Urolithin A’s Antioxidative, Anti-Inflammatory, and Antiapoptotic Activities Mitigate Doxorubicin-Induced Liver Injury in Wistar Rats
Human colon microbiota produce a metabolite called urolithin A (URO A) from ellagic acid and linked compounds, and this metabolite has been demonstrated to have antioxidant, anti-inflammatory, and antiapoptotic activities. The current work examines the various mechanisms through which URO A protects...
Ausführliche Beschreibung
Autor*in: |
Shahid Karim [verfasserIn] Batoul Madani [verfasserIn] Abdulhadi S. Burzangi [verfasserIn] Mohammed Alsieni [verfasserIn] Mohammed A. Bazuhair [verfasserIn] Maha Jamal [verfasserIn] Hussam Daghistani [verfasserIn] Mohammed O. Barasheed [verfasserIn] Huda Alkreathy [verfasserIn] Mohammad Ahmed Khan [verfasserIn] Lateef M. Khan [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2023 |
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Übergeordnetes Werk: |
In: Biomedicines - MDPI AG, 2014, 11(2023), 4, p 1125 |
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Übergeordnetes Werk: |
volume:11 ; year:2023 ; number:4, p 1125 |
Links: |
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DOI / URN: |
10.3390/biomedicines11041125 |
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Katalog-ID: |
DOAJ08989748X |
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10.3390/biomedicines11041125 doi (DE-627)DOAJ08989748X (DE-599)DOAJ02fbb5f5570d45fb9d9fb82630d25069 DE-627 ger DE-627 rakwb eng QH301-705.5 Shahid Karim verfasserin aut Urolithin A’s Antioxidative, Anti-Inflammatory, and Antiapoptotic Activities Mitigate Doxorubicin-Induced Liver Injury in Wistar Rats 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Human colon microbiota produce a metabolite called urolithin A (URO A) from ellagic acid and linked compounds, and this metabolite has been demonstrated to have antioxidant, anti-inflammatory, and antiapoptotic activities. The current work examines the various mechanisms through which URO A protects against doxorubicin (DOX)-induced liver injury in Wistar rats. In this experiment, Wistar rats were administered DOX intraperitoneally (20 mg kg<sup<−1</sup<) on day 7 while given URO A intraperitoneally (2.5 or 5 mg kg<sup<−1</sup< d<sup<−1</sup<) for 14 days. The serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma glutamyl transferase (GGT) were measured. Hematoxylin and eosin (HE) staining was used to evaluate histopathological characteristics, and then antioxidant and anti-inflammatory properties were evaluated in tissue and serum, respectively. We also looked at how active caspase 3 and cytochrome c oxidase were in the liver. The findings demonstrated that supplementary URO A therapy clearly mitigated DOX-induced liver damage. The antioxidant enzymes SOD and CAT were elevated in the liver, and the levels of inflammatory cytokines, such as TNF-α, NF-kB, and IL-6, in the tissue were significantly attenuated, all of which complemented the beneficial effects of URO A in DOX-induced liver injury. In addition, URO A was able to alter the expression of caspase 3 and cytochrome c oxidase in the livers of rats that were subjected to DOX stress. These results showed that URO A reduced DOX-induced liver injury by reducing oxidative stress, inflammation, and apoptosis. chemotherapy drug-induced liver injury urolithin A apoptosis anti-inflammatory oxidative stress Biology (General) Batoul Madani verfasserin aut Abdulhadi S. Burzangi verfasserin aut Mohammed Alsieni verfasserin aut Mohammed A. Bazuhair verfasserin aut Maha Jamal verfasserin aut Hussam Daghistani verfasserin aut Mohammed O. Barasheed verfasserin aut Huda Alkreathy verfasserin aut Mohammad Ahmed Khan verfasserin aut Lateef M. Khan verfasserin aut In Biomedicines MDPI AG, 2014 11(2023), 4, p 1125 (DE-627)750370483 (DE-600)2720867-9 22279059 nnns volume:11 year:2023 number:4, p 1125 https://doi.org/10.3390/biomedicines11041125 kostenfrei https://doaj.org/article/02fbb5f5570d45fb9d9fb82630d25069 kostenfrei https://www.mdpi.com/2227-9059/11/4/1125 kostenfrei https://doaj.org/toc/2227-9059 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2023 4, p 1125 |
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10.3390/biomedicines11041125 doi (DE-627)DOAJ08989748X (DE-599)DOAJ02fbb5f5570d45fb9d9fb82630d25069 DE-627 ger DE-627 rakwb eng QH301-705.5 Shahid Karim verfasserin aut Urolithin A’s Antioxidative, Anti-Inflammatory, and Antiapoptotic Activities Mitigate Doxorubicin-Induced Liver Injury in Wistar Rats 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Human colon microbiota produce a metabolite called urolithin A (URO A) from ellagic acid and linked compounds, and this metabolite has been demonstrated to have antioxidant, anti-inflammatory, and antiapoptotic activities. The current work examines the various mechanisms through which URO A protects against doxorubicin (DOX)-induced liver injury in Wistar rats. In this experiment, Wistar rats were administered DOX intraperitoneally (20 mg kg<sup<−1</sup<) on day 7 while given URO A intraperitoneally (2.5 or 5 mg kg<sup<−1</sup< d<sup<−1</sup<) for 14 days. The serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma glutamyl transferase (GGT) were measured. Hematoxylin and eosin (HE) staining was used to evaluate histopathological characteristics, and then antioxidant and anti-inflammatory properties were evaluated in tissue and serum, respectively. We also looked at how active caspase 3 and cytochrome c oxidase were in the liver. The findings demonstrated that supplementary URO A therapy clearly mitigated DOX-induced liver damage. The antioxidant enzymes SOD and CAT were elevated in the liver, and the levels of inflammatory cytokines, such as TNF-α, NF-kB, and IL-6, in the tissue were significantly attenuated, all of which complemented the beneficial effects of URO A in DOX-induced liver injury. In addition, URO A was able to alter the expression of caspase 3 and cytochrome c oxidase in the livers of rats that were subjected to DOX stress. These results showed that URO A reduced DOX-induced liver injury by reducing oxidative stress, inflammation, and apoptosis. chemotherapy drug-induced liver injury urolithin A apoptosis anti-inflammatory oxidative stress Biology (General) Batoul Madani verfasserin aut Abdulhadi S. Burzangi verfasserin aut Mohammed Alsieni verfasserin aut Mohammed A. Bazuhair verfasserin aut Maha Jamal verfasserin aut Hussam Daghistani verfasserin aut Mohammed O. Barasheed verfasserin aut Huda Alkreathy verfasserin aut Mohammad Ahmed Khan verfasserin aut Lateef M. Khan verfasserin aut In Biomedicines MDPI AG, 2014 11(2023), 4, p 1125 (DE-627)750370483 (DE-600)2720867-9 22279059 nnns volume:11 year:2023 number:4, p 1125 https://doi.org/10.3390/biomedicines11041125 kostenfrei https://doaj.org/article/02fbb5f5570d45fb9d9fb82630d25069 kostenfrei https://www.mdpi.com/2227-9059/11/4/1125 kostenfrei https://doaj.org/toc/2227-9059 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2023 4, p 1125 |
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10.3390/biomedicines11041125 doi (DE-627)DOAJ08989748X (DE-599)DOAJ02fbb5f5570d45fb9d9fb82630d25069 DE-627 ger DE-627 rakwb eng QH301-705.5 Shahid Karim verfasserin aut Urolithin A’s Antioxidative, Anti-Inflammatory, and Antiapoptotic Activities Mitigate Doxorubicin-Induced Liver Injury in Wistar Rats 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Human colon microbiota produce a metabolite called urolithin A (URO A) from ellagic acid and linked compounds, and this metabolite has been demonstrated to have antioxidant, anti-inflammatory, and antiapoptotic activities. The current work examines the various mechanisms through which URO A protects against doxorubicin (DOX)-induced liver injury in Wistar rats. In this experiment, Wistar rats were administered DOX intraperitoneally (20 mg kg<sup<−1</sup<) on day 7 while given URO A intraperitoneally (2.5 or 5 mg kg<sup<−1</sup< d<sup<−1</sup<) for 14 days. The serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma glutamyl transferase (GGT) were measured. Hematoxylin and eosin (HE) staining was used to evaluate histopathological characteristics, and then antioxidant and anti-inflammatory properties were evaluated in tissue and serum, respectively. We also looked at how active caspase 3 and cytochrome c oxidase were in the liver. The findings demonstrated that supplementary URO A therapy clearly mitigated DOX-induced liver damage. The antioxidant enzymes SOD and CAT were elevated in the liver, and the levels of inflammatory cytokines, such as TNF-α, NF-kB, and IL-6, in the tissue were significantly attenuated, all of which complemented the beneficial effects of URO A in DOX-induced liver injury. In addition, URO A was able to alter the expression of caspase 3 and cytochrome c oxidase in the livers of rats that were subjected to DOX stress. These results showed that URO A reduced DOX-induced liver injury by reducing oxidative stress, inflammation, and apoptosis. chemotherapy drug-induced liver injury urolithin A apoptosis anti-inflammatory oxidative stress Biology (General) Batoul Madani verfasserin aut Abdulhadi S. Burzangi verfasserin aut Mohammed Alsieni verfasserin aut Mohammed A. Bazuhair verfasserin aut Maha Jamal verfasserin aut Hussam Daghistani verfasserin aut Mohammed O. Barasheed verfasserin aut Huda Alkreathy verfasserin aut Mohammad Ahmed Khan verfasserin aut Lateef M. Khan verfasserin aut In Biomedicines MDPI AG, 2014 11(2023), 4, p 1125 (DE-627)750370483 (DE-600)2720867-9 22279059 nnns volume:11 year:2023 number:4, p 1125 https://doi.org/10.3390/biomedicines11041125 kostenfrei https://doaj.org/article/02fbb5f5570d45fb9d9fb82630d25069 kostenfrei https://www.mdpi.com/2227-9059/11/4/1125 kostenfrei https://doaj.org/toc/2227-9059 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2023 4, p 1125 |
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10.3390/biomedicines11041125 doi (DE-627)DOAJ08989748X (DE-599)DOAJ02fbb5f5570d45fb9d9fb82630d25069 DE-627 ger DE-627 rakwb eng QH301-705.5 Shahid Karim verfasserin aut Urolithin A’s Antioxidative, Anti-Inflammatory, and Antiapoptotic Activities Mitigate Doxorubicin-Induced Liver Injury in Wistar Rats 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Human colon microbiota produce a metabolite called urolithin A (URO A) from ellagic acid and linked compounds, and this metabolite has been demonstrated to have antioxidant, anti-inflammatory, and antiapoptotic activities. The current work examines the various mechanisms through which URO A protects against doxorubicin (DOX)-induced liver injury in Wistar rats. In this experiment, Wistar rats were administered DOX intraperitoneally (20 mg kg<sup<−1</sup<) on day 7 while given URO A intraperitoneally (2.5 or 5 mg kg<sup<−1</sup< d<sup<−1</sup<) for 14 days. The serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma glutamyl transferase (GGT) were measured. Hematoxylin and eosin (HE) staining was used to evaluate histopathological characteristics, and then antioxidant and anti-inflammatory properties were evaluated in tissue and serum, respectively. We also looked at how active caspase 3 and cytochrome c oxidase were in the liver. The findings demonstrated that supplementary URO A therapy clearly mitigated DOX-induced liver damage. The antioxidant enzymes SOD and CAT were elevated in the liver, and the levels of inflammatory cytokines, such as TNF-α, NF-kB, and IL-6, in the tissue were significantly attenuated, all of which complemented the beneficial effects of URO A in DOX-induced liver injury. In addition, URO A was able to alter the expression of caspase 3 and cytochrome c oxidase in the livers of rats that were subjected to DOX stress. These results showed that URO A reduced DOX-induced liver injury by reducing oxidative stress, inflammation, and apoptosis. chemotherapy drug-induced liver injury urolithin A apoptosis anti-inflammatory oxidative stress Biology (General) Batoul Madani verfasserin aut Abdulhadi S. Burzangi verfasserin aut Mohammed Alsieni verfasserin aut Mohammed A. Bazuhair verfasserin aut Maha Jamal verfasserin aut Hussam Daghistani verfasserin aut Mohammed O. Barasheed verfasserin aut Huda Alkreathy verfasserin aut Mohammad Ahmed Khan verfasserin aut Lateef M. Khan verfasserin aut In Biomedicines MDPI AG, 2014 11(2023), 4, p 1125 (DE-627)750370483 (DE-600)2720867-9 22279059 nnns volume:11 year:2023 number:4, p 1125 https://doi.org/10.3390/biomedicines11041125 kostenfrei https://doaj.org/article/02fbb5f5570d45fb9d9fb82630d25069 kostenfrei https://www.mdpi.com/2227-9059/11/4/1125 kostenfrei https://doaj.org/toc/2227-9059 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2023 4, p 1125 |
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Urolithin A’s Antioxidative, Anti-Inflammatory, and Antiapoptotic Activities Mitigate Doxorubicin-Induced Liver Injury in Wistar Rats |
abstract |
Human colon microbiota produce a metabolite called urolithin A (URO A) from ellagic acid and linked compounds, and this metabolite has been demonstrated to have antioxidant, anti-inflammatory, and antiapoptotic activities. The current work examines the various mechanisms through which URO A protects against doxorubicin (DOX)-induced liver injury in Wistar rats. In this experiment, Wistar rats were administered DOX intraperitoneally (20 mg kg<sup<−1</sup<) on day 7 while given URO A intraperitoneally (2.5 or 5 mg kg<sup<−1</sup< d<sup<−1</sup<) for 14 days. The serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma glutamyl transferase (GGT) were measured. Hematoxylin and eosin (HE) staining was used to evaluate histopathological characteristics, and then antioxidant and anti-inflammatory properties were evaluated in tissue and serum, respectively. We also looked at how active caspase 3 and cytochrome c oxidase were in the liver. The findings demonstrated that supplementary URO A therapy clearly mitigated DOX-induced liver damage. The antioxidant enzymes SOD and CAT were elevated in the liver, and the levels of inflammatory cytokines, such as TNF-α, NF-kB, and IL-6, in the tissue were significantly attenuated, all of which complemented the beneficial effects of URO A in DOX-induced liver injury. In addition, URO A was able to alter the expression of caspase 3 and cytochrome c oxidase in the livers of rats that were subjected to DOX stress. These results showed that URO A reduced DOX-induced liver injury by reducing oxidative stress, inflammation, and apoptosis. |
abstractGer |
Human colon microbiota produce a metabolite called urolithin A (URO A) from ellagic acid and linked compounds, and this metabolite has been demonstrated to have antioxidant, anti-inflammatory, and antiapoptotic activities. The current work examines the various mechanisms through which URO A protects against doxorubicin (DOX)-induced liver injury in Wistar rats. In this experiment, Wistar rats were administered DOX intraperitoneally (20 mg kg<sup<−1</sup<) on day 7 while given URO A intraperitoneally (2.5 or 5 mg kg<sup<−1</sup< d<sup<−1</sup<) for 14 days. The serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma glutamyl transferase (GGT) were measured. Hematoxylin and eosin (HE) staining was used to evaluate histopathological characteristics, and then antioxidant and anti-inflammatory properties were evaluated in tissue and serum, respectively. We also looked at how active caspase 3 and cytochrome c oxidase were in the liver. The findings demonstrated that supplementary URO A therapy clearly mitigated DOX-induced liver damage. The antioxidant enzymes SOD and CAT were elevated in the liver, and the levels of inflammatory cytokines, such as TNF-α, NF-kB, and IL-6, in the tissue were significantly attenuated, all of which complemented the beneficial effects of URO A in DOX-induced liver injury. In addition, URO A was able to alter the expression of caspase 3 and cytochrome c oxidase in the livers of rats that were subjected to DOX stress. These results showed that URO A reduced DOX-induced liver injury by reducing oxidative stress, inflammation, and apoptosis. |
abstract_unstemmed |
Human colon microbiota produce a metabolite called urolithin A (URO A) from ellagic acid and linked compounds, and this metabolite has been demonstrated to have antioxidant, anti-inflammatory, and antiapoptotic activities. The current work examines the various mechanisms through which URO A protects against doxorubicin (DOX)-induced liver injury in Wistar rats. In this experiment, Wistar rats were administered DOX intraperitoneally (20 mg kg<sup<−1</sup<) on day 7 while given URO A intraperitoneally (2.5 or 5 mg kg<sup<−1</sup< d<sup<−1</sup<) for 14 days. The serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma glutamyl transferase (GGT) were measured. Hematoxylin and eosin (HE) staining was used to evaluate histopathological characteristics, and then antioxidant and anti-inflammatory properties were evaluated in tissue and serum, respectively. We also looked at how active caspase 3 and cytochrome c oxidase were in the liver. The findings demonstrated that supplementary URO A therapy clearly mitigated DOX-induced liver damage. The antioxidant enzymes SOD and CAT were elevated in the liver, and the levels of inflammatory cytokines, such as TNF-α, NF-kB, and IL-6, in the tissue were significantly attenuated, all of which complemented the beneficial effects of URO A in DOX-induced liver injury. In addition, URO A was able to alter the expression of caspase 3 and cytochrome c oxidase in the livers of rats that were subjected to DOX stress. These results showed that URO A reduced DOX-induced liver injury by reducing oxidative stress, inflammation, and apoptosis. |
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container_issue |
4, p 1125 |
title_short |
Urolithin A’s Antioxidative, Anti-Inflammatory, and Antiapoptotic Activities Mitigate Doxorubicin-Induced Liver Injury in Wistar Rats |
url |
https://doi.org/10.3390/biomedicines11041125 https://doaj.org/article/02fbb5f5570d45fb9d9fb82630d25069 https://www.mdpi.com/2227-9059/11/4/1125 https://doaj.org/toc/2227-9059 |
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author2 |
Batoul Madani Abdulhadi S. Burzangi Mohammed Alsieni Mohammed A. Bazuhair Maha Jamal Hussam Daghistani Mohammed O. Barasheed Huda Alkreathy Mohammad Ahmed Khan Lateef M. Khan |
author2Str |
Batoul Madani Abdulhadi S. Burzangi Mohammed Alsieni Mohammed A. Bazuhair Maha Jamal Hussam Daghistani Mohammed O. Barasheed Huda Alkreathy Mohammad Ahmed Khan Lateef M. Khan |
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doi_str |
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up_date |
2024-07-04T01:06:28.996Z |
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