Effects of Lidocaine-Derived Organic Compounds on Eosinophil Activation and Survival
Lidocaine, a local anesthetic, is known to possess anti-inflammatory properties. However, its clinical use is limited by inconveniences, such as its local synesthetic effects. This study evaluated lidocaine analogs designed and synthesized to overcome the disadvantages of lidocaine, having anti-infl...
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Published in | Molecules (Basel, Switzerland) Vol. 28; no. 15; p. 5696 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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27.07.2023
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Abstract | Lidocaine, a local anesthetic, is known to possess anti-inflammatory properties. However, its clinical use is limited by inconveniences, such as its local synesthetic effects. This study evaluated lidocaine analogs designed and synthesized to overcome the disadvantages of lidocaine, having anti-inflammatory properties. Interleukin 5 (IL-5)-induced eosinophil activation and survival were evaluated using 36 lidocaine analogs with modified lidocaine structure on the aromatic or the acyl moiety or both. Eosinophil survival was evaluated using a CellTiter 96
aqueous cell proliferation assay kit. Superoxide production was determined using the superoxide dismutase-inhibitable reduction of cytochrome C method. Eosinophil cationic protein (ECP), IL-8, and transcription factor expression were determined using enzyme-linked immunosorbent assay. The platelet-activating factor (PAF)-induced migration assay was performed using a Transwell insert system. Compounds EI137 and EI341 inhibited IL-5-induced eosinophil survival and superoxide and ECP production in a concentration-dependent manner. These compounds also significantly reduced IL-8 production. Although compounds EI137 and EI341 significantly reduced phosphorylated ERK 1/2 expression, they did not influence other total and phosphorylated transcription factors. Moreover, 1000 µM of compound EI341 only inhibited PAF-induced migration of eosinophils. Lidocaine analogs EI137 and EI341 inhibited IL-5-mediated activation and survival of eosinophils. These compounds could be new therapeutic agents to treat eosinophilic inflammatory diseases. |
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AbstractList | Lidocaine, a local anesthetic, is known to possess anti-inflammatory properties. However, its clinical use is limited by inconveniences, such as its local synesthetic effects. This study evaluated lidocaine analogs designed and synthesized to overcome the disadvantages of lidocaine, having anti-inflammatory properties. Interleukin 5 (IL-5)-induced eosinophil activation and survival were evaluated using 36 lidocaine analogs with modified lidocaine structure on the aromatic or the acyl moiety or both. Eosinophil survival was evaluated using a CellTiter 96® aqueous cell proliferation assay kit. Superoxide production was determined using the superoxide dismutase-inhibitable reduction of cytochrome C method. Eosinophil cationic protein (ECP), IL-8, and transcription factor expression were determined using enzyme-linked immunosorbent assay. The platelet-activating factor (PAF)-induced migration assay was performed using a Transwell insert system. Compounds EI137 and EI341 inhibited IL-5-induced eosinophil survival and superoxide and ECP production in a concentration-dependent manner. These compounds also significantly reduced IL-8 production. Although compounds EI137 and EI341 significantly reduced phosphorylated ERK 1/2 expression, they did not influence other total and phosphorylated transcription factors. Moreover, 1000 µM of compound EI341 only inhibited PAF-induced migration of eosinophils. Lidocaine analogs EI137 and EI341 inhibited IL-5-mediated activation and survival of eosinophils. These compounds could be new therapeutic agents to treat eosinophilic inflammatory diseases. Lidocaine, a local anesthetic, is known to possess anti-inflammatory properties. However, its clinical use is limited by inconveniences, such as its local synesthetic effects. This study evaluated lidocaine analogs designed and synthesized to overcome the disadvantages of lidocaine, having anti-inflammatory properties. Interleukin 5 (IL-5)-induced eosinophil activation and survival were evaluated using 36 lidocaine analogs with modified lidocaine structure on the aromatic or the acyl moiety or both. Eosinophil survival was evaluated using a CellTiter 96 aqueous cell proliferation assay kit. Superoxide production was determined using the superoxide dismutase-inhibitable reduction of cytochrome C method. Eosinophil cationic protein (ECP), IL-8, and transcription factor expression were determined using enzyme-linked immunosorbent assay. The platelet-activating factor (PAF)-induced migration assay was performed using a Transwell insert system. Compounds EI137 and EI341 inhibited IL-5-induced eosinophil survival and superoxide and ECP production in a concentration-dependent manner. These compounds also significantly reduced IL-8 production. Although compounds EI137 and EI341 significantly reduced phosphorylated ERK 1/2 expression, they did not influence other total and phosphorylated transcription factors. Moreover, 1000 µM of compound EI341 only inhibited PAF-induced migration of eosinophils. Lidocaine analogs EI137 and EI341 inhibited IL-5-mediated activation and survival of eosinophils. These compounds could be new therapeutic agents to treat eosinophilic inflammatory diseases. Lidocaine, a local anesthetic, is known to possess anti-inflammatory properties. However, its clinical use is limited by inconveniences, such as its local synesthetic effects. This study evaluated lidocaine analogs designed and synthesized to overcome the disadvantages of lidocaine, having anti-inflammatory properties. Interleukin 5 (IL-5)-induced eosinophil activation and survival were evaluated using 36 lidocaine analogs with modified lidocaine structure on the aromatic or the acyl moiety or both. Eosinophil survival was evaluated using a CellTiter 96[sup.®] aqueous cell proliferation assay kit. Superoxide production was determined using the superoxide dismutase-inhibitable reduction of cytochrome C method. Eosinophil cationic protein (ECP), IL-8, and transcription factor expression were determined using enzyme-linked immunosorbent assay. The platelet-activating factor (PAF)-induced migration assay was performed using a Transwell insert system. Compounds EI137 and EI341 inhibited IL-5-induced eosinophil survival and superoxide and ECP production in a concentration-dependent manner. These compounds also significantly reduced IL-8 production. Although compounds EI137 and EI341 significantly reduced phosphorylated ERK 1/2 expression, they did not influence other total and phosphorylated transcription factors. Moreover, 1000 µM of compound EI341 only inhibited PAF-induced migration of eosinophils. Lidocaine analogs EI137 and EI341 inhibited IL-5-mediated activation and survival of eosinophils. These compounds could be new therapeutic agents to treat eosinophilic inflammatory diseases. Lidocaine, a local anesthetic, is known to possess anti-inflammatory properties. However, its clinical use is limited by inconveniences, such as its local synesthetic effects. This study evaluated lidocaine analogs designed and synthesized to overcome the disadvantages of lidocaine, having anti-inflammatory properties. Interleukin 5 (IL-5)-induced eosinophil activation and survival were evaluated using 36 lidocaine analogs with modified lidocaine structure on the aromatic or the acyl moiety or both. Eosinophil survival was evaluated using a CellTiter 96 ® aqueous cell proliferation assay kit. Superoxide production was determined using the superoxide dismutase-inhibitable reduction of cytochrome C method. Eosinophil cationic protein (ECP), IL-8, and transcription factor expression were determined using enzyme-linked immunosorbent assay. The platelet-activating factor (PAF)-induced migration assay was performed using a Transwell insert system. Compounds EI137 and EI341 inhibited IL-5-induced eosinophil survival and superoxide and ECP production in a concentration-dependent manner. These compounds also significantly reduced IL-8 production. Although compounds EI137 and EI341 significantly reduced phosphorylated ERK 1/2 expression, they did not influence other total and phosphorylated transcription factors. Moreover, 1000 µM of compound EI341 only inhibited PAF-induced migration of eosinophils. Lidocaine analogs EI137 and EI341 inhibited IL-5-mediated activation and survival of eosinophils. These compounds could be new therapeutic agents to treat eosinophilic inflammatory diseases. |
Audience | Academic |
Author | Geum, Sang-Yen Abdel-Aal, Abu-Baker M Chae, Mi-Hyun Aboul-Fadl, Tarek Ye, Mi-Kyung Abd El-Wahab, Hend A A Shin, Seung-Heon Abou-Ghadir, Ola F Aboraia, Ahmed S Qayed, Wesam S |
AuthorAffiliation | 1 Department of Otolaryngology-Head and Neck Surgery, School of Medicine, Daegu Catholic University, Daegu 42472, Republic of Korea; miky@cu.ac.kr (M.-K.Y.); leonen@hanmail.net (M.-H.C.); saye60@naver.com (S.-Y.G.) 2 Department of Medicinal Chemistry, Faculty of Pharmacy, Assiut University, Assiut 71526, Egypt; ahmed.mohamed15@pharm.aun.edu.eg (A.S.A.); wesam.qayed@aun.edu.eg (W.S.Q.); hendaboelmaged@aun.edu.eg (H.A.A.A.E.-w.); fadl@aun.edu.eg (T.A.-F.) 3 Department of Pharmaceutical Organic Chemistry, Faculty of Pharmacy, Assiut University, Assiut 71526, Egypt; abubaker.elsayed@pharm.aun.edu.eg (A.-B.M.A.-A.); olaghadir@aun.edu.eg (O.F.A.-G.) |
AuthorAffiliation_xml | – name: 2 Department of Medicinal Chemistry, Faculty of Pharmacy, Assiut University, Assiut 71526, Egypt; ahmed.mohamed15@pharm.aun.edu.eg (A.S.A.); wesam.qayed@aun.edu.eg (W.S.Q.); hendaboelmaged@aun.edu.eg (H.A.A.A.E.-w.); fadl@aun.edu.eg (T.A.-F.) – name: 3 Department of Pharmaceutical Organic Chemistry, Faculty of Pharmacy, Assiut University, Assiut 71526, Egypt; abubaker.elsayed@pharm.aun.edu.eg (A.-B.M.A.-A.); olaghadir@aun.edu.eg (O.F.A.-G.) – name: 1 Department of Otolaryngology-Head and Neck Surgery, School of Medicine, Daegu Catholic University, Daegu 42472, Republic of Korea; miky@cu.ac.kr (M.-K.Y.); leonen@hanmail.net (M.-H.C.); saye60@naver.com (S.-Y.G.) |
Author_xml | – sequence: 1 givenname: Seung-Heon orcidid: 0000-0002-9118-0590 surname: Shin fullname: Shin, Seung-Heon organization: Department of Otolaryngology-Head and Neck Surgery, School of Medicine, Daegu Catholic University, Daegu 42472, Republic of Korea – sequence: 2 givenname: Mi-Kyung surname: Ye fullname: Ye, Mi-Kyung organization: Department of Otolaryngology-Head and Neck Surgery, School of Medicine, Daegu Catholic University, Daegu 42472, Republic of Korea – sequence: 3 givenname: Mi-Hyun surname: Chae fullname: Chae, Mi-Hyun organization: Department of Otolaryngology-Head and Neck Surgery, School of Medicine, Daegu Catholic University, Daegu 42472, Republic of Korea – sequence: 4 givenname: Sang-Yen orcidid: 0000-0001-6996-5618 surname: Geum fullname: Geum, Sang-Yen organization: Department of Otolaryngology-Head and Neck Surgery, School of Medicine, Daegu Catholic University, Daegu 42472, Republic of Korea – sequence: 5 givenname: Ahmed S orcidid: 0000-0002-8287-3117 surname: Aboraia fullname: Aboraia, Ahmed S organization: Department of Medicinal Chemistry, Faculty of Pharmacy, Assiut University, Assiut 71526, Egypt – sequence: 6 givenname: Abu-Baker M orcidid: 0000-0003-1759-5090 surname: Abdel-Aal fullname: Abdel-Aal, Abu-Baker M organization: Department of Pharmaceutical Organic Chemistry, Faculty of Pharmacy, Assiut University, Assiut 71526, Egypt – sequence: 7 givenname: Wesam S orcidid: 0000-0001-7220-5628 surname: Qayed fullname: Qayed, Wesam S organization: Department of Medicinal Chemistry, Faculty of Pharmacy, Assiut University, Assiut 71526, Egypt – sequence: 8 givenname: Hend A A surname: Abd El-Wahab fullname: Abd El-Wahab, Hend A A organization: Department of Medicinal Chemistry, Faculty of Pharmacy, Assiut University, Assiut 71526, Egypt – sequence: 9 givenname: Ola F surname: Abou-Ghadir fullname: Abou-Ghadir, Ola F organization: Department of Pharmaceutical Organic Chemistry, Faculty of Pharmacy, Assiut University, Assiut 71526, Egypt – sequence: 10 givenname: Tarek orcidid: 0000-0002-1963-4332 surname: Aboul-Fadl fullname: Aboul-Fadl, Tarek organization: Department of Medicinal Chemistry, Faculty of Pharmacy, Assiut University, Assiut 71526, Egypt |
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SubjectTerms | Analysis anti-inflammation Asthma Cytokines Design Enzyme-linked immunosorbent assay Enzymes Hydrogen bonds Inflammation Lidocaine lidocaine analog ligand-based drug pharmacophore Superoxide Transcription factors |
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Title | Effects of Lidocaine-Derived Organic Compounds on Eosinophil Activation and Survival |
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