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Published on: April 24, 2021
Refined Qingkailing Protects MCAO Mice from Endoplasmic Reticulum Stress-Induced Apoptosis with a Broad Time Window
Fafeng Cheng1, Xianggen Zhong, Yi Lu
1College of Basic Medicine, Beijing University of Chinese Medicine, Beijing 100029, China.
Abstract:
In the current study, we are investigating effect of refined QKL on ischemia-reperfusion-induced brain injury in mice. Methods. Mice were employed to induce ischemia-reperfusion injury of brain by middle cerebral artery occlusion (MCAO). RQKL solution was administered with different doses (0, 1.5, 3, and 6 mL/kg body weight) at the same time of onset of ischemia, and with the dose of 1.5 mL/kg at different time points (0, 1.5, 3, 6, and 9 h after MCAO). Neurological function and brain infarction were examined and cell apoptosis and ROS at prefrontal cortex were evaluated 24 h after MCAO, and western blot and intracellular calcium were also researched, respectively. Results. RQKL of all doses can improve neurological function and decrease brain infarction, and it performed significant effect in 0, 1.5, 3, and 6 h groups. Moreover, RQKL was able to reduce apoptotic process by reduction of caspase-3 expression, or restraint of eIF2a phosphorylation and caspase-12 activation. It was also able to reduce ROS and modulate intracellular calcium in the brain. Conclusion. RQKL can prevent ischemic-induced brain injury with a time window of 6 h, and its mechanism might be related to suppress ER stress-mediated apoptotic signaling.
Insights
Refined QKL effectively mitigates brain injury caused by ischemia-reperfusion in mice. This neuroprotective effect, observed within a 6-hour window, involves reducing apoptosis and oxidative stress.
Area of Science:
- Neuroscience
- Pharmacology
- Cell Biology
Background:
- Ischemia-reperfusion (I/R) injury is a major cause of brain damage.
- Understanding protective mechanisms against I/R injury is critical for developing effective treatments.
Purpose of the Study:
- To investigate the neuroprotective effects of refined QKL (RQKL) on ischemia-reperfusion-induced brain injury in a mouse model.
- To determine the optimal dosage and time window for RQKL administration.
- To elucidate the underlying molecular mechanisms of RQKL's protective action.
Main Methods:
- Middle cerebral artery occlusion (MCAO) model in mice to induce I/R brain injury.
- Administration of RQKL at various doses and time points post-MCAO.
- Assessment of neurological function, brain infarction volume, cell apoptosis, reactive oxygen species (ROS), caspase-3 expression, eIF2a phosphorylation, caspase-12 activation, and intracellular calcium levels.
Main Results:
- RQKL administration significantly improved neurological function and reduced brain infarction across all tested doses.
- Optimal protective effects were observed when RQKL was administered within 6 hours of MCAO onset.
- RQKL suppressed apoptosis by reducing caspase-3 expression, inhibiting eIF2a phosphorylation and caspase-12 activation, decreasing ROS, and modulating intracellular calcium.
Conclusions:
- Refined QKL demonstrates significant neuroprotective potential against ischemic brain injury.
- The therapeutic window for RQKL is up to 6 hours post-ischemia.
- RQKL's mechanism of action involves suppressing ER stress-mediated apoptotic signaling pathways.
