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Monitoring Astrocyte Reactivity and Proliferation in Vitro Under Ischemic-Like Conditions
Published on: October 21, 2017
Bacopa monnieri inhibits apoptosis and senescence through mitophagy in human astrocytes
Sarbari Saha1, Kewal Kumar Mahapatra1, Soumya Ranjan Mishra1
1Department of Life Science, National Institute of Technology Rourkela, India.
Abstract:
Benzo[a]pyrene (B[a]P), a polycyclic aromatic hydrocarbon, is a potent neurotoxic agent that is responsible for impaired neuronal development and is associated with aging. Here, it was demonstrated that extracts of Bacopa monnieri (BM), a traditional Ayurvedic medicine, diminished the B[a]P-induced apoptosis and senescence in human astrocytes. BM was demonstrated to protect the immortalized primary fetal astrocytes (IMPHFA) from B[a]P-induced apoptosis and senescence by reducing the damaged mitochondria that produced reactive oxygen species (ROS). Furthermore, it was shown that B[a]P-triggered G2 arrest could be altered by BM, thus indicating that BM could reverse the cell cycle arrest and mediate a normal cell cycle in IMPHFA cells. In addition, the lifespan of Caenorhabditis elegans was assessed, which confirmed these effects in the presence of BM, compared to the B[a]P-treated group. Furthermore, the anti-senescence and anti-apoptotic activities of BM were observed to be mediated through the protective effect of mitophagy, and inhibition of mitophagy could not protect the astrocytes from mitochondrial ROS-induced apoptosis and senescence in BM-treated cells. Moreover, it was revealed that BM induced Parkin-dependent mitophagy to exert its cytoprotective activity in IMPHFA cells. In conclusion, the anti-senescence and anti-apoptotic effects of BM in astrocytes could combat pollution and aging-related neurological disorders.
Insights
Bacopa monnieri (BM) extracts protect human astrocytes from neurotoxicity caused by Benzo[a]pyrene (B[a]P). BM reduces B[a]P-induced cell damage and aging by promoting mitophagy, a cellular cleanup process.
Area of Science:
- Neuroscience
- Cell Biology
- Pharmacology
Background:
- Benzo[a]pyrene (B[a]P) is a neurotoxic polycyclic aromatic hydrocarbon linked to impaired neuronal development and aging.
- Astrocytes play crucial roles in neuronal health and are vulnerable to environmental toxins.
Purpose of the Study:
- To investigate the neuroprotective effects of Bacopa monnieri (BM) extracts against B[a]P-induced toxicity in human astrocytes.
- To elucidate the mechanisms underlying BM's protective actions, including its impact on apoptosis, senescence, and mitophagy.
Main Methods:
- Treatment of immortalized primary fetal astrocytes (IMPHFA) with B[a]P and BM extracts.
- Assessment of apoptosis, senescence, reactive oxygen species (ROS) production, and cell cycle progression.
- Evaluation of mitophagy induction and its role in cytoprotection.
- Lifespan studies in Caenorhabditis elegans.
Main Results:
- BM extracts significantly diminished B[a]P-induced apoptosis and senescence in IMPHFA cells.
- BM reduced B[a]P-induced mitochondrial damage and ROS production.
- BM reversed B[a]P-triggered cell cycle arrest (G2 arrest) in astrocytes.
- BM-mediated protection was dependent on Parkin-dependent mitophagy, which cleared damaged mitochondria.
Conclusions:
- Bacopa monnieri exhibits significant anti-apoptotic and anti-senescence properties in astrocytes, counteracting B[a]P neurotoxicity.
- BM's neuroprotective effects are mediated through the induction of Parkin-dependent mitophagy, reducing mitochondrial dysfunction.
- These findings suggest BM holds potential for combating neurological disorders associated with environmental pollution and aging.
