Conclusion
Our study gives credence to TQ as a promising intervention therapy for cerebral ischemia that decreases inflammation, oxidative stress, and neuronal cell death via the Nrf2/HO-1 pathway, along with modulation of apoptotic and autophagic processes.
Results
Our in vivo and in vitro results indicated that TQ significantly mitigates brain damage and motor dysfunction after ischemic stroke. These observations coincided with curtailed cell death, inflammation, oxidative stress, apoptosis, and autophagy. Most importantly, Nrf2/HO-1 signaling pathway activation by TQ was vital in the modulation of the above processes. Lastly, we found TQ to have minimal toxicity in liver tissue.