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RISS 인기검색어
- 검색키워드
- 저자 : Po-Len Liu (검색결과 3 건)
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Antioxidative and Hepatoprotective Effects of Magnolol on Acetaminophen-induced Liver Damage in Rats
Yung-Hsiang Chen,Feng-Yen Lin,Po-Len Liu,Yi-Tsau Huang,Jen-Hwey Chiu,Yi-Chun Chang,Kee-Ming Man,Chuang-Ye Hong,Yen-Yi Ho,Ming-Tsung Lai 대한약학회 2009 Archives of Pharmacal Research Vol.32 No.2
Acute liver failure (ALF), an often fatal condition characterized by massive hepatocyte necrosis, is frequently caused by drug poisoning, particularly with acetaminophen (N-acetyl-p-aminophenol/APAP). Hepatocyte necrosis is consecutive to glutathione (GSH) depletion and mitochondrial damage caused by reactive oxygen species (ROS) overproduction. Magnolol, one major phenolic constituent of Magnolia officinalis, have been known to exhibit potent antioxidative activity. In this study, the anti-hepatotoxic activity of magnolol on APAP-induced toxicity in the Sprague-Dawley rat liver was examined. After evaluating the changes of several biochemical parameters in serum, the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) were elevated by APAP (500 mg/kg) intraperitoneal administration (8 and 24 h) and reduced by treatment with magnolol (0.5 h after APAP administration; 0.01, 0.1, and 1 μg/kg). Histological changes around the hepatic central vein, lipid peroxidation (thiobarbituric acid-reactive substance/TBARS), and GSH depletion in liver tissue induced by APAP were also recovered by magnolol treatment. The data show that oxidative stress followed by lipid peroxidation may play a very important role in the pathogenesis of APAP-induced hepatic injury; treatment with lipid-soluble antioxidant, magnolol, exerts anti-hepatotoxic activity. Our study points out the potential interest of magnolol in the treatment of toxic ALF.
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Magnolol induces apoptosis via caspase-independent pathways in non-small cell lung cancer cells
Tsai, Jong-Rung,Chong, Inn-Wen,Chen, Yung-Hsiang,Hwang, Jhi-Jhu,Yin, Wei-Hsian,Chen, Hsiu-Lin,Chou, Shah-Hwa,Chiu, Chien-Chih,Liu, Po-Len 대한약학회 2014 Archives of Pharmacal Research Vol.37 No.4
Magnolol, a hydroxylated biphenyl agent isolated from herbal planet Magnolia officinalis, is a component of traditional Asian herbal teas. It has been reported to have anti-microbial, anti-inflammatory, and anti-cancer activity. Non-small cell lung cancer (NSCLC) cell lines (A549, H441 and H520) and normal human bronchial epithelial cells (HBECs) were used to evaluate the cytotoxic effect of magnolol. We show that magnolol inhibited cellular proliferation, increased DNA fragmentation, and decreased mitochondrial membrane potential in all NSCLC cells, but had no cytotoxic effect on HBECs. Magnolol triggered the release of pro-apoptotic proteins: Bid, Bax and cytochrome c from mitochondria, but did not activate the caspase-3, -8, and -9, suggesting that magnolol induces apoptosis of NSCLC cell lines via a caspase-independent pathway. The caspase-independent pathway is mediated through the activation of nuclear translocation of apoptosis-inducing factor, endonuclease G and cleaved poly(-ADP-ribose) polymerase, which played important roles in mediating cell death. Furthermore, magnolol inhibited PI3K/AKT and ERK1/2 activity, but up-regulated p38 and JNK activity in A549 cell lines. The results of this study provided a basis for understanding and developing magnolol as a novel treatment of NSCLC.
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Magnolol induces apoptosis via caspase-independent pathways in non-small cell lung cancer cells
Jong-Rung Tsai,Inn-Wen Chong,Yung-Hsiang Chen,Jhi-Jhu Hwang,Wei-Hsian Yin,Hsiu-Lin Chen,Shah-Hwa Chou,Chien-Chih Chiu,Po-Len Liu 대한약학회 2014 Archives of Pharmacal Research Vol.37 No.4
Magnolol, a hydroxylated biphenyl agent isolatedfrom herbal planet Magnolia officinalis, is a componentof traditional Asian herbal teas. It has been reported tohave anti-microbial, anti-inflammatory, and anti-canceractivity. Non-small cell lung cancer (NSCLC) cell lines(A549, H441 and H520) and normal human bronchialepithelial cells (HBECs) were used to evaluate the cytotoxiceffect of magnolol. We show that magnolol inhibitedcellular proliferation, increased DNA fragmentation, anddecreased mitochondrial membrane potential in all NSCLCcells, but had no cytotoxic effect on HBECs. Magnololtriggered the release of pro-apoptotic proteins: Bid, Bax and cytochrome c from mitochondria, but did not activatethe caspase-3, -8, and -9, suggesting that magnolol inducesapoptosis of NSCLC cell lines via a caspase-independentpathway. The caspase-independent pathway is mediatedthrough the activation of nuclear translocation of apoptosis-inducing factor, endonuclease G and cleaved poly(-ADP-ribose) polymerase, which played important roles inmediating cell death. Furthermore, magnolol inhibitedPI3K/AKT and ERK1/2 activity, but up-regulated p38 andJNK activity in A549 cell lines. The results of this studyprovided a basis for understanding and developing magnololas a novel treatment of NSCLC.
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