah,
  • K. Pundarikakshudu,
  • Vijay Kevlani,
  • Maitreyi Zaveri

摘要

Introduction

Avipattikar Churna is prescribed for gastric conditions in Ayurveda. The herbs present in churna have anti-inflammatory, antioxidant, and cytoprotective activities and the sugar part of churna is responsible for acid neutralization. We investigated the mechanism of action of Avipattikar churna against peptic ulcer using network pharmacology, in-vitro, ex-vivo and in vivo studies.

Methods

Network pharmacology of churna was performed to identify the protein and pathways targeted by phytoconstituents of churna. In the phytochemical analysis the quantification of phenols, flavonoids, tannins, in vitro studies including acid neutralizing capacity, ex-vivo studies including proton pump inhibition and antioxidant activities of three extracts of churna (aqueous, alcoholic and hydro-alcoholic) and in vivo studies were performed.

Results

Network analysis revealed Quercetin, Ellagic acid, Turpetholic acid, Copaene, and Eugenol having activity in peptic ulcer. The quantitative estimation of total phenols, flavonoids and tannins were found to be 12.467 ± 0.273% w/w, 4.734 ± 0.091% w/w, and 8.0368 ± 0.138% w/w respectively. The proton pump inhibition activity of all three extracts was concentration-dependent, with the hydroalcohol extract being the most effective at 250 ug/mL. Aqueous and hydroalcoholic extracts were found to improve levels of SOD, catalase and glutathione. Additionally, in-vivo studies revealed decrease in NFκB, TNF-α, and IL-6 post treatment. The ulcer protective effect was supported by histopathology results.

Conclusion

From the experimental data we conclude that Avipattikar churna may act via various mechanisms including acid neutralization, proton pump inhibition and antioxidant activity. Further in vivo studies suggest that churna may suppress the NF-κB signaling pathway, which is associated with significant reductions in TNF-α and IL-6 levels, decreased inflammatory cell infiltration, promotion of ulcer healing, and induction of apoptosis.