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Sun Mi Kim Hae Sun Park Do Youn Jun Hyun Ju Woo Mi Hee Woo Chae Ha Yang Young Ho Kim 《Toxicology and applied pharmacology》2009,241(2):210-220
Exposure of Jurkat T cells to mollugin (15–30 μM), purified from the roots of Rubia cordifolia L., caused cytotoxicity and apoptotic DNA fragmentation along with mitochondrial membrane potential disruption, mitochondrial cytochrome c release, phosphorylation of c-Jun N-terminal kinase (JNK), activation of caspase-12, -9, -7, -3, and -8, cleavage of FLIP and Bid, and PARP degradation, without accompanying necrosis. While these mollugin-induced cytotoxicity and apoptotic events including activation of caspase-8 and mitochondria-dependent activation of caspase cascade were completely prevented by overexpression of Bcl-xL, the activation of JNK and caspase-12 was prevented to much lesser extent. Pretreatment of the cells with the pan-caspase inhibitor (z-VAD-fmk), the caspase-9 inhibitor (z-LEHD-fmk), the caspase-3 inhibitor (z-DEVD-fmk) or the caspase-12 inhibitor (z-ATAD-fmk) at the minimal concentration to prevent mollugin-induced apoptosis appeared to completely block the activation of caspase-7 and -8, and PARP degradation, but failed to block the activation of caspase-9 and -3 with allowing a slight enhancement in the level of JNK phosphorylation. Both FADD-positive wild-type Jurkat clone A3 and FADD-deficient Jurkat clone I2.1 exhibited a similar susceptibility to the cytotoxicity of mollugin, excluding involvement of Fas/FasL system in triggering mollugin-induced apoptosis. Normal peripheral T cells were more refractory to the cytotoxicity of mollugin than were Jurkat T cells. These results demonstrated that mollugin-induced cytotoxicity in Jurkat T cells was mainly attributable to apoptosis provoked via endoplasmic reticulum (ER) stress-mediated activation of JNK and caspase-12, and subsequent mitochondria-dependent activation of caspase-9 and -3, leading to activation of caspase-7 and -8, which could be regulated by Bcl-xL. 相似文献
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目的:观察大叶茜草素(mollugin)对大鼠肝星状细胞系CFSC-2G活化和胶原合成的影响并探讨其分子机制。方法:小剂量(10μmol/L)过氧化氢(H_2O_2)诱导CFSC-2G细胞30 min后,再加入不同浓度(0、20、40、60和120μmol/L)的mollugin处理。MTT法检测细胞活力,real-time PCR和Western blot法分别检测核因子E2相关因子2(Nrf2)、血红素加氧酶-1(HO-1)、核因子κB(NF-κB)p65、Bcl-2、Bcl-x L、Bax以及肝星状细胞活化标志物α-平滑肌肌动蛋白和Ⅰ型胶原蛋白的mRNA和蛋白表达,并用Western blot法检测p38丝裂原活化蛋白激酶(p38MAPK)的磷酸化水平。结果:低剂量H_2O_2可以诱导CFSC-2G细胞活化,mollugin明显促进p38 MAPK磷酸化,上调Nrf2和HO-1的mRNA和蛋白表达,下调NF-κB p65、Bcl-2和Bcl-x L的mRNA和蛋白表达,抑制H_2O_2诱导活化的CFSC-2G细胞活力和胶原合成(P0.05)。结论:Mollugin可能通过上调Nrf2和HO-1并下调NF-κB p65和Bcl-2表达,抑制CFSC-2G细胞活化和胶原合成。 相似文献
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目的:使用茜草细胞悬浮培养体系研究茜草中萘醌类成分生合成途径原料IPP的来源,以及茉莉酸甲酯、氯胺和洛伐他丁对蒽醌和萘醌的积累情况。方法:建立茜草细胞悬浮培养体系,分别在培养基中添加茉莉酸甲酯、氯胺和洛伐他丁。每3天取样一次。使用高效液相色谱法测定紫色素和大叶茜草素含量并计算出产量。结果:洛伐他丁处理组中紫色素和大叶茜草素产量均有显著增加。氯胺处理组中紫色素和大叶茜草素产量明显下降。茉莉酸甲酯处理组中紫色素产量增加,同时大叶茜草素产量降低。结论:在茜草细胞中萘醌类成分的IPP可能是通过MEP途径合成的;要解释茉莉酸甲酯对蒽醌和萘醌积累的不同作用,基因表达水平方面的研究尤其是对1,4-二羟基-2-萘甲酸异戊烯基化的基因表达研究应该受到更多关注。 相似文献
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OBJECTIVE A HPLC method for the determination of Mollugin in BiYuan DiWan was improve in virtue of DAD.METHODS A DiamonsilTMC18 column was used with methanol-water-furanidine(84:15:1) as mobile phase.Content was detected at double wavelength of 250nm and 相似文献
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Jeong GS Lee DS Kim DC Jahng Y Son JK Lee SH Kim YC 《European journal of pharmacology》2011,(3):6-234
Mollugin, a bioactive phytochemical isolated from Rubia cordifolia L. (Rubiaceae), exhibits antimutagenic activity, antitumor activity, antiviral activity, and inhibitory activity in arachidonic acid- and collagen-induced platelet aggregation. In this study, we investigated the effects of mollugin as a neuroprotective agent in glutamate-induced neurotoxicity in the mouse hippocampal HT22 cell line and as an anti-inflammatory agent in lipopolysaccharide-induced microglial activation in BV2 cells. Mollugin showed potent neuroprotective effects against glutamate-induced neurotoxicity and reactive oxygen species generation in mouse hippocampal HT22 cells. In addition, the anti-inflammatory effects of mollugin were demonstrated by the suppression of pro-inflammatory mediators, including pro-inflammatory enzymes (inducible nitric oxide synthase and cyclooxygenase-2) and cytokines (tumor necrosis factor-α and interleukin-6). Furthermore, we found that the neuroprotective and anti-inflammatory effects of mollugin were linked to the up-regulation of the expression of heme oxygenase (HO)-1 and the activity of HO in HT22 and BV2 cells. In addition, the effects of mollugin resulted in the nuclear accumulation of nuclear factor-E2-related factor 2 (Nrf2) in HT22 and BV2 cells. Furthermore, mollugin also activated the p38 mitogen-activated protein kinase (MAPK) pathway both in HT22 and BV2 cells. These results suggest that mollugin may be a promising candidate for the treatment of neurodegenerative diseases related to neuroinflammation. 相似文献
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