CAJ | 학술논문

目的：探讨Y‐27632对低氧性肺动脉收缩的作用及其机制。方法建立小鼠低氧损伤模型；采用微血管张力实验测定肺动脉收缩力，WB检测TRPC6蛋白表达，离子影像技术测定平滑肌细胞全细胞钙变化。结果与对照组比较，CPA诱导低氧组肺动脉的收缩（加强到了167．9％±68．6％，倡 P＜0．05；Y‐27632可显著抑制这一变化（抑制率为47．3％±17．8％，＃ P＜0．05）；低氧可致肺动脉血管T RPC6蛋白表达显著增加（增加到154．8％±34．3％，倡 P＜0．05），这一变化可被Y‐27632显著降低（降低到134．2％±18．2％，＃ P＜0．05）；CPA诱导低氧组肺动脉平滑肌细胞[Ca2＋]i 显著升高（荧光比率升高到188．9％±46．6％，倡 P＜0．05），此作用可被Y‐27632显著抑制（荧光比率降低了46．7％±14．5％，＃ P＜0．05）。结论 ROCK抑制剂Y‐27632可通过调控T RPC6蛋白表达及其介导的[Ca2＋]i 变化，重要性地参与低氧性肺动脉收缩。
목적：탐토Y‐27632대저양성폐동맥수축적작용급기궤제。방법건립소서저양손상모형；채용미혈관장력실험측정폐동맥수축력，WB검측TRPC6단백표체，리자영상기술측정평활기세포전세포개변화。결과여대조조비교，CPA유도저양조폐동맥적수축（가강도료167．9％±68．6％，창 P＜0．05；Y‐27632가현저억제저일변화（억제솔위47．3％±17．8％，＃ P＜0．05）；저양가치폐동맥혈관T RPC6단백표체현저증가（증가도154．8％±34．3％，창 P＜0．05），저일변화가피Y‐27632현저강저（강저도134．2％±18．2％，＃ P＜0．05）；CPA유도저양조폐동맥평활기세포[Ca2＋]i 현저승고（형광비솔승고도188．9％±46．6％，창 P＜0．05），차작용가피Y‐27632현저억제（형광비솔강저료46．7％±14．5％，＃ P＜0．05）。결론 ROCK억제제Y‐27632가통과조공T RPC6단백표체급기개도적[Ca2＋]i 변화，중요성지삼여저양성폐동맥수축。
Objective To investigate the effect of Y‐27632 on hypoxic pulmonary vasoconstriction and the potential mechanism . Methods Hypoxia‐induced injury model was made in mouse .CPA‐induced muscle contraction was detected by capillary tension experiment .To explore the expression of TRPC6 ,WB and immunofluorescence staining experiments were performed .Ca2+ was measured using a fluorescence imaging system .Results CPA‐induced muscle contraction was enhanced by 167 .9% ± 68 .6% in hypoxic pulmonary artery compared with control ,which was markedly inhibited by Y‐27632 (inhibition ratio was 47 .3% ± 17 .8% ,# P<0 .05) .The expression of TRPC6 induced by hypoxia was markedly increased (to 154 .8% ± 34 .3% ,* P<0 .05) . After treatment with Y‐27632 ,the expression of TRPC6 was significantly decreased compared with hypoxia mice (to 134 .2% ± 18 .2% ,# P<0 .05) .Ca2+ influx in pulmonary artery smooth muscle cells elicited by store depletion using CPA were dramatically augmented in hypoxia group by 188 .9% ± 46 .6% in the ratio of 340 nm/380 nm(* P<0 .05) .However ,Y‐27632 obviously at‐tenuated this change by 46 .7% ± 14 .5% (# P<0 .05) .Conclusion Inhibition of ROCK by Y‐27632 can importantly take part in HPV via the regulation of TRPC6 expression in pulmonary artery ,which mediated extracellular Ca2+ influx .