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      • KCI등재

        Galangin Prevents Acute Hepatorenal Toxicity in Novel Propacetamol-Induced Acetaminophen-Overdosed Mice

        Ming-Shiun Tsai,Chia-Chih Chien,Ting-Hui Lin,Chia-Chi Liu,Rosa Huang Liu,Hong-Lin Su,Yung-Tsung Chiu,Sue-Hong Wang 한국식품영양과학회 2015 Journal of medicinal food Vol.18 No.11

        Acetaminophen (APAP) overdose causes severe liver and kidney damage. APAP-induced liver injury (AILI) represents the most frequent cause of drug-induced liver failure. APAP is relatively insoluble and can only be taken orally; however, its prodrug, propacetamol, is water soluble and usually injected directly. In this study, we examined the timedependent effects of AILI after propacetamol injection in mice. After analyses of alanine aminotransferase and aspartate aminotransferase activities and liver histopathology, we demonstrated that a novel AILI mouse model can be established by single propacetamol injection. Furthermore, we compared the protective and therapeutic effects of galangin with a known liver protective extract, silymarin, and the only clinical agent for treating APAP toxicity, N-acetylcysteine (NAC), at the same dose in the model mice. We observed that galangin and silymarin were more effective than NAC for protecting against AILI. However, only NAC greatly improved both the survival time and rate consequent to a lethal dose of propacetamol. To decipher the hepatic protective mechanism(s) of galangin, galangin pretreatment significantly decreased the hepatic oxidative stress, increased hepatic glutathione level, and decreased hepatic microsomal CYP2E1 levels induced by propacetamol injection. In addition, propacetamol injection also reproduced the probability of APAP-induced kidney injury (AIKI), appearing similar to a clinical APAP overdose. Only galangin pretreatment showed the protective effect of AIKI. Thus, we have established a novel mouse model for AILI and AIKI using a single propacetamol injection. We also demonstrated that galangin provides significant protection against AILI and AIKI in this mouse model.

      • Penetration Processes of Soft Solid Materials by Needle-Free Micro-Injections

        ( Muh Rong Wang ),( Chun Hsien Chiu ),( Chien Chih Huang ),( Li Jay Cheng ),( Yang Sheng Huang ),( Min Chen ) 한국액체미립화학회 2010 한국액체미립화학회 학술강연회 논문집 Vol.2010 No.-

        Penetration characteristics of the single pulse micro-jets into the soft solid materials of gelatin gels and porcine colons are investigated in this paper. The images of penetration processes were taken by IDT high-speed digital camera at the sampling rate of 2500 frames per second. The evolution of the penetration process, penetration depth, volume of infection and penetration rate is investigated. Gelatin gel is a good model material for the observation of the penetration processes because of the translucent property. In vitro penetrations of porcine colons were also tested for the prior study of endoscopic needle-free injection. The penetration test was performed under the single-pulsed mode at injection time of 0.1, 0.25 and 0.5 seconds. The injection pressure was in the range of 50 to 125 bar. The diameter of the injectors, do, is 250 and 300 m. According to the high-speed photos of the gel penetration, the injection processes can be described as four steps: 1. Initial compression period: the elastic compression of the soft solid material at the penetration site and the neighborhood. 2. Material failure period: the jet penetrates inside the gelatin gel including the initial surface crack and growth of the injected volume. 3. Elastic rebounding period: It takes place when the injection is stopped. The injected water starts to be squeezed out of the gelatin gel under the compression of the gelatin gel during the elastic relaxation processes until the final penetration depth and width. 4. Final stable period: the penetration depth and width inside the gelatin gel are fixed afterward. Furthermore, the injection tests on the porcine colon show the penetration into submucosal layer is possible under the injection pressure less than 60 bar with the orifice of 300 m and injection time of 0.1 sec. The injection power is 16 W under this condition. However, higher injection power is needed for the punch through injection of porcine colon. The failure stress of the porcine colon is 1.077 0.333 MPa by the deep penetration test.

      • SCIESCOPUSKCI등재

        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.

      • KCI등재

        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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