CAJ | 학술논문

目的：研究羟基红花黄色素A（hydroxysafflor yellow A，HSYA）对心肌细胞模拟缺血/再灌注（simulated ischemia/reperfusion，SI/R）损伤的保护作用。方法采用H9c2心肌细胞建立SI/R损伤模型，检测心肌细胞存活率、乳酸脱氢酶（LDH）水平，TUNEL染色法检测细胞凋亡，Western blot检测Akt/eNOS信号通路蛋白的表达。结果与SI/R组比较，20μM HSYA预处理能显著提高SI/R损伤的H9c2细胞的存活率，（69.7±5.8）%vs.（79.9±5.8）%，差异有统计学意义（P＜0.05）。与Control 组相比，SI/R组心肌细胞LDH释放增加，（43.3±9.4）U/Lvs.（129.5±11.9）U/L，差异有统计学意义（P＜0.05）。与SI/R组相比，HSYA可显著降低LDH的释放，而加入PI3K的抑制剂LY29004后，这种作用消失。与Control组比较，SI/R损伤显著增加H9c2心肌细胞的凋亡率，差异有统计学意义（P＜0.05）；与SI/R组相比，SI/R+HSYA组细胞凋亡率显著下降，而加入LY29004后，逆转了HSYA的抑制凋亡的作用。与SI/R组相比， SI/R+HSYA组 p-Akt蛋白的表达显著升高，差异有统计学意义（P＜0.05），加入LY29004后 p-Akt 蛋白的表达被明显抑制。与SI/R组比较，SI/R+HSYA组 p-eNOS 蛋白的表达明显升高，差异有统计学意义（P＜0.05），加入LY29004后 p-eNOS蛋白的表达被明显抑制。结论羟基红花黄色素A能增强H9c2细胞活力，减少心肌细胞损伤，抑制心肌细胞凋亡，并通过激活Akt/eNOS信号通路发挥保护作用。
목적：연구간기홍화황색소A（hydroxysafflor yellow A，HSYA）대심기세포모의결혈/재관주（simulated ischemia/reperfusion，SI/R）손상적보호작용。방법채용H9c2심기세포건립SI/R손상모형，검측심기세포존활솔、유산탈경매（LDH）수평，TUNEL염색법검측세포조망，Western blot검측Akt/eNOS신호통로단백적표체。결과여SI/R조비교，20μM HSYA예처리능현저제고SI/R손상적H9c2세포적존활솔，（69.7±5.8）%vs.（79.9±5.8）%，차이유통계학의의（P＜0.05）。여Control 조상비，SI/R조심기세포LDH석방증가，（43.3±9.4）U/Lvs.（129.5±11.9）U/L，차이유통계학의의（P＜0.05）。여SI/R조상비，HSYA가현저강저LDH적석방，이가입PI3K적억제제LY29004후，저충작용소실。여Control조비교，SI/R손상현저증가H9c2심기세포적조망솔，차이유통계학의의（P＜0.05）；여SI/R조상비，SI/R+HSYA조세포조망솔현저하강，이가입LY29004후，역전료HSYA적억제조망적작용。여SI/R조상비， SI/R+HSYA조 p-Akt단백적표체현저승고，차이유통계학의의（P＜0.05），가입LY29004후 p-Akt 단백적표체피명현억제。여SI/R조비교，SI/R+HSYA조 p-eNOS 단백적표체명현승고，차이유통계학의의（P＜0.05），가입LY29004후 p-eNOS단백적표체피명현억제。결론간기홍화황색소A능증강H9c2세포활력，감소심기세포손상，억제심기세포조망，병통과격활Akt/eNOS신호통로발휘보호작용。
Objective To study the preventive effect of hydroxysafflor yellow A (HSYA) on simulated cardiomyocyte ischemia-reperfusion (SI/R) injury.Methods The model of SI/R injury was established by using H9c2 cardiomyocyte. The survival rate of cardiomyocyte and level of lactate dehydrogenase (LDH) were detected, apoptosis was detected by using TUNEL staining assay, and Akt/eNOS protein expressions were detected by using Western blot test.Resutls The survival rate of H9c2 cardiomyocyte with SI/R injury increased significantly in SI/R+HSYA group compared with SI/R group [(69.7±5.8) % vs. (79.9±5.8)%, P<0.05]. The release of LDH increased in SI/R group compared with control group [(43.3±9.4) U/L vs. (129.5±11.9) U/L, P<0.05]. HSYA decreased significantly the release of LDH, which disappeared after LY29004 (PI3K inhibitor) added. The apoptosis rate of H9c2 cardiomyocyte increased significantly in SI/R group compared with control group (P<0.05). The apoptosis rate of H9c2 cardiomyocyte decreased significantly in SI/R+HSYA group compared with SI/R group, which was reversed after LY29004 added. The expression of p-Akt increased significantly in SI/R+HSYA group compared with SI/R group (P<0.05), which was significantly inhibited after LY29004 added. The expression of p-eNOS increased significantly in SI/R+HSYA group compared with SI/R group (P<0.05), which was significantly inhibited after LY29004 added.Conclusion HSYA can improve the viability of H9c2 cardiomyocyte, relieve cardiomyocyte injury, inhibit cardiomyocyte apoptosis, and play a protective role through activating Akt/eNOS signal path.