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Exploring the Therapeutic Potential of Camalexin in Benomyl- induced Parkinson’s Disease in Mice: In vitro, In vivo and Aldehyde Dehydrogenase Insights
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Abstract
Camalexin was selected in this study due to its ALDH-enhancing gene and its aldehyde dehydrogenase and dopamine protective roles have been evaluated. Also, the role of Benomyl in affecting the aldehyde dehydrogenase enzyme (both ALDH1A1 and ALDH2) was countered with the effect of pesticides on the neurological system of humans. The work aims to provide a suitable multi-targeted molecule that can be used as a supplement for the existing PD drugs by evaluating its role using invitro cell lines, animal and alternative to animal models. MTT assay was performed using SH-SY5Y cell lines and IC50 of camalexin was determined. The role of Camalexin in promoting ALDH1A1 was exposed by utilizing DOPAL and alpha-synuclein as PD markers in western blot studies. Real-time PCR was performed to determine the promoting of ALDH2 gene expression in the SH-SY5Y cells by Camalexin. Camalexin was proven to be beneficial in promoting the motor coordination and improve the cognitive parameters in mice studies. The dopamine and serotonin concentration were improved; whereas, mono amino oxidases were reduced by Camalexin treatment in animals. Camalexin was shown to hold a prominent role in reduction of free radicals (lipid peroxidation products) and improving the anti-oxidant enzymes (SOD, CAT, GPX, GSH) and the brain samples were histopathologically analyzed for the α-synuclein deposits. camalexin holds promise as a supplementary treatment for PD, with potential benefits for ALDH enhancement, neuroprotection, and oxidative stress reduction.
Springer Science and Business Media LLC
Title: Exploring the Therapeutic Potential of Camalexin in Benomyl- induced Parkinson’s Disease in Mice: In vitro, In vivo and Aldehyde Dehydrogenase Insights
Description:
Abstract
Camalexin was selected in this study due to its ALDH-enhancing gene and its aldehyde dehydrogenase and dopamine protective roles have been evaluated.
Also, the role of Benomyl in affecting the aldehyde dehydrogenase enzyme (both ALDH1A1 and ALDH2) was countered with the effect of pesticides on the neurological system of humans.
The work aims to provide a suitable multi-targeted molecule that can be used as a supplement for the existing PD drugs by evaluating its role using invitro cell lines, animal and alternative to animal models.
MTT assay was performed using SH-SY5Y cell lines and IC50 of camalexin was determined.
The role of Camalexin in promoting ALDH1A1 was exposed by utilizing DOPAL and alpha-synuclein as PD markers in western blot studies.
Real-time PCR was performed to determine the promoting of ALDH2 gene expression in the SH-SY5Y cells by Camalexin.
Camalexin was proven to be beneficial in promoting the motor coordination and improve the cognitive parameters in mice studies.
The dopamine and serotonin concentration were improved; whereas, mono amino oxidases were reduced by Camalexin treatment in animals.
Camalexin was shown to hold a prominent role in reduction of free radicals (lipid peroxidation products) and improving the anti-oxidant enzymes (SOD, CAT, GPX, GSH) and the brain samples were histopathologically analyzed for the α-synuclein deposits.
camalexin holds promise as a supplementary treatment for PD, with potential benefits for ALDH enhancement, neuroprotection, and oxidative stress reduction.
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