Beneficial effects of apigenin on the transgenic Drosophila model of Alzheimer's disease

Siddique, Yasir Hasan; Rahul, .; Ara, Gulshan; Afzal, Muhammad; Varshney, Himanshi; Gaur, Kajal; Subhan, Iqra; Mantasha, I; Shahid, M.

doi:10.1016/j.cbi.2022.110120

Cited by 21 publications

(10 citation statements)

References 60 publications

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“…Mechanistic studies suggest several mechanisms by which apigenin could increase sleep quality and quantity ( Table 1 ). In Drosophila , dietary supplementation with apigenin decreased oxidative stress and acetylcholinesterase activity ( 70 ), reduced glutathione- S - transferase activity and lipid peroxidation, and increased glutathione levels, all of which are thought to support healthy sleep ( 71 , 72 ). Apigenin supplementation in rodents decreased corticosterone levels and increased levels of Bdnf ( 73 ), CREB, phosphorylated CREB, and serotonin in the hippocampus ( 74 , 75 ).…”

Section: Apigenin and Sleepmentioning

confidence: 99%

“…In this model, apigenin partially reversed the lifespan-shortening effects of D-galactose ( 92 ). In a separate transgenic Drosophila model of Alzheimer’s disease (AD) expressing Amyloid Beta-42 in neurons and producing AD-like amyloid beta aggregates, a daily diet containing apigenin for 30 days was shown to delay the loss of climbing typically seen in this model ( 70 ). Apigenin similarly increases survival in a fly model of PD ( 54 ) and, in Caenorhabditis elegans , dietary supplementation with apigenin or apigenin glycosides increases lifespan ( 93 , 94 ).…”

Section: Apigenin and Agingmentioning

confidence: 99%

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Apigenin: a natural molecule at the intersection of sleep and aging

Kramer,

Johnson

2024

Front. Nutr.

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NAD+, a pivotal coenzyme central to metabolism, exhibits a characteristic decline with age. In mice, NAD+ levels can be elevated via treatment with apigenin, a natural flavonoid that inhibits the NAD+-consuming glycoprotein CD38. In animal models, apigenin positively impacts both sleep and longevity. For example, apigenin improves learning and memory in older mice, reduces tumor proliferation in a mouse xenograft model of triple-negative breast cancer, and induces sedative effects in mice and rats. Moreover, apigenin elongates survival in fly models of neurodegenerative disease and apigenin glycosides increase lifespan in worms. Apigenin’s therapeutic potential is underscored by human clinical studies using chamomile extract, which contains apigenin as an active ingredient. Collectively, chamomile extract has been reported to alleviate anxiety, improve mood, and relieve pain. Furthermore, dietary apigenin intake positively correlates with sleep quality in a large cohort of adults. Apigenin’s electron-rich flavonoid structure gives it strong bonding capacity to diverse molecular structures across receptors and enzymes. The effects of apigenin extend beyond CD38 inhibition, encompassing agonistic and antagonistic modulation of various targets, including GABA and inflammatory pathways. Cumulatively, a large body of evidence positions apigenin as a unique molecule capable of influencing both aging and sleep. Further studies are warranted to better understand apigenin’s nuanced mechanisms and clinical potential.

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Section: Apigenin and Sleepmentioning

confidence: 99%

Section: Apigenin and Agingmentioning

confidence: 99%

Apigenin: a natural molecule at the intersection of sleep and aging

Kramer,

Johnson

2024

Front. Nutr.

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“…[5][6][7][8][9][10][11] These AD models exhibited AD-like pathological and behavioral changes. [5][6][7][8][9][10][11][12][13][14] Arctic mutant Aβ 42 (E22G) is an important mutation of Aβ 42 in familial Alzheimer's disease (FAD). 15 Expression of Aβ arc (arctic mutant Aβ 42 ) was more neurotoxic than expression of Aβ 40 and Aβ 42 in Drosophila 13,16 consistent with the aggregative abilities of these peptides found in vitro.…”

Section: Introductionmentioning

confidence: 99%

“…Drosophila has been extensively used to build AD models due to its small size, ease of reproduction, and ease of genetic manipulation 5–7 . Drosophila AD models were almost generated by expression of human Aβ, APP, presenilin, and BACE 5–11 . These AD models exhibited AD‐like pathological and behavioral changes 5–14 .…”

Section: Introductionmentioning

confidence: 99%

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Icaritin greatly attenuates β‐amyloid‐induced toxicity in vivo

Li,

Wei,

Tang

et al. 2023

CNS Neurosci Ther

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AimsThe accumulation and deposition of β‐amyloid (Aβ) has always been considered a major pathological feature of Alzheimer's disease (AD). The latest and mainstream amyloid cascade hypothesis indicates that all the main pathological changes in AD are attributed to the accumulation of soluble Aβ. However, the exploration of therapeutic drugs for Aβ toxicity has progressed slowly. This study aims to investigate the protective effects of Icaritin on the Aβ‐induced Drosophila AD model and its possible mechanism.MethodsTo identify the effects of Icaritin on AD, we constructed an excellent Drosophila AD model named Aβarc (arctic mutant Aβ42) Drosophila. Climbing ability, flight ability, and longevity were used to evaluate the effects of Icaritin on AD phenotypes. Aβarc was determined by immunostaining and ELISA. To identify the effects of Icaritin on oxidative stress, we performed the detection of ROS, hydrogen peroxide, MDA, SOD, catalase, GST, and Caspase‐3. To identify the effects of Icaritin on energy metabolism, we performed the detection of ATP and lactate. Transcriptome analysis and qRT‐PCR verifications were used to detect the genes directly involved in oxidative stress and energy metabolism. Mitochondrial structure and function were detected by an electron microscopy assay, a mitochondrial membrane potential assay, and a mitochondrial respiration assay.ResultsWe discovered that Icaritin almost completely rescues the climbing ability, flight ability, and longevity of Aβarc Drosophila. Aβarc was dramatically reduced by Icaritin treatment. We also found that Icaritin significantly reduces oxidative stress and greatly improves impaired energy metabolism. Importantly, transcriptome analysis and qRT‐PCR verifications showed that many key genes, directly involved in oxidative stress and energy metabolism, are restored by Icaritin. Next, we found that Icaritin perfectly restores the integrity of mitochondrial structure and function damaged by Aβarc toxicity.ConclusionThis study suggested that Icaritin is a potential drug to deal with the toxicity of Aβarc, at least partially realized by restoring the mitochondria/oxidative stress/energy metabolism axis, and holds potential for translation to human AD.

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The hepatoprotective potential of tannic acid against doxorubicin‐induced hepatotoxicity: Insights into its antioxidative, anti‐inflammatory, and antiapoptotic mechanisms

Özturk,

Ceylan,

Demir

2024

J Biochem & Molecular Tox

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Doxorubicin (DOX), which is frequently used in cancer treatment, has limited clinical use due to adverse effects on healthy tissues, especially the liver. Therefore, it is necessary to research the molecular basis of DOX‐induced organ and tissue damage and protective agents. In this study, we aimed to examine the protective effects of tannic acid (TA) against DOX‐induced hepatoxicity in experimental rat models. Rats were randomly divided into four experimental groups: the untreated control, DOX, TA, and cotreatment (DOX + TA) groups. We investigated the antioxidant system's main components and oxidative stress indicators. Moreover, we examined alterations in the mRNA expression of critical regulators that modulate apoptosis, inflammation, and cell metabolism to better understand the underlying factors of DOX‐induced liver toxicity. The results showed that DOX exposure caused an increase in MDA levels and a significant depletion of GSH content in rat liver tissues. Consistent with oxidative stress‐related metabolites, DOX was found to significantly suppress both mRNA expression and enzyme activities of antioxidant system components. Moreover, DOX exposure had significant adverse effects on regulating the other regulatory genes studied. However, it was determined that TA could alleviate many of the negative changes caused by DOX. The results of the present study indicated that TA might be considered a versatile candidate that could prevent DOX‐induced hepatotoxicity, possibly by preserving cell physiology, viability, and especially redox balance.

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Beneficial effects of apigenin on the transgenic Drosophila model of Alzheimer's disease

Cited by 21 publications

References 60 publications

Apigenin: a natural molecule at the intersection of sleep and aging

Apigenin: a natural molecule at the intersection of sleep and aging

Icaritin greatly attenuates β‐amyloid‐induced toxicity in vivo

The hepatoprotective potential of tannic acid against doxorubicin‐induced hepatotoxicity: Insights into its antioxidative, anti‐inflammatory, and antiapoptotic mechanisms

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