Bratislavske lekarske listy · 2020
Protease-activated receptor 1 inhibitor improves brain edema in rats with intracerebral hemorrhage.
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Huang P, He X Y, Xu M
Аннотация
AIM: To investigate the changes of water content in brain tissue, the expression of AQP4mRNA after cerebral hemorrhage in rats, and the intervention effect of Protease activated receptor 1 inhibitor (PAR1 inhibitor) on both.
METHODS: Establish sham operation group (Sham group), ICH group, ICH+PAR1 inhibitor high-dose group (PI(H)group), ICH+PAR1 inhibitor low-dose group (PI(L)group), 25 in each group. Neural dysfunction scores were performed at 1d, 3d, 7d, 14d, and 21d after surgery, and brain water content and AQP4mRNA content were measured.
RESULTS: Results: The neurological dysfunction and cerebral edema of rats with cerebral hemorrhage reached the peak at 3 days after operation. With the increase of time, the water content and AQP4mRNA content in the PL(H)group were higher than those in the PI(L)group. The differences were statistically significant.
CONCLUSIONS: Appropriate inhibition of PAR1 can alleviate cerebral edema around the hematoma and play a role in improving the function of nerve defects. The mechanism may be realized by down-regulating the expression of AQP4mRNA in brain tissue (Tab. 3, Fig. 3, Ref. 25).
METHODS: Establish sham operation group (Sham group), ICH group, ICH+PAR1 inhibitor high-dose group (PI(H)group), ICH+PAR1 inhibitor low-dose group (PI(L)group), 25 in each group. Neural dysfunction scores were performed at 1d, 3d, 7d, 14d, and 21d after surgery, and brain water content and AQP4mRNA content were measured.
RESULTS: Results: The neurological dysfunction and cerebral edema of rats with cerebral hemorrhage reached the peak at 3 days after operation. With the increase of time, the water content and AQP4mRNA content in the PL(H)group were higher than those in the PI(L)group. The differences were statistically significant.
CONCLUSIONS: Appropriate inhibition of PAR1 can alleviate cerebral edema around the hematoma and play a role in improving the function of nerve defects. The mechanism may be realized by down-regulating the expression of AQP4mRNA in brain tissue (Tab. 3, Fig. 3, Ref. 25).