Solanum nigrum L. Extract Decreases Parkinsonism‐Induced Oxidative Neurodegeneration Through the Inhibition of TRPM2 Channel.
Saved in:
| Title: | Solanum nigrum L. Extract Decreases Parkinsonism‐Induced Oxidative Neurodegeneration Through the Inhibition of TRPM2 Channel. |
|---|---|
| Authors: | Majmudar, Mohit Ashish1,2 (AUTHOR), Nazıroğlu, Ayşenur3 (AUTHOR), Baxi, Darshee B.2 (AUTHOR), Upadhyay, Khushali2 (AUTHOR), Nazıroğlu, Mustafa1,4,5 (AUTHOR) mustafanaziroglu@sdu.edu.tr, Bose, Anupama (AUTHOR) abose@wiley.com |
| Source: | Journal of Food Biochemistry. 6/10/2026, Vol. 2026, p1-16. 16p. |
| Subjects: | Solanum nigrum, Parkinson's disease, Neurodegeneration, Intracellular calcium, Oxidative stress, Antioxidants, Ion channels, Apoptosis |
| Abstract: | Parkinson's disease is caused by the 1‐methyl‐4‐phenylpyridinium (MPP)‐induced stimulation of the TRPM2 channel and the generation of free reactive oxygen species (ROS). The stimulation in SH‐SY5Y neuronal cells may be suppressed by the antioxidant Solanum nigrum L. (SNL) extract and TRPM2 antagonist (N‐(p‐amylcinnamoyl) anthranilic acid, ACA). The antioxidant and anti‐apoptotic properties of SNL were investigated in Parkinsonism (MPP)‐induced dopaminergic SH‐SY5Y cells by reducing the TRPM2 signaling molecular pathways. Four primary groups of SH‐SY5Y cells were generated: control (CNT), SNL (12.5 μg/mL for 24 h), MPP (0.5 mM for 6 h), and MPP + SNL. TRPM2 current density, cytosolic cation (Ca2+, Fe2+, and Zn2+) concentrations, and the cell death percentage were increased due to the MPP incubation. MPP reduced antioxidants (glutathione peroxidase and glutathione) and cell viability while increasing apoptotic (caspases‐3, ‐8, and ‐9) and oxidant (lipid peroxidation, mitochondrial membrane dysfunction, and ROS) indicators. These indicators were further elevated by TRPM2 stimulation, although they were attenuated through TRPM2 inhibition by the treatment of SNL and ACA. In conclusion, the antioxidant property of SNL incubation decreased MPP‐induced mitochondrial oxidative cytotoxicity and cell death by blocking TRPM2‐mediated Ca2+ signaling. SNL is a potential treatment for MPP‐induced Parkinsonism associated with excessive ROS generation, apoptosis, and Ca2+ influx. [ABSTRACT FROM AUTHOR] |
| Copyright of Journal of Food Biochemistry is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) | |
| Database: | Engineering Source |
|
Full text is not displayed to guests.
Login for full access.
|
|
| Abstract: | Parkinson's disease is caused by the 1‐methyl‐4‐phenylpyridinium (MPP)‐induced stimulation of the TRPM2 channel and the generation of free reactive oxygen species (ROS). The stimulation in SH‐SY5Y neuronal cells may be suppressed by the antioxidant Solanum nigrum L. (SNL) extract and TRPM2 antagonist (N‐(p‐amylcinnamoyl) anthranilic acid, ACA). The antioxidant and anti‐apoptotic properties of SNL were investigated in Parkinsonism (MPP)‐induced dopaminergic SH‐SY5Y cells by reducing the TRPM2 signaling molecular pathways. Four primary groups of SH‐SY5Y cells were generated: control (CNT), SNL (12.5 μg/mL for 24 h), MPP (0.5 mM for 6 h), and MPP + SNL. TRPM2 current density, cytosolic cation (Ca2+, Fe2+, and Zn2+) concentrations, and the cell death percentage were increased due to the MPP incubation. MPP reduced antioxidants (glutathione peroxidase and glutathione) and cell viability while increasing apoptotic (caspases‐3, ‐8, and ‐9) and oxidant (lipid peroxidation, mitochondrial membrane dysfunction, and ROS) indicators. These indicators were further elevated by TRPM2 stimulation, although they were attenuated through TRPM2 inhibition by the treatment of SNL and ACA. In conclusion, the antioxidant property of SNL incubation decreased MPP‐induced mitochondrial oxidative cytotoxicity and cell death by blocking TRPM2‐mediated Ca2+ signaling. SNL is a potential treatment for MPP‐induced Parkinsonism associated with excessive ROS generation, apoptosis, and Ca2+ influx. [ABSTRACT FROM AUTHOR] |
|---|---|
| ISSN: | 01458884 |
| DOI: | 10.1155/jfbc/7519232 |
