8- O -( E - p -methoxycinnamoyl)harpagide Inhibits Influenza A Virus Infection by Suppressing Intracellular Calcium
Calcium (Ca ) dependent signaling circuit plays a critical role in influenza A virus (IAV) infection. The 8- -( - -methoxycinnamoyl)harpagide (MCH) exhibits pharmacological activities that exert neuroprotective, hepatoprotective, anti-inflammatory and other biological effects. However, not have repo...
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Published in | Molecules (Basel, Switzerland) Vol. 26; no. 4; p. 1029 |
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Main Authors | , , , , |
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Language | English |
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Abstract | Calcium (Ca
) dependent signaling circuit plays a critical role in influenza A virus (IAV) infection. The 8-
-(
-
-methoxycinnamoyl)harpagide (MCH) exhibits pharmacological activities that exert neuroprotective, hepatoprotective, anti-inflammatory and other biological effects. However, not have reports of antiviral effects. To investigate the antiviral activity of MCH on IAV-infected human lung cells mediated by calcium regulation. We examined the inhibitory effect of MCH on IAV infections and measured the level of viral proteins upon MCH treatment using Western blotting. We also performed molecular docking simulation with MCH and IAV M2 protein. Finally, we analyzed MCH's suppression of intracellular calcium and ROS (reactive oxygen species) in IAV-infected human lung cells using a flow cytometer. The results shown that MCH inhibited the infection of IAV and increased the survival of the infected human lung cells. The levels of IAV protein M1, M2, NS1 and PA were inhibited in MCH-treated human lung cells compared to that in infected and untreated cells. Also, docking simulation suggest that MCH interacted with M2 on its hydrophobic wall (L40 and I42) and polar amino acids (D44 and R45), which formed intermolecular contacts and were a crucial part of the channel gate along with W41. Lastly, MCH inhibited IAV infection by reducing intracellular calcium and mitochondrial Ca
/ROS levels in infected human lung cells. Taken together, these data suggest that MCH inhibits IAV infection and increases the survival of infected human lung cells by suppressing calcium levels. These results indicate that MCH is useful for developing IAV treatments. |
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AbstractList | Calcium (Ca2+) dependent signaling circuit plays a critical role in influenza A virus (IAV) infection. The 8-O-(E-p-methoxycinnamoyl)harpagide (MCH) exhibits pharmacological activities that exert neuroprotective, hepatoprotective, anti-inflammatory and other biological effects. However, not have reports of antiviral effects. To investigate the antiviral activity of MCH on IAV-infected human lung cells mediated by calcium regulation. We examined the inhibitory effect of MCH on IAV infections and measured the level of viral proteins upon MCH treatment using Western blotting. We also performed molecular docking simulation with MCH and IAV M2 protein. Finally, we analyzed MCH’s suppression of intracellular calcium and ROS (reactive oxygen species) in IAV-infected human lung cells using a flow cytometer. The results shown that MCH inhibited the infection of IAV and increased the survival of the infected human lung cells. The levels of IAV protein M1, M2, NS1 and PA were inhibited in MCH-treated human lung cells compared to that in infected and untreated cells. Also, docking simulation suggest that MCH interacted with M2 on its hydrophobic wall (L40 and I42) and polar amino acids (D44 and R45), which formed intermolecular contacts and were a crucial part of the channel gate along with W41. Lastly, MCH inhibited IAV infection by reducing intracellular calcium and mitochondrial Ca2+/ROS levels in infected human lung cells. Taken together, these data suggest that MCH inhibits IAV infection and increases the survival of infected human lung cells by suppressing calcium levels. These results indicate that MCH is useful for developing IAV treatments. Calcium (Ca 2+ ) dependent signaling circuit plays a critical role in influenza A virus (IAV) infection. The 8- O -( E - p -methoxycinnamoyl)harpagide (MCH) exhibits pharmacological activities that exert neuroprotective, hepatoprotective, anti-inflammatory and other biological effects. However, not have reports of antiviral effects. To investigate the antiviral activity of MCH on IAV-infected human lung cells mediated by calcium regulation. We examined the inhibitory effect of MCH on IAV infections and measured the level of viral proteins upon MCH treatment using Western blotting. We also performed molecular docking simulation with MCH and IAV M2 protein. Finally, we analyzed MCH’s suppression of intracellular calcium and ROS (reactive oxygen species) in IAV-infected human lung cells using a flow cytometer. The results shown that MCH inhibited the infection of IAV and increased the survival of the infected human lung cells. The levels of IAV protein M1, M2, NS1 and PA were inhibited in MCH-treated human lung cells compared to that in infected and untreated cells. Also, docking simulation suggest that MCH interacted with M2 on its hydrophobic wall (L40 and I42) and polar amino acids (D44 and R45), which formed intermolecular contacts and were a crucial part of the channel gate along with W41. Lastly, MCH inhibited IAV infection by reducing intracellular calcium and mitochondrial Ca 2+ /ROS levels in infected human lung cells. Taken together, these data suggest that MCH inhibits IAV infection and increases the survival of infected human lung cells by suppressing calcium levels. These results indicate that MCH is useful for developing IAV treatments. Calcium (Ca ) dependent signaling circuit plays a critical role in influenza A virus (IAV) infection. The 8- -( - -methoxycinnamoyl)harpagide (MCH) exhibits pharmacological activities that exert neuroprotective, hepatoprotective, anti-inflammatory and other biological effects. However, not have reports of antiviral effects. To investigate the antiviral activity of MCH on IAV-infected human lung cells mediated by calcium regulation. We examined the inhibitory effect of MCH on IAV infections and measured the level of viral proteins upon MCH treatment using Western blotting. We also performed molecular docking simulation with MCH and IAV M2 protein. Finally, we analyzed MCH's suppression of intracellular calcium and ROS (reactive oxygen species) in IAV-infected human lung cells using a flow cytometer. The results shown that MCH inhibited the infection of IAV and increased the survival of the infected human lung cells. The levels of IAV protein M1, M2, NS1 and PA were inhibited in MCH-treated human lung cells compared to that in infected and untreated cells. Also, docking simulation suggest that MCH interacted with M2 on its hydrophobic wall (L40 and I42) and polar amino acids (D44 and R45), which formed intermolecular contacts and were a crucial part of the channel gate along with W41. Lastly, MCH inhibited IAV infection by reducing intracellular calcium and mitochondrial Ca /ROS levels in infected human lung cells. Taken together, these data suggest that MCH inhibits IAV infection and increases the survival of infected human lung cells by suppressing calcium levels. These results indicate that MCH is useful for developing IAV treatments. |
Author | Li, Wei Kwon, Eun-Bin Choi, Jang-Gi Yang, Hye-Jin Kim, Young-Soo |
AuthorAffiliation | Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, Daegu 41062, Korea; wrld2931@kiom.re.kr (E.-B.K.); hjyang@kiom.re.kr (H.-J.Y.); yskim527@kiom.re.kr (Y.-S.K.) |
AuthorAffiliation_xml | – name: Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, Daegu 41062, Korea; wrld2931@kiom.re.kr (E.-B.K.); hjyang@kiom.re.kr (H.-J.Y.); yskim527@kiom.re.kr (Y.-S.K.) |
Author_xml | – sequence: 1 givenname: Eun-Bin surname: Kwon fullname: Kwon, Eun-Bin organization: Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, Daegu 41062, Korea – sequence: 2 givenname: Hye-Jin surname: Yang fullname: Yang, Hye-Jin organization: Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, Daegu 41062, Korea – sequence: 3 givenname: Young-Soo orcidid: 0000-0003-0605-1231 surname: Kim fullname: Kim, Young-Soo organization: Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, Daegu 41062, Korea – sequence: 4 givenname: Wei orcidid: 0000-0001-7272-7290 surname: Li fullname: Li, Wei organization: Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, Daegu 41062, Korea – sequence: 5 givenname: Jang-Gi surname: Choi fullname: Choi, Jang-Gi organization: Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, Daegu 41062, Korea |
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Keywords | intracellular calcium 8-O-(E-p-methoxycinnamoyl)harpagide reactive oxygen species M2 ion channel influenza A virus |
Language | English |
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Snippet | Calcium (Ca
) dependent signaling circuit plays a critical role in influenza A virus (IAV) infection. The 8-
-(
-
-methoxycinnamoyl)harpagide (MCH) exhibits... Calcium (Ca2+) dependent signaling circuit plays a critical role in influenza A virus (IAV) infection. The 8-O-(E-p-methoxycinnamoyl)harpagide (MCH) exhibits... Calcium (Ca 2+ ) dependent signaling circuit plays a critical role in influenza A virus (IAV) infection. The 8- O -( E - p -methoxycinnamoyl)harpagide (MCH)... |
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SubjectTerms | 8-O-(E-p-methoxycinnamoyl)harpagide A549 Cells Antiviral Agents - pharmacology Antiviral Agents - therapeutic use Calcium - metabolism Communication Humans influenza A virus Influenza A virus - drug effects Influenza, Human - drug therapy Influenza, Human - virology intracellular calcium Intracellular Space - metabolism Ion Channels - metabolism Iridoid Glycosides - chemistry Iridoid Glycosides - pharmacology Iridoid Glycosides - therapeutic use M2 ion channel Mitochondria - drug effects Mitochondria - pathology Molecular Docking Simulation Pyrans - chemistry Pyrans - pharmacology Pyrans - therapeutic use reactive oxygen species Viral Matrix Proteins |
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Title | 8- O -( E - p -methoxycinnamoyl)harpagide Inhibits Influenza A Virus Infection by Suppressing Intracellular Calcium |
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