The Experts below are selected from a list of 189 Experts worldwide ranked by ideXlab platform
Hala F. Zaki - One of the best experts on this subject based on the ideXlab platform.
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zafirlukast and Vincamine ameliorate tamoxifen induced oxidative stress and inflammation role of the jnk erk pathway
Life Sciences, 2018Co-Authors: Ahmed M Eldessouki, Mai A. Abd El Fattah, Azza S. Awad, Hala F. ZakiAbstract:Abstract Aims This study investigated the hepatoprotective effects of both zafirlukast and Vincamine and their possible role in the treatment of tamoxifen-induced liver injury in rats. Materials and methods Female Wistar rats were divided into five groups (10 rats each). Groups I and II received 1% Tween 80 and served as normal and tamoxifen controls, respectively. Groups III, IV and V were treated with zafirlukast (80 mg/kg), Vincamine (10 mg/kg) and a combination of zafirlukast (80 mg/kg) and Vincamine (10 mg/kg), respectively for 10 successive days. Tamoxifen was given orally to all groups, except for 1st group, in the dose of 45 mg/kg for 10 days to induce liver injury. Subsequently, rats were sacrificed for biochemical, histopathological, Immunohistochemistry, PCR and western blot assessment. Key findings Tamoxifen-induced liver injury was reflected by alterations in estimated biochemical parameters, activation of JNK/ERK pathway, increased expression of NF-κB, liver oxidative stress and inflammatory markers parallel to histopathological changes in liver tissue. Treatment of rats with zafirlukast and Vincamine ameliorated tamoxifen induced hepatic cell injury via suppressing oxidative stress, inflammatory markers, caspases-3, p-JNK/p-ERK and NF-κB pathways. Significance Zafirlukast and Vincamine may be regarded as potential therapeutic strategies with antioxidant and anti-inflammatory activities against tamoxifen-induced oxidative damage in rat liver.
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Zafirlukast and Vincamine ameliorate tamoxifen-induced oxidative stress and inflammation: Role of the JNK/ERK pathway.
Life sciences, 2018Co-Authors: Ahmed M. El-dessouki, Mai A. Abd El Fattah, Azza S. Awad, Hala F. ZakiAbstract:Abstract Aims This study investigated the hepatoprotective effects of both zafirlukast and Vincamine and their possible role in the treatment of tamoxifen-induced liver injury in rats. Materials and methods Female Wistar rats were divided into five groups (10 rats each). Groups I and II received 1% Tween 80 and served as normal and tamoxifen controls, respectively. Groups III, IV and V were treated with zafirlukast (80 mg/kg), Vincamine (10 mg/kg) and a combination of zafirlukast (80 mg/kg) and Vincamine (10 mg/kg), respectively for 10 successive days. Tamoxifen was given orally to all groups, except for 1st group, in the dose of 45 mg/kg for 10 days to induce liver injury. Subsequently, rats were sacrificed for biochemical, histopathological, Immunohistochemistry, PCR and western blot assessment. Key findings Tamoxifen-induced liver injury was reflected by alterations in estimated biochemical parameters, activation of JNK/ERK pathway, increased expression of NF-κB, liver oxidative stress and inflammatory markers parallel to histopathological changes in liver tissue. Treatment of rats with zafirlukast and Vincamine ameliorated tamoxifen induced hepatic cell injury via suppressing oxidative stress, inflammatory markers, caspases-3, p-JNK/p-ERK and NF-κB pathways. Significance Zafirlukast and Vincamine may be regarded as potential therapeutic strategies with antioxidant and anti-inflammatory activities against tamoxifen-induced oxidative damage in rat liver.
Daniele Passarella - One of the best experts on this subject based on the ideXlab platform.
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Vincamine by synthesis and semi-synthesis
Phytochemistry Reviews, 2020Co-Authors: Elisa Bonandi, Francesca Foschi, Cristina Marucci, Giuseppe Paladino, Marcello Luzzani, Daniele PassarellaAbstract:This review summarizes the main strategies aimed at the total synthesis of Vincamine and congeners. Then, our contribution in this field is presented: we describe (+)-Vincamine semi-synthesis using tabersonine as starting material. Characterization and quantification of the main impurities are discussed, and HPLC conditions, structural elucidation and NMR data of four of them are reported.
Mai A. Abd El Fattah - One of the best experts on this subject based on the ideXlab platform.
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zafirlukast and Vincamine ameliorate tamoxifen induced oxidative stress and inflammation role of the jnk erk pathway
Life Sciences, 2018Co-Authors: Ahmed M Eldessouki, Mai A. Abd El Fattah, Azza S. Awad, Hala F. ZakiAbstract:Abstract Aims This study investigated the hepatoprotective effects of both zafirlukast and Vincamine and their possible role in the treatment of tamoxifen-induced liver injury in rats. Materials and methods Female Wistar rats were divided into five groups (10 rats each). Groups I and II received 1% Tween 80 and served as normal and tamoxifen controls, respectively. Groups III, IV and V were treated with zafirlukast (80 mg/kg), Vincamine (10 mg/kg) and a combination of zafirlukast (80 mg/kg) and Vincamine (10 mg/kg), respectively for 10 successive days. Tamoxifen was given orally to all groups, except for 1st group, in the dose of 45 mg/kg for 10 days to induce liver injury. Subsequently, rats were sacrificed for biochemical, histopathological, Immunohistochemistry, PCR and western blot assessment. Key findings Tamoxifen-induced liver injury was reflected by alterations in estimated biochemical parameters, activation of JNK/ERK pathway, increased expression of NF-κB, liver oxidative stress and inflammatory markers parallel to histopathological changes in liver tissue. Treatment of rats with zafirlukast and Vincamine ameliorated tamoxifen induced hepatic cell injury via suppressing oxidative stress, inflammatory markers, caspases-3, p-JNK/p-ERK and NF-κB pathways. Significance Zafirlukast and Vincamine may be regarded as potential therapeutic strategies with antioxidant and anti-inflammatory activities against tamoxifen-induced oxidative damage in rat liver.
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Zafirlukast and Vincamine ameliorate tamoxifen-induced oxidative stress and inflammation: Role of the JNK/ERK pathway.
Life sciences, 2018Co-Authors: Ahmed M. El-dessouki, Mai A. Abd El Fattah, Azza S. Awad, Hala F. ZakiAbstract:Abstract Aims This study investigated the hepatoprotective effects of both zafirlukast and Vincamine and their possible role in the treatment of tamoxifen-induced liver injury in rats. Materials and methods Female Wistar rats were divided into five groups (10 rats each). Groups I and II received 1% Tween 80 and served as normal and tamoxifen controls, respectively. Groups III, IV and V were treated with zafirlukast (80 mg/kg), Vincamine (10 mg/kg) and a combination of zafirlukast (80 mg/kg) and Vincamine (10 mg/kg), respectively for 10 successive days. Tamoxifen was given orally to all groups, except for 1st group, in the dose of 45 mg/kg for 10 days to induce liver injury. Subsequently, rats were sacrificed for biochemical, histopathological, Immunohistochemistry, PCR and western blot assessment. Key findings Tamoxifen-induced liver injury was reflected by alterations in estimated biochemical parameters, activation of JNK/ERK pathway, increased expression of NF-κB, liver oxidative stress and inflammatory markers parallel to histopathological changes in liver tissue. Treatment of rats with zafirlukast and Vincamine ameliorated tamoxifen induced hepatic cell injury via suppressing oxidative stress, inflammatory markers, caspases-3, p-JNK/p-ERK and NF-κB pathways. Significance Zafirlukast and Vincamine may be regarded as potential therapeutic strategies with antioxidant and anti-inflammatory activities against tamoxifen-induced oxidative damage in rat liver.
Azza S. Awad - One of the best experts on this subject based on the ideXlab platform.
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zafirlukast and Vincamine ameliorate tamoxifen induced oxidative stress and inflammation role of the jnk erk pathway
Life Sciences, 2018Co-Authors: Ahmed M Eldessouki, Mai A. Abd El Fattah, Azza S. Awad, Hala F. ZakiAbstract:Abstract Aims This study investigated the hepatoprotective effects of both zafirlukast and Vincamine and their possible role in the treatment of tamoxifen-induced liver injury in rats. Materials and methods Female Wistar rats were divided into five groups (10 rats each). Groups I and II received 1% Tween 80 and served as normal and tamoxifen controls, respectively. Groups III, IV and V were treated with zafirlukast (80 mg/kg), Vincamine (10 mg/kg) and a combination of zafirlukast (80 mg/kg) and Vincamine (10 mg/kg), respectively for 10 successive days. Tamoxifen was given orally to all groups, except for 1st group, in the dose of 45 mg/kg for 10 days to induce liver injury. Subsequently, rats were sacrificed for biochemical, histopathological, Immunohistochemistry, PCR and western blot assessment. Key findings Tamoxifen-induced liver injury was reflected by alterations in estimated biochemical parameters, activation of JNK/ERK pathway, increased expression of NF-κB, liver oxidative stress and inflammatory markers parallel to histopathological changes in liver tissue. Treatment of rats with zafirlukast and Vincamine ameliorated tamoxifen induced hepatic cell injury via suppressing oxidative stress, inflammatory markers, caspases-3, p-JNK/p-ERK and NF-κB pathways. Significance Zafirlukast and Vincamine may be regarded as potential therapeutic strategies with antioxidant and anti-inflammatory activities against tamoxifen-induced oxidative damage in rat liver.
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Zafirlukast and Vincamine ameliorate tamoxifen-induced oxidative stress and inflammation: Role of the JNK/ERK pathway.
Life sciences, 2018Co-Authors: Ahmed M. El-dessouki, Mai A. Abd El Fattah, Azza S. Awad, Hala F. ZakiAbstract:Abstract Aims This study investigated the hepatoprotective effects of both zafirlukast and Vincamine and their possible role in the treatment of tamoxifen-induced liver injury in rats. Materials and methods Female Wistar rats were divided into five groups (10 rats each). Groups I and II received 1% Tween 80 and served as normal and tamoxifen controls, respectively. Groups III, IV and V were treated with zafirlukast (80 mg/kg), Vincamine (10 mg/kg) and a combination of zafirlukast (80 mg/kg) and Vincamine (10 mg/kg), respectively for 10 successive days. Tamoxifen was given orally to all groups, except for 1st group, in the dose of 45 mg/kg for 10 days to induce liver injury. Subsequently, rats were sacrificed for biochemical, histopathological, Immunohistochemistry, PCR and western blot assessment. Key findings Tamoxifen-induced liver injury was reflected by alterations in estimated biochemical parameters, activation of JNK/ERK pathway, increased expression of NF-κB, liver oxidative stress and inflammatory markers parallel to histopathological changes in liver tissue. Treatment of rats with zafirlukast and Vincamine ameliorated tamoxifen induced hepatic cell injury via suppressing oxidative stress, inflammatory markers, caspases-3, p-JNK/p-ERK and NF-κB pathways. Significance Zafirlukast and Vincamine may be regarded as potential therapeutic strategies with antioxidant and anti-inflammatory activities against tamoxifen-induced oxidative damage in rat liver.
Ghada A. Badawi - One of the best experts on this subject based on the ideXlab platform.
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Vincamine protects against cisplatin induced nephrotoxicity via activation of Nrf2/HO-1 and hindering TLR4/ IFN-γ/CD44 cells inflammatory cascade
Life sciences, 2021Co-Authors: Rehab M. El-sayed, Rehab E. Abo El Gheit, Ghada A. BadawiAbstract:Abstract Cisplatin is a commonly prescribed chemotherapeutic agent for the treatment of different types of solid tumors. However, the high incidence of cisplatin-induced nephrotoxicity largely restricts its clinical efficacy in absence of both preventive and treatment options to combat its serious and life-threatening effects. Therefore, the current study investigated the reno-protective molecular mechanisms of Vincamine against cisplatin nephrotoxicity. Vincamine (40 mg/kg P.O.) was given for 7 days, cisplatin was injected as single dose (10 mg/kg i.p.) at the seven day of the experiments. Animals were sacrificed after 72 h of cisplatin injection to allow nephrotoxicity. Vincamine pretreatment improved kidney functions and decreased kidney function tests as urea, creatinine and kidney injury molecule-1 (KIM-1), as well as it exhibited antioxidant properties by restoring balance between pro and anti-oxidants of malondialdehyde (MDA), myeloperoxidase (MPO), nuclear factor erythroid 2-related factor 2 (Nrf2) and hemeoxygenase-1 (HO-1). Moreover, Vincamine hindered the inflammatory cascade via mediating Toll like receptor 4 (TLR4)- interferon gamma (IFNγ)-CD44 cells pathway and transforming growth factor beta (TGFβ1). Additionally, Vincamine retained DNA fragmentation. In conclusion, Vincamine represents a promising intervention in limiting cisplatin nephrotoxicity by its anti-oxidant, anti-inflammatory, antiapoptotic mechanistic activities. Therefore, Vincamine can be used as adjunct therapy with cisplatin to mitigate cisplatin-induced-AKI.
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Vincamine protects against cisplatin induced nephrotoxicity via activation of nrf2 ho 1 and hindering tlr4 ifn γ cd44 cells inflammatory cascade
Life Sciences, 2021Co-Authors: Rehab M Elsayed, Rehab E. Abo El Gheit, Ghada A. BadawiAbstract:Abstract Cisplatin is a commonly prescribed chemotherapeutic agent for the treatment of different types of solid tumors. However, the high incidence of cisplatin-induced nephrotoxicity largely restricts its clinical efficacy in absence of both preventive and treatment options to combat its serious and life-threatening effects. Therefore, the current study investigated the reno-protective molecular mechanisms of Vincamine against cisplatin nephrotoxicity. Vincamine (40 mg/kg P.O.) was given for 7 days, cisplatin was injected as single dose (10 mg/kg i.p.) at the seven day of the experiments. Animals were sacrificed after 72 h of cisplatin injection to allow nephrotoxicity. Vincamine pretreatment improved kidney functions and decreased kidney function tests as urea, creatinine and kidney injury molecule-1 (KIM-1), as well as it exhibited antioxidant properties by restoring balance between pro and anti-oxidants of malondialdehyde (MDA), myeloperoxidase (MPO), nuclear factor erythroid 2-related factor 2 (Nrf2) and hemeoxygenase-1 (HO-1). Moreover, Vincamine hindered the inflammatory cascade via mediating Toll like receptor 4 (TLR4)- interferon gamma (IFNγ)-CD44 cells pathway and transforming growth factor beta (TGFβ1). Additionally, Vincamine retained DNA fragmentation. In conclusion, Vincamine represents a promising intervention in limiting cisplatin nephrotoxicity by its anti-oxidant, anti-inflammatory, antiapoptotic mechanistic activities. Therefore, Vincamine can be used as adjunct therapy with cisplatin to mitigate cisplatin-induced-AKI.