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Tranexamic acid protects against rotenone-induced apoptosis in human neuroblastoma SH-SY5Y cells
Hak-Jae Kim1, Hae Jeong Park, Hyun Kyung Park
1Kohwang Medical Research Institute, Kyung Hee University, Seoul 130-701, Republic of Korea.
Abstract:
Rotenone is a pesticide that has been shown to induce the pathological symptoms of Parkinson's disease (PD) in animal models. In this study, we investigated the protective effects of tranexamic acid (TA) on rotenone-induced apoptosis in human dopaminergic SH-SY5Y cells. TA blocked the rotenone-induced phosphorylation of JNK and P38, the downregulation of BCL2 and the upregulation of BAX. Furthermore, TA not only decreased the rotenone-induced cleavage of caspase 9, PARP, and caspase 3, but also increased caspase 3 enzymatic activity. Our findings indicate that TA is able to protect neuronal cells against apoptosis and suggest that TA might potentially serve as an agent for prevention or therapy of PD.
Insights
Tranexamic acid (TA) protects human neuronal cells from rotenone-induced Parkinson's disease (PD) pathology. TA inhibits apoptosis pathways, suggesting its potential as a therapeutic agent for PD prevention and treatment.
Area of Science:
- Neuroscience
- Pharmacology
- Cell Biology
Background:
- Rotenone pesticide exposure is linked to Parkinson's disease (PD) pathology in animal models.
- Dopaminergic neuron apoptosis is a key feature of Parkinson's disease pathogenesis.
- Identifying neuroprotective agents is crucial for PD therapeutic strategies.
Purpose of the Study:
- To investigate the protective effects of tranexamic acid (TA) against rotenone-induced apoptosis in human dopaminergic SH-SY5Y cells.
- To elucidate the molecular mechanisms underlying TA's neuroprotection in a cellular model of PD.
Main Methods:
- Utilized human dopaminergic SH-SY5Y cells exposed to rotenone.
- Assessed the impact of tranexamic acid (TA) on key apoptosis markers.
- Measured phosphorylation of JNK and P38 kinases.
- Quantified expression levels of BCL2 and BAX proteins.
- Analyzed cleavage of executioner caspases (caspase 9, caspase 3) and PARP.
- Determined caspase 3 enzymatic activity.
Main Results:
- Tranexamic acid (TA) inhibited rotenone-induced phosphorylation of JNK and P38 signaling pathways.
- TA prevented the downregulation of the anti-apoptotic protein BCL2 and the upregulation of the pro-apoptotic protein BAX.
- TA significantly decreased the cleavage of caspase 9, PARP, and caspase 3.
- TA treatment led to increased caspase 3 enzymatic activity in rotenone-exposed cells.
Conclusions:
- Tranexamic acid (TA) demonstrates significant neuroprotective effects against rotenone-induced apoptosis in human dopaminergic cells.
- TA acts by modulating key apoptotic signaling pathways and effector proteins.
- These findings suggest tranexamic acid (TA) as a potential therapeutic candidate for Parkinson's disease prevention and treatment.
