Costunolide and Parthenolide Ameliorate MPP+ Induced Apoptosis in the Cellular Parkinson’s Disease Model
Monoamine oxidase B (MAO-B) is an enzyme that metabolizes several chemicals, including dopamine. MAO-B inhibitors are used in the treatment of Parkinson’s Disease (PD), and the inhibition of this enzyme reduces dopamine turnover and oxidative stress. The absence of dopamine results in PD pathogenesi...
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MDPI AG
2023-03-01
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| author | Mehmet Enes Arslan Hasan Türkez Yasemin Sevim Harun Selvitopi Abdurrahim Kadi Sena Öner Adil Mardinoğlu |
| author_facet | Mehmet Enes Arslan Hasan Türkez Yasemin Sevim Harun Selvitopi Abdurrahim Kadi Sena Öner Adil Mardinoğlu |
| author_sort | Mehmet Enes Arslan |
| collection | DOAJ |
| description | Monoamine oxidase B (MAO-B) is an enzyme that metabolizes several chemicals, including dopamine. MAO-B inhibitors are used in the treatment of Parkinson’s Disease (PD), and the inhibition of this enzyme reduces dopamine turnover and oxidative stress. The absence of dopamine results in PD pathogenesis originating from decreased Acetylcholinesterase (AChE) activity and elevated oxidative stress. Here, we performed a molecular docking analysis for the potential use of costunolide and parthenolide terpenoids as potential MAO-B inhibitors in the treatment of PD. Neuroprotective properties of plant-originated costunolide and parthenolide terpenoids were investigated in a cellular PD model that was developed by using MPP<sup>+</sup> toxicity. We investigated neuroprotection mechanisms through the analysis of oxidative stress parameters, acetylcholinesterase activity and apoptotic cell death ratios. Our results showed that 100 µg/mL and 50 µg/mL of costunolide, and 50 µg/mL of parthenolide applied to the cellular disease model ameliorated the cytotoxicity caused by MPP<sup>+</sup> exposure. We found that acetylcholinesterase activity assays exhibited that terpenoids could ameliorate and restore the enzyme activity as in negative control levels. The oxidative stress parameter analyses revealed that terpenoid application could enhance antioxidant levels and decrease oxidative stress in the cultures. In conclusion, we reported that these two terpenoid molecules could be used in the development of efficient treatment strategies for PD patients. |
| first_indexed | 2024-03-11T05:41:03Z |
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| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-11T05:41:03Z |
| publishDate | 2023-03-01 |
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| record_format | Article |
| series | Cells |
| spelling | doaj.art-8c82d5d56e3b44b28100eeb91f65dda92023-11-17T16:27:45ZengMDPI AGCells2073-44092023-03-0112799210.3390/cells12070992Costunolide and Parthenolide Ameliorate MPP+ Induced Apoptosis in the Cellular Parkinson’s Disease ModelMehmet Enes Arslan0Hasan Türkez1Yasemin Sevim2Harun Selvitopi3Abdurrahim Kadi4Sena Öner5Adil Mardinoğlu6Department of Molecular Biology and Genetics, Faculty of Science, Erzurum Technical University, 25100 Erzurum, TurkeyDepartment of Medical Biology, Faculty of Medicine, Atatürk University, 25240 Erzurum, TurkeyDepartment of Molecular Biology and Genetics, Faculty of Science, Erzurum Technical University, 25100 Erzurum, TurkeyDepartment of Mathematics, Faculty of Science, Erzurum Technical University, 25100 Erzurum, TurkeyDepartment of Molecular Biology and Genetics, Faculty of Science, Erzurum Technical University, 25100 Erzurum, TurkeyDepartment of Molecular Biology and Genetics, Faculty of Science, Erzurum Technical University, 25100 Erzurum, TurkeyScience for Life Laboratory, KTH-Royal Institute of Technology, SE-17121 Stockholm, SwedenMonoamine oxidase B (MAO-B) is an enzyme that metabolizes several chemicals, including dopamine. MAO-B inhibitors are used in the treatment of Parkinson’s Disease (PD), and the inhibition of this enzyme reduces dopamine turnover and oxidative stress. The absence of dopamine results in PD pathogenesis originating from decreased Acetylcholinesterase (AChE) activity and elevated oxidative stress. Here, we performed a molecular docking analysis for the potential use of costunolide and parthenolide terpenoids as potential MAO-B inhibitors in the treatment of PD. Neuroprotective properties of plant-originated costunolide and parthenolide terpenoids were investigated in a cellular PD model that was developed by using MPP<sup>+</sup> toxicity. We investigated neuroprotection mechanisms through the analysis of oxidative stress parameters, acetylcholinesterase activity and apoptotic cell death ratios. Our results showed that 100 µg/mL and 50 µg/mL of costunolide, and 50 µg/mL of parthenolide applied to the cellular disease model ameliorated the cytotoxicity caused by MPP<sup>+</sup> exposure. We found that acetylcholinesterase activity assays exhibited that terpenoids could ameliorate and restore the enzyme activity as in negative control levels. The oxidative stress parameter analyses revealed that terpenoid application could enhance antioxidant levels and decrease oxidative stress in the cultures. In conclusion, we reported that these two terpenoid molecules could be used in the development of efficient treatment strategies for PD patients.https://www.mdpi.com/2073-4409/12/7/992Parkinson’s diseaseterpenoidsantioxidantsacetylcholinesteraseapoptosis |
| spellingShingle | Mehmet Enes Arslan Hasan Türkez Yasemin Sevim Harun Selvitopi Abdurrahim Kadi Sena Öner Adil Mardinoğlu Costunolide and Parthenolide Ameliorate MPP+ Induced Apoptosis in the Cellular Parkinson’s Disease Model Cells Parkinson’s disease terpenoids antioxidants acetylcholinesterase apoptosis |
| title | Costunolide and Parthenolide Ameliorate MPP+ Induced Apoptosis in the Cellular Parkinson’s Disease Model |
| title_full | Costunolide and Parthenolide Ameliorate MPP+ Induced Apoptosis in the Cellular Parkinson’s Disease Model |
| title_fullStr | Costunolide and Parthenolide Ameliorate MPP+ Induced Apoptosis in the Cellular Parkinson’s Disease Model |
| title_full_unstemmed | Costunolide and Parthenolide Ameliorate MPP+ Induced Apoptosis in the Cellular Parkinson’s Disease Model |
| title_short | Costunolide and Parthenolide Ameliorate MPP+ Induced Apoptosis in the Cellular Parkinson’s Disease Model |
| title_sort | costunolide and parthenolide ameliorate mpp induced apoptosis in the cellular parkinson s disease model |
| topic | Parkinson’s disease terpenoids antioxidants acetylcholinesterase apoptosis |
| url | https://www.mdpi.com/2073-4409/12/7/992 |
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