Han Yong Hwan, Moon Hwa Jin, You Bo Ra, Kim Sung Zoo, Kim Suhn Hee, Park Woo Hyun
Department of Physiology, Medical School, Centers for Healthcare Technology Development Institute for Medical Sciences, Chonbuk National University, JeonJu 561-180, Korea.
Int J Mol Med. 2009 Nov;24(5):717-22. doi: 10.3892/ijmm_00000284.
Pyrogallol (PG) as a polyphenol compound induces apoptosis in several types of cells. Here, we investigated the effects of MAPK inhibitors on PG-treated calf pulmonary artery endothelial cells (CPAEC) in relation to cell death, ROS and GSH. PG inhibited the growth of CPAEC and also induced cell death, which was accompanied by the loss of mitochondrial membrane potential (MMP; DeltaPsi(m)). PG decreased the ROS level and increased the GSH depleted cell number in CPAEC. JNK inhibitor intensified the growth inhibition by PG whereas p38 inhibitor attenuated the growth inhibition. While MEK and p38 inhibitors decreased CPAEC death by PG, JNK inhibitor increased. None of the MAPK inhibitors significantly increased ROS level in PG-treated CPAEC. JNK inhibitor increased GSH depleted cell number in PG-treated CPAEC whereas p38 inhibitor decreased the number. MAPK inhibitors differently affected cell growth, death, ROS and GSH levels in control CPACE. In conclusion, PG induced apoptosis via the loss of MMP (DeltaPsi(m)) in CPAEC, which is accompanied by GSH depletion. JNK and p38 inhibitors increased and decreased apoptosis in PG-treated CPAEC, respectively, which were correlated with GSH depletion.
连苯三酚（PG）作为一种多酚化合物可诱导多种类型细胞发生凋亡。在此，我们研究了丝裂原活化蛋白激酶（MAPK）抑制剂对PG处理的小牛肺动脉内皮细胞（CPAEC）细胞死亡、活性氧（ROS）和谷胱甘肽（GSH）的影响。PG抑制CPAEC的生长并诱导细胞死亡，同时伴有线粒体膜电位（MMP；ΔΨm）的丧失。PG降低了CPAEC中的ROS水平并增加了GSH耗竭的细胞数量。JNK抑制剂增强了PG对生长的抑制作用，而p38抑制剂减弱了这种生长抑制。虽然MEK和p38抑制剂减少了PG诱导的CPAEC死亡，但JNK抑制剂却增加了这种死亡。在PG处理的CPAEC中，没有一种MAPK抑制剂能显著增加ROS水平。JNK抑制剂增加了PG处理的CPAEC中GSH耗竭的细胞数量，而p38抑制剂则减少了该数量。MAPK抑制剂对对照CPAEC中的细胞生长、死亡、ROS和GSH水平有不同影响。总之，PG通过导致CPAEC中MMP（ΔΨm）丧失诱导凋亡，同时伴有GSH耗竭。JNK和p38抑制剂分别增加和减少了PG处理的CPAEC中的凋亡，这与GSH耗竭相关。
