Objective : This study was conducted to evaluate the inhibitory effect of Angelicae gigas extract (AGE) on contraction of pericytes and Human Umbilical Vein Endothelial Cells (HUVEC). Materials and Method : Pericytes and HUVEC were pretreated with different concentration (100㎍/㎖, 200㎍/㎖) of AGE ...
Objective : This study was conducted to evaluate the inhibitory effect of Angelicae gigas extract (AGE) on contraction of pericytes and Human Umbilical Vein Endothelial Cells (HUVEC). Materials and Method : Pericytes and HUVEC were pretreated with different concentration (100㎍/㎖, 200㎍/㎖) of AGE for 30 minutes at 37℃ and then exposed to cold (25℃) for 30 minutes to estimate active RhoA. Pericytes and HUVEC were pretreated with AGE (200㎍/㎖) for 30 minutes at 37℃ and then cultured in cold temperature (25℃) for 30 minutes to estimate p-cofilin, p-LIMK1/2, TESK1, chronophin. Pericytes were pretreated with AGE (200㎍/㎖) for 30 minutes in 37℃ and then treated with endothelin-1 (100n㏖/L) for 30 minutes in 37℃ to examine active RhoA, p-cofilin, p-LIMK1/2, TESK1, chronophin. After each of the experiment, western blot analysis was conducted to measure active RhoA, p-cofilin, p-LIMK1/2, TESK1, and chronophin. Results : AGE inhibited active RhoA in pericytes and HUVEC exposed to 25℃, at both concentration (100㎍/㎖, 200㎍/㎖). AGE (200㎍/㎖) decreased p-cofilin and increased p-LIMK1/2 in cold-exposed pericytes, and decreased p-cofilin, p-LIMK1/2 in cold-exposed HUVEC. Meanwhile, AGE (200㎍/㎖) decreased active RhoA, p-cofilin, TESK1 and increased chronophin in endothelin-1 exposed pericytes. Conclusion : AGE showed inhibitory effect on contraction of pericytes exposed to either cold or endothelin-1, and HUVEC exposed to cold.
Objective : This study was conducted to evaluate the inhibitory effect of Angelicae gigas extract (AGE) on contraction of pericytes and Human Umbilical Vein Endothelial Cells (HUVEC). Materials and Method : Pericytes and HUVEC were pretreated with different concentration (100㎍/㎖, 200㎍/㎖) of AGE for 30 minutes at 37℃ and then exposed to cold (25℃) for 30 minutes to estimate active RhoA. Pericytes and HUVEC were pretreated with AGE (200㎍/㎖) for 30 minutes at 37℃ and then cultured in cold temperature (25℃) for 30 minutes to estimate p-cofilin, p-LIMK1/2, TESK1, chronophin. Pericytes were pretreated with AGE (200㎍/㎖) for 30 minutes in 37℃ and then treated with endothelin-1 (100n㏖/L) for 30 minutes in 37℃ to examine active RhoA, p-cofilin, p-LIMK1/2, TESK1, chronophin. After each of the experiment, western blot analysis was conducted to measure active RhoA, p-cofilin, p-LIMK1/2, TESK1, and chronophin. Results : AGE inhibited active RhoA in pericytes and HUVEC exposed to 25℃, at both concentration (100㎍/㎖, 200㎍/㎖). AGE (200㎍/㎖) decreased p-cofilin and increased p-LIMK1/2 in cold-exposed pericytes, and decreased p-cofilin, p-LIMK1/2 in cold-exposed HUVEC. Meanwhile, AGE (200㎍/㎖) decreased active RhoA, p-cofilin, TESK1 and increased chronophin in endothelin-1 exposed pericytes. Conclusion : AGE showed inhibitory effect on contraction of pericytes exposed to either cold or endothelin-1, and HUVEC exposed to cold.
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