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안구적출에 따른 위둔덕의 Calbindin D-28k과 c-fos의 변화에 관한 연구
김명,김기훈,김주영,하현철,안명수,김장민,조향훈,정명섭,장인엽 朝鮮大學校 附設 醫學硏究所 2005 The Medical Journal of Chosun University Vol.30 No.2
Changes of Calbindin D-28k- and c-fos-immunoreactivities in the superior collicuclus after Eye Enucleation. Objective and methods: Calcium-binding proteins (CBPs) play an important role in the protection, differentiation and reorganization of the central nervous system. The effects of neonatal retinal deafferentation on a CBPs, calbindin D-28k were examined immunohistochemically in the superficial layer of the rat superior colliculus. Also early gene familly c-fos was examined to evaluate the neuronal characteristics in the superior colliculus after monocular enucleation. Results: On the experimental side of superior colliculus, the number of calbindin D-28k-immunoreactive (IR) cells was reduced (77.4% compared to control), but not fibers. Appearance of c-fos-like immunoreactivity was represented much more in the ipsilateral superior colliculus than contralateral side within 24h after eye enucleation. Conclusion: These results suggest that the changes of retinotectal projection may alter the expressional pattern of calbindin D-28k and c-fos expression.
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.