Nigella sativa L. (Black Cumin): A Promising Natural Remedy for Wide Range of Illnesses
Identifieur interne : 000A80 ( Pmc/Checkpoint ); précédent : 000A79; suivant : 000A81Nigella sativa L. (Black Cumin): A Promising Natural Remedy for Wide Range of Illnesses
Auteurs : Ebrahim M. Yimer [Éthiopie] ; Kald Beshir Tuem [Éthiopie] ; Aman Karim [Éthiopie] ; Najeeb Ur-Rehman [Arabie saoudite] ; Farooq Anwar [Pakistan]Source :
- Evidence-based Complementary and Alternative Medicine : eCAM [ 1741-427X ] ; 2019.
Abstract
The seed of
Url:
DOI: 10.1155/2019/1528635
PubMed: 31214267
PubMed Central: 6535880
Affiliations:
Links toward previous steps (curation, corpus...)
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PMC:6535880Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en"><italic>Nigella sativa</italic> L. (Black Cumin): A Promising Natural Remedy for Wide Range of Illnesses</title><author><name sortKey="Yimer, Ebrahim M" sort="Yimer, Ebrahim M" uniqKey="Yimer E" first="Ebrahim M." last="Yimer">Ebrahim M. Yimer</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Pharmacology and Toxicology, College of Health Sciences, Mekelle University, Ethiopia</nlm:aff><country xml:lang="fr">Éthiopie</country><wicri:regionArea>Department of Pharmacology and Toxicology, College of Health Sciences, Mekelle University</wicri:regionArea><wicri:noRegion>Mekelle University</wicri:noRegion></affiliation></author><author><name sortKey="Tuem, Kald Beshir" sort="Tuem, Kald Beshir" uniqKey="Tuem K" first="Kald Beshir" last="Tuem">Kald Beshir Tuem</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Pharmacology and Toxicology, College of Health Sciences, Mekelle University, Ethiopia</nlm:aff><country xml:lang="fr">Éthiopie</country><wicri:regionArea>Department of Pharmacology and Toxicology, College of Health Sciences, Mekelle University</wicri:regionArea><wicri:noRegion>Mekelle University</wicri:noRegion></affiliation></author><author><name sortKey="Karim, Aman" sort="Karim, Aman" uniqKey="Karim A" first="Aman" last="Karim">Aman Karim</name><affiliation wicri:level="1"><nlm:aff id="I2">Department of Pharmacognosy, College of Health Sciences, Mekelle University, Ethiopia</nlm:aff><country xml:lang="fr">Éthiopie</country><wicri:regionArea>Department of Pharmacognosy, College of Health Sciences, Mekelle University</wicri:regionArea><wicri:noRegion>Mekelle University</wicri:noRegion></affiliation></author><author><name sortKey="Ur Rehman, Najeeb" sort="Ur Rehman, Najeeb" uniqKey="Ur Rehman N" first="Najeeb" last="Ur-Rehman">Najeeb Ur-Rehman</name><affiliation wicri:level="1"><nlm:aff id="I3">Department of Pharmacology, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Al-Kharj, Saudi Arabia</nlm:aff><country xml:lang="fr">Arabie saoudite</country><wicri:regionArea>Department of Pharmacology, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Al-Kharj</wicri:regionArea><wicri:noRegion>Al-Kharj</wicri:noRegion></affiliation></author><author><name sortKey="Anwar, Farooq" sort="Anwar, Farooq" uniqKey="Anwar F" first="Farooq" last="Anwar">Farooq Anwar</name><affiliation wicri:level="1"><nlm:aff id="I4">Department of Chemistry, University of Sargodha, Sargodha, Pakistan</nlm:aff><country xml:lang="fr">Pakistan</country><wicri:regionArea>Department of Chemistry, University of Sargodha, Sargodha</wicri:regionArea><wicri:noRegion>Sargodha</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31214267</idno><idno type="pmc">6535880</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6535880</idno><idno type="RBID">PMC:6535880</idno><idno type="doi">10.1155/2019/1528635</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000946</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000946</idno><idno type="wicri:Area/Pmc/Curation">000946</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000946</idno><idno type="wicri:Area/Pmc/Checkpoint">000A80</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000A80</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main"><italic>Nigella sativa</italic> L. (Black Cumin): A Promising Natural Remedy for Wide Range of Illnesses</title><author><name sortKey="Yimer, Ebrahim M" sort="Yimer, Ebrahim M" uniqKey="Yimer E" first="Ebrahim M." last="Yimer">Ebrahim M. Yimer</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Pharmacology and Toxicology, College of Health Sciences, Mekelle University, Ethiopia</nlm:aff><country xml:lang="fr">Éthiopie</country><wicri:regionArea>Department of Pharmacology and Toxicology, College of Health Sciences, Mekelle University</wicri:regionArea><wicri:noRegion>Mekelle University</wicri:noRegion></affiliation></author><author><name sortKey="Tuem, Kald Beshir" sort="Tuem, Kald Beshir" uniqKey="Tuem K" first="Kald Beshir" last="Tuem">Kald Beshir Tuem</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Pharmacology and Toxicology, College of Health Sciences, Mekelle University, Ethiopia</nlm:aff><country xml:lang="fr">Éthiopie</country><wicri:regionArea>Department of Pharmacology and Toxicology, College of Health Sciences, Mekelle University</wicri:regionArea><wicri:noRegion>Mekelle University</wicri:noRegion></affiliation></author><author><name sortKey="Karim, Aman" sort="Karim, Aman" uniqKey="Karim A" first="Aman" last="Karim">Aman Karim</name><affiliation wicri:level="1"><nlm:aff id="I2">Department of Pharmacognosy, College of Health Sciences, Mekelle University, Ethiopia</nlm:aff><country xml:lang="fr">Éthiopie</country><wicri:regionArea>Department of Pharmacognosy, College of Health Sciences, Mekelle University</wicri:regionArea><wicri:noRegion>Mekelle University</wicri:noRegion></affiliation></author><author><name sortKey="Ur Rehman, Najeeb" sort="Ur Rehman, Najeeb" uniqKey="Ur Rehman N" first="Najeeb" last="Ur-Rehman">Najeeb Ur-Rehman</name><affiliation wicri:level="1"><nlm:aff id="I3">Department of Pharmacology, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Al-Kharj, Saudi Arabia</nlm:aff><country xml:lang="fr">Arabie saoudite</country><wicri:regionArea>Department of Pharmacology, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Al-Kharj</wicri:regionArea><wicri:noRegion>Al-Kharj</wicri:noRegion></affiliation></author><author><name sortKey="Anwar, Farooq" sort="Anwar, Farooq" uniqKey="Anwar F" first="Farooq" last="Anwar">Farooq Anwar</name><affiliation wicri:level="1"><nlm:aff id="I4">Department of Chemistry, University of Sargodha, Sargodha, Pakistan</nlm:aff><country xml:lang="fr">Pakistan</country><wicri:regionArea>Department of Chemistry, University of Sargodha, Sargodha</wicri:regionArea><wicri:noRegion>Sargodha</wicri:noRegion></affiliation></author></analytic><series><title level="j">Evidence-based Complementary and Alternative Medicine : eCAM</title><idno type="ISSN">1741-427X</idno><idno type="eISSN">1741-4288</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The seed of<italic> Nigella sativa</italic> (<italic>N. sativa</italic>) has been used in different civilization around the world for centuries to treat various animal and human ailments. So far, numerous studies demonstrated the seed of<italic> Nigella sativa </italic>and its main active constituent, thymoquinone, to be medicinally very effective against various illnesses including different chronic illness: neurological and mental illness, cardiovascular disorders, cancer, diabetes, inflammatory conditions, and infertility as well as various infectious diseases due to bacterial, fungal, parasitic, and viral infections. In spite of limited studies conducted so far, the promising efficacy of<italic> N. sativa</italic> against HIV/AIDS can be explored as an alternative option for the treatment of this pandemic disease after substantiating its full therapeutic efficacy. Moreover, the strong antioxidant property of this valued seed has recently gained increasing attention with regard to its potential role as dietary supplement with minimal side effects. Besides, when combined with different conventional chemotherapeutic agents, it synergizes their effects resulting in reducing the dosage of concomitantly used drugs with optimized efficacy and least and/or no toxicity. A number of pharmaceutical and biological properties have been ascribed to seeds of<italic> N. sativa</italic>. The present review focuses on the profile of high-value components along with traditional medicinal and biological principles of<italic> N. sativa </italic>seed and its oil so as to explore functional food and nutraceutical potential of this valued herb.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Jamshidi Kia, F" uniqKey="Jamshidi Kia F">F. Jamshidi-Kia</name></author><author><name sortKey="Lorigooini, Z" uniqKey="Lorigooini Z">Z. Lorigooini</name></author><author><name sortKey="Amini Khoei, H" uniqKey="Amini Khoei H">H. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Evid Based Complement Alternat Med</journal-id><journal-id journal-id-type="iso-abbrev">Evid Based Complement Alternat Med</journal-id><journal-id journal-id-type="publisher-id">ECAM</journal-id><journal-title-group><journal-title>Evidence-based Complementary and Alternative Medicine : eCAM</journal-title></journal-title-group><issn pub-type="ppub">1741-427X</issn><issn pub-type="epub">1741-4288</issn><publisher><publisher-name>Hindawi</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31214267</article-id><article-id pub-id-type="pmc">6535880</article-id><article-id pub-id-type="doi">10.1155/2019/1528635</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review Article</subject></subj-group></article-categories><title-group><article-title><italic>Nigella sativa</italic> L. (Black Cumin): A Promising Natural Remedy for Wide Range of Illnesses</article-title></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid" authenticated="false">http://orcid.org/0000-0003-3140-4967</contrib-id><name><surname>Yimer</surname><given-names>Ebrahim M.</given-names></name><email>ebrahim99muhammed@gmail.com</email><xref ref-type="aff" rid="I1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">http://orcid.org/0000-0003-2847-1392</contrib-id><name><surname>Tuem</surname><given-names>Kald Beshir</given-names></name><xref ref-type="aff" rid="I1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">http://orcid.org/0000-0001-6198-1664</contrib-id><name><surname>Karim</surname><given-names>Aman</given-names></name><xref ref-type="aff" rid="I2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Ur-Rehman</surname><given-names>Najeeb</given-names></name><xref ref-type="aff" rid="I3"><sup>3</sup></xref></contrib><contrib contrib-type="author"><name><surname>Anwar</surname><given-names>Farooq</given-names></name><xref ref-type="aff" rid="I4"><sup>4</sup></xref></contrib></contrib-group><aff id="I1"><sup>1</sup>Department of Pharmacology and Toxicology, College of Health Sciences, Mekelle University, Ethiopia</aff><aff id="I2"><sup>2</sup>Department of Pharmacognosy, College of Health Sciences, Mekelle University, Ethiopia</aff><aff id="I3"><sup>3</sup>Department of Pharmacology, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Al-Kharj, Saudi Arabia</aff><aff id="I4"><sup>4</sup>Department of Chemistry, University of Sargodha, Sargodha, Pakistan</aff><author-notes><fn fn-type="other"><p>Academic Editor: Nativ Dudai</p></fn></author-notes><pub-date pub-type="collection"><year>2019</year></pub-date><pub-date pub-type="epub"><day>12</day><month>5</month><year>2019</year></pub-date><pub-date pub-type="pmc-release"><day>12</day><month>5</month><year>2019</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on the
<volume>2019</volume><elocation-id>1528635</elocation-id><history><date date-type="received"><day>20</day><month>10</month><year>2018</year></date><date date-type="rev-recd"><day>26</day><month>2</month><year>2019</year></date><date date-type="accepted"><day>30</day><month>4</month><year>2019</year></date></history><permissions><copyright-statement>Copyright © 2019 Ebrahim M. Yimer et al.</copyright-statement><copyright-year>2019</copyright-year><license xlink:href="https://creativecommons.org/licenses/by/4.0/"><license-p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p></license></permissions><abstract><p>The seed of<italic> Nigella sativa</italic> (<italic>N. sativa</italic>) has been used in different civilization around the world for centuries to treat various animal and human ailments. So far, numerous studies demonstrated the seed of<italic> Nigella sativa </italic>and its main active constituent, thymoquinone, to be medicinally very effective against various illnesses including different chronic illness: neurological and mental illness, cardiovascular disorders, cancer, diabetes, inflammatory conditions, and infertility as well as various infectious diseases due to bacterial, fungal, parasitic, and viral infections. In spite of limited studies conducted so far, the promising efficacy of<italic> N. sativa</italic> against HIV/AIDS can be explored as an alternative option for the treatment of this pandemic disease after substantiating its full therapeutic efficacy. Moreover, the strong antioxidant property of this valued seed has recently gained increasing attention with regard to its potential role as dietary supplement with minimal side effects. Besides, when combined with different conventional chemotherapeutic agents, it synergizes their effects resulting in reducing the dosage of concomitantly used drugs with optimized efficacy and least and/or no toxicity. A number of pharmaceutical and biological properties have been ascribed to seeds of<italic> N. sativa</italic>. The present review focuses on the profile of high-value components along with traditional medicinal and biological principles of<italic> N. sativa </italic>seed and its oil so as to explore functional food and nutraceutical potential of this valued herb.</p></abstract></article-meta></front><floats-group><table-wrap id="tab1" orientation="portrait" position="float"><label>Table 1</label><caption><p>The effects of <italic>N. sativa</italic> and its active component, thymoquinone (TQ) on neurological and mental disorders.</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left" rowspan="1" colspan="1">Neurological or mental Disorders</th><th align="left" rowspan="1" colspan="1">Model used and intervention (s)</th><th align="left" rowspan="1" colspan="1">Finding (mechanism)</th><th align="center" rowspan="1" colspan="1">References</th></tr></thead><tbody><tr><td rowspan="2" align="left" colspan="1">Alzheimer's disease (AD)</td><td align="left" rowspan="1" colspan="1">Lipopolysaccharide-induced AD in mice, received TQ (2.5 & 5mg/kg) for 7 days.</td><td align="left" rowspan="1" colspan="1">(i) ↓ TBARS & 5-LOX levels <break></break>(ii) ↑ GSH extent and SOD action<break></break>(iii) Causes disaggregation of A<italic>β</italic> peptide<break></break>(iv) prevents declining of neurons<break></break>(v) Slows degeneration of cognitive ability</td><td align="center" rowspan="1" colspan="1">[<xref rid="B64" ref-type="bibr">64</xref>, <xref rid="B65" ref-type="bibr">65</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">A<italic>β</italic>-induced neurotoxicity (analyzed by culturing hippocampus and cortical neurons).<break></break>TQ is administered along with A<italic>β</italic><sub>1−42</sub> for 72 hours</td><td align="left" rowspan="1" colspan="1">(i) Reducing A<italic>β</italic>-induced neurotoxicity. (Improved cell viability) by:<break></break>(ii) Inhibiting mitochondrial membrane potential depolarization <break></break>(iii) Hindering reactive oxygen species generation</td><td align="center" rowspan="1" colspan="1">[<xref rid="B66" ref-type="bibr">66</xref>]<break></break></td></tr><tr><td colspan="4" rowspan="1"><hr></hr></td></tr><tr><td rowspan="2" align="left" colspan="1">Parkinson's disease (PD)</td><td align="left" rowspan="1" colspan="1">1-methyl-4-phenylpyridinium (MPP<sup>+</sup>) and rotenone-induced neurotoxicity in PD model, cultures were treated with TQ (0.01, 0.1, 1 and, 10 <italic>μ</italic>M) on day 8th for 4 days.</td><td align="left" rowspan="1" colspan="1">(i) Rescued dopaminergic neurons through:<break></break>(ii) Its antioxidant and anti-inflammatory effects</td><td align="center" rowspan="1" colspan="1">[<xref rid="B67" ref-type="bibr">67</xref>]<break></break></td></tr><tr><td align="left" rowspan="1" colspan="1">Experimental model of early PD induced by 6-hydroxydopamine neurotoxicity, pretreatment of daily TQ (5 & 10 mg/kg) and one additional dose after surgery were used.</td><td align="left" rowspan="1" colspan="1">(i) ↓ MDA level <break></break>(ii) Prevents loss of neurons in substantia nigra<break></break>(iii) Protects hippocampal & human induced pluripotent stem cell against <italic>α</italic>-synuclein induced synaptic toxicity</td><td align="center" rowspan="1" colspan="1"> [<xref rid="B68" ref-type="bibr">68</xref>, <xref rid="B69" ref-type="bibr">69</xref>]<break></break></td></tr><tr><td colspan="4" rowspan="1"><hr></hr></td></tr><tr><td rowspan="3" align="left" colspan="1">Depression and anxiety</td><td align="left" rowspan="1" colspan="1">(i) Open field and elevated plus maze models; forced swim test <break></break>(ii) Locomotor behavior in familiar and new environment in rats, <italic>N. sativa </italic> oil (0.1 mL/day) aqueous seed extract (2 mL/day) orally for 4-6 weeks</td><td align="left" rowspan="1" colspan="1">(i) ↑ in open field activity & struggling time<break></break>(ii) ↑ 5-HT <break></break>(iii) ↓ 5HIAA level in the brain <break></break>(iv) ↑ tryptophan level in plasma & brain<break></break>(v) ↑ locomotors activity in novel environment <break></break>(vi) ↑ brain DA level</td><td align="center" rowspan="1" colspan="1">[<xref rid="B59" ref-type="bibr">59</xref>, <xref rid="B70" ref-type="bibr">70</xref>, <xref rid="B71" ref-type="bibr">71</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Stressed and unstressed mice, 10 and 20 mg/kg of TQ for 4 weeks</td><td align="left" rowspan="1" colspan="1">Unstressed mice: at 10 & 20 mg/Kg showed anti-anxiety <break></break>(i) without altering nitrite levels<break></break>(ii) ↑ GABA content (only 20mg/Kg).<break></break>Stressed mice: 20 mg/kg showed anxiolytic effects with <break></break>(i) ↓ plasma nitrite level<break></break>(ii) Reversal of reduced GABA</td><td align="center" rowspan="1" colspan="1">[<xref rid="B72" ref-type="bibr">72</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Randomized control trial on healthy human subjects, <italic>N. sativa</italic> capsule (500 mg) daily for 4 weeks.</td><td align="left" rowspan="1" colspan="1">(i) Stabilize disturbed mood<break></break>(ii) ↓ anxiety<break></break>(iii) Modulate memory positively</td><td align="center" rowspan="1" colspan="1">[<xref rid="B73" ref-type="bibr">73</xref>]</td></tr><tr><td colspan="4" rowspan="1"><hr></hr></td></tr><tr><td rowspan="2" align="left" colspan="1">Epilepsy</td><td align="left" rowspan="1" colspan="1">Pentylenetetrazole-induced seizure, <italic>N. sativa</italic> oil; TQ</td><td align="left" rowspan="1" colspan="1">(i) Prevented seizure occurrence<break></break>(ii) ↓ Reactive oxygen species generation<break></break>(iii) Reduced seizure score <break></break>(iv) Showed additive effects with phenobarbitone</td><td align="center" rowspan="1" colspan="1">[<xref rid="B74" ref-type="bibr">74</xref>–<xref rid="B76" ref-type="bibr">76</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Double-blinded placebo randomized control trial (refractory epilepsy), TQ as adjunctive therapy for 4 weeks</td><td align="left" rowspan="1" colspan="1">(i) Significant reduction of seizure frequency (those who received combination therapy)</td><td align="center" rowspan="1" colspan="1">[<xref rid="B77" ref-type="bibr">77</xref>]</td></tr><tr><td colspan="4" rowspan="1"><hr></hr></td></tr><tr><td rowspan="2" align="left" colspan="1">Opioid dependence and Tolerance</td><td align="left" rowspan="1" colspan="1">Morphine brought tolerance and dependency in mice, 4mL/kg of <italic>N. sativa</italic> oil along with morphine (5mg/kg)</td><td align="left" rowspan="1" colspan="1">(i) Attenuated the development of tolerance<break></break>(ii) Inhibited nitric oxide overproduction <break></break>(iii) ↓ in brain MDA level</td><td align="center" rowspan="1" colspan="1">[<xref rid="B78" ref-type="bibr">78</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Randomized trial (on 35 known addicts of opiates), 500 mg <italic>N. Sativa </italic>three times daily<break></break></td><td align="left" rowspan="1" colspan="1">(i) ↓ the withdrawal effects significantly<break></break>(ii) ↑ appetite (no significant weight gain)<break></break>(iii) No changes in physiological parameters (blood pressure, pulse and respiratory rate)</td><td align="center" rowspan="1" colspan="1">[<xref rid="B79" ref-type="bibr">79</xref>]</td></tr></tbody></table><table-wrap-foot><fn><p>TBARs= Thiobarbituric acid reactive substances, GABA= gamma amino butyric acid, 5-HT= 5 hydroxytryptamine, MDA= malondialdehyde, DA= dopamine, 5HIAA= 5 hydroxyindoleacetic acid, GSH= glutathione peroxidase, SOD= superoxide dismutase, TQ= thymoquinone, A<italic>β</italic>= beta amyloid peptides, ↑=increase, ↓=decrease.</p></fn></table-wrap-foot></table-wrap><table-wrap id="tab2" content-type="sidewaystable" orientation="portrait" position="float"><label>Table 2</label><caption><p>Effects of <italic>N. sativa</italic> and thymoquinone against various types of cancer models and their effects on anticancer agents.</p></caption><table frame="hsides" rules="groups"><thead><tr><th colspan="2" align="center" rowspan="1">Cancer models or effects of anticancer agents</th><th align="left" rowspan="1" colspan="1">Intervention (s)</th><th align="left" rowspan="1" colspan="1">Findings (Mechanisms)</th><th align="center" rowspan="1" colspan="1">References</th></tr></thead><tbody><tr><td rowspan="8" align="left" colspan="1"><italic>In vitro </italic>studies</td><td align="left" rowspan="1" colspan="1">Doxorubicin-resistant <break></break>human breast cancer cells line (MCF-7/DOX cells)</td><td align="left" rowspan="1" colspan="1">TQ (25, 50 or 100 <italic>µ</italic>M) for 48 hours & NSO Nano emulsion</td><td align="left" rowspan="1" colspan="1">(i) Concentration dependent growth inhibition<break></break>(ii) Induce apoptosis, p53 protein <break></break>(iii) Upregulation of PTEN (inhibit PI3K/Akt pathway)</td><td align="center" rowspan="1" colspan="1">[<xref rid="B125" ref-type="bibr">124</xref>, <xref rid="B126" ref-type="bibr">125</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Human cervical squamous <break></break>cancer cells</td><td align="left" rowspan="1" colspan="1">TQ (1.0 to 30 <italic>μ</italic>g/mL) for 24, 48 and 72 hours</td><td align="left" rowspan="1" colspan="1">(i) More cytotoxic than cisplatin towards this cancerous cell (but less cytotoxicity towards normal cells)<break></break>(ii) Downregulates Bcl-2 protein</td><td align="center" rowspan="1" colspan="1">[<xref rid="B127" ref-type="bibr">126</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Myeloblastic leukemia <break></break>(HL-60 cells)</td><td align="left" rowspan="1" colspan="1">TQ</td><td align="left" rowspan="1" colspan="1">(i) Induces apoptosis, disrupts mitochondrial membrane potential, triggers the activation of caspases 3, 8 & 9 in HL-60 cells</td><td align="center" rowspan="1" colspan="1"> [<xref rid="B128" ref-type="bibr">127</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Human bladder cancer cells (T24 and 253J)</td><td align="left" rowspan="1" colspan="1">TQ (20-160 <italic>µ</italic>mol/L) for different periods (24h, 48h, and 72h)</td><td align="left" rowspan="1" colspan="1">(i) TQ showed marked cytotoxicity on bladder cancer cells<break></break>(ii) It inhibited cancerous cells rapid multiplication and evoked apoptosis via activation of caspase.<break></break>(iii) TQ also resulted in activation of ER stress, mitochondrial disturbance and enhanced mitochondrial mediated apoptotic path.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B129" ref-type="bibr">128</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Renal cell cancer (RCC) cell lines (786-O and ACHN)</td><td align="left" rowspan="1" colspan="1">TQ (40 <italic>μ</italic>mol/L) for 24 hours</td><td align="left" rowspan="1" colspan="1">(i) TQ suppressed migration, invasion and epithelial-mesenchymal transition in RCC cells.<break></break>(ii) TQ exhibited significant inhibition of the metastasis of RCC cells through induction of autophagy via AMPK/mTOR signalling.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B130" ref-type="bibr">129</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Human renal tubular epithelial cell (HK2) and the human RCC cell lines (769-P & 786-O)</td><td align="left" rowspan="1" colspan="1">TQ (0.5, 1, 2.5, 5, 10, 15 & 20 <italic>µ</italic>M) at various durations (0, 24, 48 & 72 h).</td><td align="left" rowspan="1" colspan="1">(i) TQ markedly inhibited the migration and invasion of the human RCC 769-P and 786-O cell lines.<break></break>(ii) TQ also increased the expression of E-cadherin and reduced the expression of Snail, ZEB1 and vimentin at the mRNA as well as protein levels in dose-dependent fashion.<break></break>(iii) As a result, the extents of phosphorylation of hepatic kinase B1 and AMPK were upregulated.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B131" ref-type="bibr">130</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Human prostate cancer cell lines (DU145 and C3)</td><td align="left" rowspan="1" colspan="1">TQ (2.5, 5.0 & 10 <italic>µ</italic>M) for 24 hours.</td><td align="left" rowspan="1" colspan="1">(i) TQ substantially arrested the proliferation of prostate cancer.<break></break>(ii) It inhibited the migrating and invading capability of prostate cancer DU145 and PC3 cells.<break></break>(iii) TQ also downregulated the expression of TGF-<italic>β</italic>, Smad2 and Smad3 in prostate cancer cells.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B132" ref-type="bibr">131</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Hepatocellular cancer cell line (HepG2)</td><td align="left" rowspan="1" colspan="1">TQ (3–24 <italic>µ</italic>M) for 24 hours.</td><td align="left" rowspan="1" colspan="1">(i) Decreased both the no. of viable HepG2 cells and the levels<break></break>(ii) TQ induced cell cycle arrest and apoptosis<break></break>(iii) Increased total antioxidant status (dose dependently) <break></break>(iv) TQ reduced the release of VEGF of HepG2 cells</td><td align="center" rowspan="1" colspan="1">[<xref rid="B133" ref-type="bibr">132</xref>]</td></tr><tr><td colspan="5" rowspan="1"><hr></hr></td></tr><tr><td rowspan="5" align="left" colspan="1"><italic>In vivo </italic>studies</td><td align="left" rowspan="1" colspan="1">Diethyl nitrosamine inducedhepatocarcinogenesis in Wistar rats</td><td align="left" rowspan="1" colspan="1">Ethanolic extract of NS (250 mg/kg) for 5 consecutive days.</td><td align="left" rowspan="1" colspan="1">(i) The chemical induced increment of liver weight, hepato-somatic indices, serum AFP and VEGF levels, and hepatic HGF<italic>β</italic> protein expression were significantly reversed by the extract.<break></break>(ii) The histopathological alteration of the livers due to the chemical was decreased in NS extract received rats without harmful effects.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B134" ref-type="bibr">133</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Orthotopic model inmice [triple-negative breast cancer (TNBC) cell lines]</td><td align="left" rowspan="1" colspan="1">TQ (20 or 100 mg/k) once every 3 days</td><td align="left" rowspan="1" colspan="1">(i) TQ markedly reduced the growth of MDA-MB-231 tumor.<break></break>(ii) TQ decreased TNBC cell viability and proliferation as well as the migration and invasion of TNBC cells.<break></break>(iii) TQ also downregulated the expression of eEF-2K (via modulation of the NF-<italic>κ</italic>B/miR-603), Src/FAK, and Akt in TNBC cells.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B135" ref-type="bibr">134</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Colon carcinogenesis of rats model</td><td align="left" rowspan="1" colspan="1">NSO for 14 weeks</td><td align="left" rowspan="1" colspan="1">(i) NSO revealed a significant antiproliferative activity in both initiation and post-initiation phases<break></break>(ii) Inhibited colon carcinogenesis of rats mainly in the post-initiation stage with no evident of adverse effects</td><td align="center" rowspan="1" colspan="1">[<xref rid="B136" ref-type="bibr">135</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Mouse model of colorectal carcinogenesis & C26 cell</td><td align="left" rowspan="1" colspan="1">TQ (5 mg/kg) for 3 weeks & TQ (0, 20, 40, 60 <italic>μ</italic>M) <italic>in vitro</italic></td><td align="left" rowspan="1" colspan="1">(i) TQ reduced tumor multiplicity<break></break>(ii) TQ impeded tumor growth and induce apoptosis in HCT116 xenografts<break></break>(iii) Sub-cytotoxic conc. of TQ (40<italic>μ</italic>M) also reduced C26 cell invasion<break></break>(iv) Anti-neoplastic and pro-apoptotic p53-dependent mechanism</td><td align="center" rowspan="1" colspan="1">[<xref rid="B137" ref-type="bibr">136</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Rat multi-organ <break></break>carcinogenesis</td><td align="left" rowspan="1" colspan="1">NSO for 30 weeks</td><td align="left" rowspan="1" colspan="1">(i) Reduction in malignant and benign colon tumor sizes, tumors in the lungs and in diverse parts of the alimentary canal principally the oesophagus and fore stomach</td><td align="center" rowspan="1" colspan="1">[<xref rid="B138" ref-type="bibr">137</xref>]</td></tr><tr><td colspan="5" rowspan="1"><hr></hr></td></tr><tr><td rowspan="4" align="left" colspan="1">Effect on anti-cancer drugs</td><td align="left" rowspan="1" colspan="1">Cyclophosphamide <break></break>Induced toxicity (abnormal RF & LFT and reduced Hgb) in rat</td><td align="left" rowspan="1" colspan="1">NSO (1ml/kg) and TQ (10 mg/kg) EOD for 12 days</td><td align="left" rowspan="1" colspan="1">(i) Substantial reduction in overall cyclophosphamide induced toxicity in both NSO and TQ treated groups.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B139" ref-type="bibr">138</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Antitumor Effect of TQ and gemcitabine on xenograft mouse and PANC-1, AsPC-1 and BxPC-3 cell lines of pancreatic cancer models,</td><td align="left" rowspan="1" colspan="1">TQ (0–50 <italic>µ</italic>mol/L) & 1.0 mg/ mouse daily<break></break></td><td align="left" rowspan="1" colspan="1">(i) TQ pre-treatment synergistically increased the gemcitabine actions of apoptotic and tumor growth inhibition of pancreatic cancer cells.<break></break>(ii) Concomitant uses resulted in the change of several molecular signaling, including the downregulation of Notch1, NICD associated with up-regulation of PTEN, via the inactivation of Akt/mTOR/S6 signaling.<break></break>(iii) TQ and gemcitabine also induced suppression of anti-apoptotic Bcl-2, Bcl-xL, XIAP and overexpression and activation Caspase-3, Caspase-9, & Bax.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B140" ref-type="bibr">139</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Cytotoxicity assay of TQ and paclitaxel on mouse breast cancer cell line (4T1) and animal models</td><td align="left" rowspan="1" colspan="1">TQ (6.25, 12.5, 25, 50, & 100 <italic>μ</italic>M) for 24 & 48 hours; (0.64, 2.4 & 3.2 mg/kg of mouse body weight).</td><td align="left" rowspan="1" colspan="1">(i) TQ induced marked cytotoxicity and apoptosis, while inhibiting wound healing and migration of 4T1 cells.<break></break>(ii) Co-administration of TQ and paclitaxel significantly induced cytotoxicity and apoptosis compared to separate administration.<break></break>(iii) The combination of paclitaxel and the lower dose TQ markedly inhibited the tumor growth.<break></break>(iv) Both agents also modulated the apoptosis genes, p53 and JAK-STAT signaling, while overexpressing the levels of Caspase-3, Caspase-7, and Caspase-12.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B141" ref-type="bibr">140</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Anti-tumor activity of TQ and topotecan in colorectal cancer cell line (HT-29)</td><td align="left" rowspan="1" colspan="1">TQ (40, 55 & 60 <italic>µ</italic>M)<break></break></td><td align="left" rowspan="1" colspan="1">(i) TQ significantly enhanced the anti-tumor effect of non-cytotoxic dose of topotecan.<break></break>(ii) Both drugs induced apoptosis via a p53-independent mechanism, while the expression of p21 was only noted in TQ therapy.<break></break>(iii) TQ improved the effectiveness of topotecan by inhibiting proliferationand lowering toxicity via p53- and Bax/Bcl2-independent mechanisms.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B142" ref-type="bibr">141</xref>]</td></tr></tbody></table><table-wrap-foot><fn><p>AMPK: Adenosine monophosphate-activated protein kinase, NS: <italic>Nigella sativa</italic>, NSO: <italic>Nigella sativa</italic> oil, TQ: Thymoquinone, PTEN: phosphatase and tensin homolog, MCF-7: Michigan Cancer Foundation-7, EOD: every other day, mTOR: Mammalian Target of Rapamycin.</p></fn></table-wrap-foot></table-wrap></floats-group></pmc><affiliations><list><country><li>Arabie saoudite</li><li>Pakistan</li><li>Éthiopie</li></country></list><tree><country name="Éthiopie"><noRegion><name sortKey="Yimer, Ebrahim M" sort="Yimer, Ebrahim M" uniqKey="Yimer E" first="Ebrahim M." last="Yimer">Ebrahim M. Yimer</name></noRegion><name sortKey="Karim, Aman" sort="Karim, Aman" uniqKey="Karim A" first="Aman" last="Karim">Aman Karim</name><name sortKey="Tuem, Kald Beshir" sort="Tuem, Kald Beshir" uniqKey="Tuem K" first="Kald Beshir" last="Tuem">Kald Beshir Tuem</name></country><country name="Arabie saoudite"><noRegion><name sortKey="Ur Rehman, Najeeb" sort="Ur Rehman, Najeeb" uniqKey="Ur Rehman N" first="Najeeb" last="Ur-Rehman">Najeeb Ur-Rehman</name></noRegion></country><country name="Pakistan"><noRegion><name sortKey="Anwar, Farooq" sort="Anwar, Farooq" uniqKey="Anwar F" first="Farooq" last="Anwar">Farooq Anwar</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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