Actin cytoskeleton as a putative target of the neem limonoid Azadirachtin A

Anuradha, A.; Annadurai, R. S.; Shashidhara, L.S.

doi:10.1016/j.ibmb.2007.03.009

Cited by 54 publications

(32 citation statements)

References 30 publications

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“…Azadirachtin is known to be effective in insect cells (7,(21)(22)(23)(24) and also to induce cell death in human cell lines at higher concentrations (7,25). We are reporting for the first time that it inhibits inflammatory responses in diverse (15), but azadirachtin does not do so.…”

Section: Discussionmentioning

confidence: 89%

Azadirachtin Interacts with the Tumor Necrosis Factor (TNF) Binding Domain of Its Receptors and Inhibits TNF-induced Biological Responses

Thoh

Kumar

Nagarajaram

et al. 2010

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 89%

Azadirachtin Interacts with the Tumor Necrosis Factor (TNF) Binding Domain of Its Receptors and Inhibits TNF-induced Biological Responses

Thoh

Kumar

Nagarajaram

et al. 2010

Journal of Biological Chemistry

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“…However, NEEM at 3.13 µg cm −2 Aza concentration and the Cd positive control at 0.01 µg cm −2 concentration on filter paper significantly increased the number of binucleate coelomocytes (Table 2). This is in agreement with Anuradha et al [27] who reported that Aza A, the major limonoid of neem seed extracts, induces depolymerization of actin leading to arrest of cells and subsequently apoptosis in a caspase-independent manner. This could be because Aza has chemical characteristics similar to colchicine, an antimitotic metabolite affecting synthesis and depolymerization of spindle fibers [28].…”

Section: Discussionsupporting

confidence: 92%

Toxicity of Commercial Neem Extract to Earthworms (Pheretima peguana)

Muangphra

Gooneratne

2011

Applied and Environmental Soil Science

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The LC 50 of commercial neem extract (Sadao Thai III containing azadirachtin; NEEM) on filter paper in the earthworm Pheretima peguana at 48 h and 72 h was 3.79 and 3.33 µg cm −2 , respectively. In earthworms exposed to five NEEM concentrations from 0.39 (∼10% of 48-h LC 50 ) to 3.13 (∼80% of 48-h LC 50 ) µg cm −2 , the radial thickness of the epidermis and body wall significantly (P < .05) decreased, and thickness of intestinal epithelium increased but only at high doses, approximately 25-fold above the concentration permitted for use as an insecticide in field applications (0.09 µg cm −2 ). NEEM significantly (P < .05) increased the number of binucleated coelomocytes in the micronucleus test (detects chromosomal aberrations) at 3.13 µg cm −2 , approximately 35-fold higher than the recommended dose, but it did not cause coelomocyte DNA single-strand breaks in the comet assay. Thus, NEEM is cytotoxic (increase in binucleates through the inhibition of cytokinesis) but not genotoxic to earthworm coelomocytes. This study demonstrates that the recommended dosage of commercial neem extract as an insecticide in agricultural practices is safe for earthworms.

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“…Salehzadeh et al [38] provided evidence to show that azadirachtin interferes with the polymerisation of tubulin, a protein essential for chromosomal organization and separation during mitosis. Anuradha et al [39] demonstrated that azadirachtin causes actin depolymerization, cell cycle arrest and caspaseindependent apoptosis in Drosophila melanogaster.…”

Section: Stimulation By Azadirachtin and Nimbolidementioning

confidence: 99%

The neem limonoids azadirachtin and nimbolide inhibit cell proliferation and induce apoptosis in an animal model of oral oncogenesis

et al. 2009

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Limonoids from the neem tree (Azadirachta indica) have attracted considerable research attention for their cytotoxicity against human cancer cell lines. However, the antiproliferative and apoptosis inducing effects of neem limonoids have not been tested in animal tumour models. The present study was therefore designed to evaluate the relative chemopreventive potential of the neem limonoids azadirachtin and nimbolide in the hamster buccal pouch (HBP) carcinogenesis model by analyzing the expression of proliferating cell nuclear antigen (PCNA), p21(waf1), cyclin D1, glutathione S-transferase pi (GST-P), NF-kappaB, inhibitor of kappaB (IkappaB), p53, Fas, Bcl-2, Bax, Bid, Apaf-1, cytochrome C, survivin, caspases-3, -6, -8 and -9, and poly(ADP-ribose) polymerase (PARP) by RT-PCR, immunohistochemical, and Western blot analyses. The results provide compelling evidence that azadirachtin and nimbolide mediate their antiproliferative effects by downregulating proteins involved in cell cycle progression and transduce apoptosis by both the intrinsic and extrinsic pathways. On a comparative basis, nimbolide was found to be a more potent antiproliferative and apoptosis inducing agent and offers promise as a candidate agent in multitargeted prevention and treatment of cancer.

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Actin cytoskeleton as a putative target of the neem limonoid Azadirachtin A

Cited by 54 publications

References 30 publications

Azadirachtin Interacts with the Tumor Necrosis Factor (TNF) Binding Domain of Its Receptors and Inhibits TNF-induced Biological Responses

Azadirachtin Interacts with the Tumor Necrosis Factor (TNF) Binding Domain of Its Receptors and Inhibits TNF-induced Biological Responses

Toxicity of Commercial Neem Extract to Earthworms (Pheretima peguana)

The neem limonoids azadirachtin and nimbolide inhibit cell proliferation and induce apoptosis in an animal model of oral oncogenesis

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