Li Xue-feng, Shi Xiao-hua, Luo Qi-zhi
Institute of Burn Research, Southwest Hospital, State Key Laboratory of Trauma, Burns and Combined Injury, the Third Military Medical University, Chongqing 400038, China.
Zhonghua Shao Shang Za Zhi. 2011 Jun;27(3):169-72.
To investigate the protective effect of ginsenoside Re on myocardial cells of neonatal SD rat with hypoxia injury, and to explore its mechanism.
The primary passage of myocardial cells collected from neonatal SD rats were divided into A group (with ordinary treatment), B group [exposed to hypoxia (1% O2, 5% CO2, 94% N(2)) for 12 hours after being cultured for 48 hours], C group (pretreated with 80 g/L ginsenoside Re for 30 minutes after 48 hours of ordinary culture, then exposed to hypoxia for 12 hours), D group (received the same treatment as used in C group except for using 40 g/L ginsenoside Re), E group (received the same treatment as used in C group except for using 20 g/L ginsenoside Re) according to the random number table, with 6 samples in each group. Myocardial cell supernatants were collected for determination of content of lactate dehydrogenase (LDH) with enzyme linked immunosorbent assay. Fluorescence recovery after photobleaching technique was used to detect gap junction intercellular communication (GJIC). Result was observed by laser scanning confocal microscope. Data were processed with paired t test.
(1) Compared with that in B group [(403 ± 22) U/L], contents of LDH in E, D, and C groups were obviously decreased [(255 ± 16), (241 ± 13), (237 ± 24) U/L, with t value respectively 5.1, 5.2, 8.3, P values all below 0.05]. (2) The fluorescence recovery rate in A group was (74.8 ± 3.6)% 10 min after quenching, which was higher than that in B group [(13.2 ± 5.6)%, t = 15.2, P < 0.01]. The fluorescence recovery rate in C, D, and E groups was respectively (39.5 ± 2.9)%, (36.2 ± 3.1)%, and (34.3 ± 3.9)% 10 min after quenching, all higher than that in B group (with t value respectively -6.6, -41.9, 18.3, P values all below 0.05).
Ginsenoside Re pretreatment, particularly with a dose of 20 g/L, can protect myocardial cells from hypoxia injury, and the effect may be attributable to inhibition of release of LDH and improvement of the GJIC function.
探讨人参皂苷Re对新生SD大鼠缺氧损伤心肌细胞的保护作用及其机制。
将新生SD大鼠原代培养的心肌细胞按随机数字表法分为A组（常规处理）、B组（培养48小时后置于缺氧环境中12小时，缺氧条件为1%O₂、5%CO₂、94%N₂）、C组（常规培养48小时后用80g/L人参皂苷Re预处理30分钟，再置于缺氧环境中12小时）、D组（处理同C组，人参皂苷Re浓度为40g/L）、E组（处理同C组，人参皂苷Re浓度为20g/L），每组6个样本。收集心肌细胞上清液，采用酶联免疫吸附法测定乳酸脱氢酶（LDH）含量。运用光漂白后荧光恢复技术检测缝隙连接细胞间通讯（GJIC），通过激光扫描共聚焦显微镜观察结果。数据采用配对t检验进行处理。
（1）与B组[（403±22）U/L]比较，E、D、C组LDH含量明显降低[（255±16）、（241±13）、（237±24）U/L，t值分别为5.1、5.2、8.3，P值均<0.05]。（2）淬灭10分钟后A组荧光恢复率为（74.8±3.6）%，高于B组[（13.2±5.6）%，t = 15.2，P<0.01]。淬灭10分钟后C、D、E组荧光恢复率分别为（39.5±2.9）%、（36.2±3.1）%、（34.3±3.9）%，均高于B组（t值分别为-6.6、-41.9、18.3，P值均<0.05）。
人参皂苷Re预处理，尤其是20g/L剂量，可保护心肌细胞免受缺氧损伤，其作用可能与抑制LDH释放及改善GJIC功能有关。
