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Published on: July 13, 2018
Green Tea Catechin Prevents Hypoxia/Reperfusion-Evoked Oxidative Stress-Regulated Autophagy-Activated Apoptosis and
Chang-Mu Chen1, Cheng-Tien Wu2, Ting-Hua Yang3
1Division of Neurosurgery, Department of Surgery, National Taiwan University Hospital and National Taiwan University, College of Medicine , Taipei, Taiwan.
Abstract:
Defective activation and proliferation in microglial cells has been suggested to be associated with the increase of cerebral ischemia/reperfusion injury. We investigated the protection and molecular mechanism of green tea catechin on hypoxia/reperfusion-induced microglial cell injury in vitro. Microglial cells were cultured in hypoxia condition (O2 < 1%) and then re-incubated to the complete normal culture medium (reperfusion). Hypoxia/reperfusion obviously decreased cell viability and induced apoptosis in microglial cells, but not in neuronal cells. Catechin significantly inhibited the hypoxia/reperfusion-induced decreased cell viability and increased reactive oxygen species (ROS) and apoptosis in microglia. The administration of both PI3K/Akt inhibitor LY294002 and mTOR inhibitor rapamycin demonstrated that Akt/mTOR-regulated autophagy was involved in the hypoxia/reperfusion-induced microglia apoptosis/death. Catechin up-regulated the Akt and mTOR phosphorylation and inhibited the hypoxia/reperfusion-induced autophagy in microglia. These results suggest that hypoxia/reperfusion can evoke autophagy-activated microglia apoptosis/death via an ROS-regulated Akt/mTOR signaling pathway, which can be reversed by catechin.
Insights
Green tea catechin protects microglia from hypoxia/reperfusion injury by inhibiting reactive oxygen species (ROS) and autophagy. This mechanism involves the Akt/mTOR signaling pathway, offering a potential therapeutic strategy for cerebral ischemia.
Area of Science:
- Neuroscience
- Cell Biology
- Pharmacology
Background:
- Microglial cell dysfunction is linked to cerebral ischemia/reperfusion (I/R) injury.
- Investigating protective mechanisms against I/R-induced microglial damage is crucial.
Purpose of the Study:
- To explore the protective effects and molecular mechanisms of green tea catechin against hypoxia/reperfusion (H/R)-induced microglial injury in vitro.
- To elucidate the role of the Akt/mTOR signaling pathway and autophagy in H/R-induced microglial apoptosis.
Main Methods:
- Microglial cells were subjected to hypoxia followed by reoxygenation (H/R).
- Cell viability, apoptosis, and reactive oxygen species (ROS) production were assessed.
- The involvement of PI3K/Akt and mTOR signaling pathways was investigated using specific inhibitors (LY294002, rapamycin).
- Autophagy levels and Akt/mTOR phosphorylation were analyzed.
Main Results:
- H/R significantly reduced microglial viability and increased apoptosis and ROS levels.
- Catechin treatment attenuated H/R-induced cell death, ROS production, and apoptosis.
- Akt/mTOR signaling pathway and autophagy were implicated in H/R-induced microglial apoptosis.
- Catechin upregulated Akt and mTOR phosphorylation and inhibited H/R-induced autophagy.
Conclusions:
- Hypoxia/reperfusion induces microglial apoptosis via an ROS-regulated Akt/mTOR-autophagy signaling pathway.
- Green tea catechin demonstrates neuroprotective effects by reversing H/R-induced microglial injury.
- Catechin's mechanism involves modulating the Akt/mTOR pathway and inhibiting autophagy, suggesting therapeutic potential for cerebral ischemia.
