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<p>Alzheimer’s disease (AD) is a neurodegenerative disease with no cure, with aggregates of amyloid-beta (Aβ) plaques, neurofibrillary tangles, and permanent neurodegeneration. Current therapies have been found to provide complementary effects; therefore, there is a need to establish new therapeutic strategies. The neuroprotective activity of <i>Kalanchoe pinnata</i> (KP) was explored in this study using network pharmacology, molecular docking, and in vitro studies. Bioactive compounds with good pharmacokinetic properties have been identified as the 10 bioactive compounds of KP, such as bryotoxin B, kaempferol, and quercetin. A total of 449 common targets of KP and AD that participate in the PI3K-Akt, MAP, and cAMP signaling pathways were identified (AKT1, TNF, and STAT3). Molecular docking results indicated good binding affinities of these KP compounds with AD-related targets. KP aqueous extract (KPAE) inhibited protrophic cytokines and PI3K/Akt signaling in BV-2 microglial cells in a dose-dependent manner by inhibiting Aβ aggregation, antioxidant activity, and neuroinflammation. The above observations indicate that KP has a multi-target effect against AD, which should be proven by preclinical and clinical trials.</p>

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Investigating the ameliorative effect of Kalanchoe pinnata on neuroinflammation-associated Alzheimer’s disease using network pharmacology, molecular docking, and in vitro studies

  • 期刊论文

  • 发表日期：

    2025年10月24日

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  • Pratima Khandayataray,
  • Meesala Krishna Murthy

摘要

Alzheimer’s disease (AD) is a neurodegenerative disease with no cure, with aggregates of amyloid-beta (Aβ) plaques, neurofibrillary tangles, and permanent neurodegeneration. Current therapies have been found to provide complementary effects; therefore, there is a need to establish new therapeutic strategies. The neuroprotective activity of Kalanchoe pinnata (KP) was explored in this study using network pharmacology, molecular docking, and in vitro studies. Bioactive compounds with good pharmacokinetic properties have been identified as the 10 bioactive compounds of KP, such as bryotoxin B, kaempferol, and quercetin. A total of 449 common targets of KP and AD that participate in the PI3K-Akt, MAP, and cAMP signaling pathways were identified (AKT1, TNF, and STAT3). Molecular docking results indicated good binding affinities of these KP compounds with AD-related targets. KP aqueous extract (KPAE) inhibited protrophic cytokines and PI3K/Akt signaling in BV-2 microglial cells in a dose-dependent manner by inhibiting Aβ aggregation, antioxidant activity, and neuroinflammation. The above observations indicate that KP has a multi-target effect against AD, which should be proven by preclinical and clinical trials.