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研究生:璩敬賢
研究生(外文):Ching-Hsien Chu
論文名稱:靈芝萃取物對於乙醯胺酚引發ICR小鼠肝損傷之保護效果
論文名稱(外文):The protective effect of Ganoderma lucidum extract on acetaminophen-induced liver damage in ICR mice
指導教授:李旭生李旭生引用關係
指導教授(外文):Shiuh-Sheng Lee
學位類別:碩士
校院名稱:國立陽明大學
系所名稱:生物化學研究所
學門:生命科學學門
學類:生物化學學類
論文種類:學術論文
論文出版年:2004
畢業學年度:92
語文別:中文
論文頁數:86
中文關鍵詞:靈芝乙醯胺酚保肝
外文關鍵詞:ganoderma lucidumacetaminophenhepatoprotective
相關次數:
  • 被引用被引用:1
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摘要
  藥用真菌- 靈芝 (Ganoderma lucidum) 是已經被廣泛用來治療許多不同疾病的傳統中藥材,其中包括治療肝疾病。乙醯胺酚 (acetaminophen) 則是被廣泛使用的退燒及止痛藥物之一,但是過量服用後會造成人及實驗動物的肝臟損傷。雖然乙醯胺酚的肝毒性已經被廣泛地研究了許多年,但是確切的毒性機制則尚未被了解。本研究主要的實驗目標為: 了解氧化壓力是否牽涉在乙醯胺酚所引起的肝毒性中,以及靈芝萃取物 (GLP) 對於乙醯胺酚在ICR小鼠所引發的肝損傷,是否具有保護效果。我們也分別比較了靈芝萃取物中酒精可溶 (AS) 及不可溶 (AI) 兩部分的保肝效果,以釐清靈芝萃取物中可能的活性成分。實驗結果顯示餵食靈芝萃取物可以顯著降低乙醯胺酚中毒小鼠血中天門冬胺酸轉胺基酶 (AST) 的活性及肝組織壞死的情形。雖然靈芝萃取物中酒精可溶及不可溶兩部分皆可顯著降低乙醯胺酚中毒小鼠肝組織壞死的情形,但對於血中的轉胺基酶活性則沒有影響。餵食乙醯胺酚小鼠肝臟中的麩胱胺酸 (glutathione) 濃度比正常控制組 (NC) 有顯著增加,但是在GLPヽAI及AS組之間則沒有顯著差異。抗氧化酵素活性分析的結果顯示,negative組及GLP組小鼠肝臟中的麩胱胺酸過氧化物酶 (glutathione peroxidase) 活性皆比normal control (NC) 組小鼠顯著為低。餵食乙醯胺酚小鼠肝臟中銅鋅超氧化物歧化酶 (Cu, Zn-SOD) 及過氧化氫酶 (catalase) 的活性皆有顯著上升,但在其他的實驗組中則沒有顯著差異。肝臟中的thiobarbituric acid reactive substances (TBARS) 在實驗組中也是沒有顯著差異。在細胞研究中,以methylthiazoletetrazolium (MTT) 測定細胞的存活率。靈芝萃取物處理過的Huh7肝癌細胞株,隨著靈芝萃取物劑量上升而細胞存活率有下降的趨勢。但是在乙醯胺酚處理Huh7及HepG2肝癌細胞株之前,預先處理靈芝萃取物24小時,可以使細胞的存活率有顯著的上升。此外,以流式細胞儀測定自由基生成。結果顯示各實驗組之間 reactive oxygen species (ROS) 產生量並無顯著差異。這結果顯示氧化壓力與乙醯胺酚引發肝損傷之間並不相關。本研究顯示靈芝萃取物在活體及離體實驗中,對乙醯胺酚所引發的肝細胞損傷都具有保護效果。我們也以二維電泳搭配質譜儀分析的方法,針對小鼠肝臟檢體作蛋白質體的分析,並且以西方墨漬法來確認結果。結果顯示靈芝萃取物餵食後的小鼠,血漿中高密度脂蛋白的主要脂蛋白元apoAI表現量有顯著上升。這暗示著靈芝萃取物可能也會對於動脈粥狀硬化的預防具有正面的效用。
Abstract
  Ganoderma lucidum, a medical fungi, has been widely used as a traditional Chinese medicine to treat several different diseases including hepatopathy. Acetaminophen (APAP) is one of the most commonly used antipyretic and analgesic, but APAP overdose can cause liver damage in human and experimental animals. Although APAP hepatotoxicity has been studied widely for many years, the precise mechanism by which acetaminophen causes cell death remains unknown. The objectives of this study were to investigate whether oxidative stress play a role in APAP-induced liver damage, and whether Ganoderma lucidum extract (GLP) can protect APAP-induced liver damage in ICR mice. We also compared the hepatoprotective effects of the alcohol-soluble (AS) and alcohol-insoluble (AI) fractions of GLP, respectively. The result showed that GLP treatment significantly reduced plasma aspartate aminotransferase (AST) activity and hepatic necrosis in APAP-intoxicated mice. Although both AS and AI treatment significantly reduced hepatic necrosis, there was no influence on activities of plasma transaminase in APAP-intoxicated mice. Hepatic concentration of glutathione was induced in mice treated with APAP compared with the normal control group, but no difference in glutathione level was found among GLP, AI, and AS groups. From the analysis of antioxidant enzyme activities, levels of glutathione peroxidase activity were decreased in negative control and GLP-treated mice as compared to the result of normal control group. Activities of hepatic cuprozinc-superoxide dismutase (Cu, Zn-SOD) and catalase were induced in mice under APAP administration, but no difference was found among other experimental groups. Levels of hepatic thiobarbituric acid reactive substances (TBARS) were also not different among experimental groups. In cellular study, cell viability was determined by methylthiazoletetrazolium (MTT) assay. Cell viability was decreased in Huh7 cells treated with GLP in a dose-dependent manner, but a significant increase in cell viability was observed in Huh7 and HepG2 cells pretreated with 5mg/ml and 20 mg /ml GLP, respectively, for 24 hours prior to APAP exposure. Moreover, free radical generation was determined by flow cytometry. It seems that production of reactive oxygen species (ROS) was not different among experimental groups. The results indicate that oxidative stress was not associated with APAP-induced liver damage. In this study, GLP was found to protect APAP-induced liver cell damage both in vivo and in vitro system. We also conducted a proteomic study by 2D-gel electrophoresis followed by matrix assisted laser desorption /ionization-mass spectrometry on the mouse liver samples. Western blot analysis also confirmed the result of proteomics study. The result showed that plasma apoAI, a major apolipoprotein of high-density lipoprotein (HDL), was induced in mice treated with GLP. This suggests that GLP may also be beneficial for the prevention of atherosclerosis.
參考文獻
1. Alexopoulos, C.J., Mims, C.W., and Blackwell, M. (1996) Introductory mycology. 4th ed. New York: John Wiley & Sons, Inc. pp: 563-597.
2. Iwatsuki, K., Akihisa, T., Tokuda, H., Ukiya, M., Oshikubo, M., Kimura, Y., Asano, T., Nomura, A., and Nishino, H. (2003) Lucidenic acids P and Q, methyl lucidenate P, and other triterpenoids from the fungus Ganoderma lucidum and their inhibitory effects on Epstein-Barr Virus Activation. J Nat Prod. 66: 1582-1585.
3. Zhang, H.N., Hea, J.H., Yuan, L., Lin, Z.B. (2003) In vitro and in vivo protective effect of Ganoderma lucidum polysaccharides on alloxan-induced pancreatic islets damage. Life Sci. 73: 2307-2319.
4. Cao, L.Z.,and Lin, Z.B. (2003) Regulatory effect of Ganoderma lucidum polysaccharides on cytotoxic T-lymphocytes induced by dendritic cells in vitro. Acta Pharmacol Sin. 24: 321-326.
5. Hikino, H., Kinno, C., Mirin, Y., Hayashi, T. (1985) Isolation and hypoglycemic activity of Ganoderans A and B, glycans of Ganoderma lucidum fruit bodies. Planta Med. 4: 339-340.
6. Hikino, H., Ishiyama, M., Suzuki, Y., and Konno, C. (1989) Mechanisms of hypoglycemic activity of ganoderan B: a glycan of Ganoderma lucidum fruit bodies. Planta Med. 55: 423-428.
7. Zhang, H.N., and Lin, Z.B. (2004) Hypoglycemic effect of Ganoderma lucidum polysaccharides. Acta Pharmacol Sin. 25: 191-195.
8. Gao, Y., Zhou, S., Wen, J., Huang, M., Xu, A. (2002) Mechanism of the antiulcerogenic effect of Ganoderma lucidum polysaccharides on indomethacin-induced lesions in the rat. Life Sci. 72: 731-745.
9. You, Y.H.,and LIN, Z.B. (2002) Protective effects of Ganoderma lucidum polysaccharides peptide on injury of macrophages induced by reactive oxygen species. Acta Pharmacol Sin. 23: 787-791.
10. Zhang, J., Tang, Q., Zimmerman-Kordmann, M., Reutter, W., and Fan, H. (2002) Activation of B lymphocytes by GLIS, a bioactive proteoglycan from Ganoderma lucidum. Life Sci. 71: 623-638.
11. Eo, S.K., Kim, Y.S., Lee, C.K., Han, S.S. (2000) Possible mode of antiviral activity of acidic protein bound polysaccharide isolated from Ganoderma lucidum on herpes simplex viruses. J Ethnopharmacol. 72: 475-481.
12. Park, E.J., Ko, G., Kim, J., and Sohn, D.H. (1997) Antifibrotic effects of a polysaccharide extracted from Ganoderma lucidum, Glycyrrhizin, and Pentoxifylline in rats with cirrhosis induced by biliary obstruction. Biol Pharm Bull. 20: 417-420.
13. Zhang, G.L., Wang, Y.H., Ni, W., Teng, H.L.,and Lin, Z.B. (2002) Hepatoprotective role of Ganoderma lucidum polysaccharide against BCG-induced immune liver injury in mice. World J Gastroenterol. 8: 728-733.
14. Liu, F., Ooi,V.E., and Chang, S.T. (1997) Free radical scavenging activities of mush room polysaccharide extracts. Life Sci. 60: 763-771.
15. Kim, H.W., Shim, M.J., and Kim, B.K. (2001) Biologically active lanostane-type triterpenoids of Ganoderrna lucidiurn. Proc Int Symposium Ganoderrna Sci Auckland: 21-30.
16. Lin, S.B., Li, C.H., Lee, S.S., and Kan, L.S. (2003) Triterpene-enriched extracts from Ganoderma lucidum inhibit growth of hepatoma cells via suppressing protein kinase C, activating mitogen-activated protein kinases and G2-phase cell cycle arrest. Life Sci 72: 2381-2390.
17. Min, B.S., Nakamura, N., Miyashiro, H., Bae, K.W., and Hattori, M. (1998) Triterpenes from the Ganoderma lucidum and their inhibitory activity against HIV-1 protease. Chem Pharm Bull. 46: 1607-1612.
18. Koyama, K., Imaizumi, T., Akiba, M., Kinoshita, K., Takahashi, K., Suzuki, A., Yano, S., Horie, S., Watanabe, K., and Naoi, Y. (1997) Antinociceptive components of Ganoderma lucidum. Planta Med. 63: 224-227.
19. Kohda, H., Tokumoto, W., Sakamoto, K., Fujii, M., Hirai, Y., Yamasaki, K., Komoda, Y., Nakamura, H., Ishihara, S., and Uchida, M. (1985) The biologically active constituents of Ganoderma lucidum (Fr.) Karst. Histamine release-inhibitory triterpenes. Chem Pharm Bull. 85: 1367-1374.
20. Wu, T.S., Shi, L.S., and Kuo, S.C. (2001) Cytotoxicity of Ganoderma lucidum Triterpenes. J Nat Prod. 64: 1121-1122.
21. Gao, J.J., Min, B.S., Ahn, E.M. Nakamura, N., Lee, H.K., and Hattori, M. (2002) New triterpene aldehydes, Lucialdehydes A-C, from Ganoderma lucidum and their cytotoxicity against murine and human tumor cells. Chem Pharm Bull. 50: 837-840.
22. Su, C.Y., Shiao, M.S., and Wang, C.T. (1999) Predominant inhibition of ganodermic acid S on the thromboxane A2 dependent pathway in human platelets response to collagen. Biochim Biophys Acta. 1437: 223-234.
23. Kim, D.H., Shim, S.B., Kim, N.J., and Jang, I.S. (1999) β-Glucuronidase-inhibitory activity and hepatoprotective effect of Ganoderma lucidum. Biol Pharm Bull. 22: 162-164.
24. Hirotani, M., and Furuya, T. (1986) Studies on the metabolites of higher fungi. Part5. Ganoderic acid derivatives, highly oxygenated lanostane-type triterpenids, from Ganoderma lucidum. Phytochemistry 25: 1189-1193.
25. Kino, K., Yamashita, A., Yamaoka, K., Watanabe, J., Tanaka, S., KO, K., Shimizu, K., and Tsunoo, H. (1989) Isolation and Characterization of a New Immunomodulatory Protein, Ling Zhi-8 (LZ-8), from Ganoderrna lucidurn. J Biol Chem. 264: 472-478.
26. Haak-Frendscho, M., Kino, K., Sone, T., and Jardieu, P. (1993) Ling Zhi 8: A novel T cell mitogen induces cytokine production and up regulation of ICAM-1 expression. Cell Immunol. 150: 101-113.
27. Thomas, S. (1993) Paracetamol (acetaminophen) poisoning. Pharmacol Ther. 60: 91-120.
28. Dahlin, D.C., Miwa, G.T., Lu, A.Y., and Nelson, S.D. (1984) N-acetyl-p-benzoquinone imine: A cytochrome P-450-mediated oxidation product of acetaminophen. Proc Natl Acad Sci U S A. 81: 1327-1331.
29. Nelson, S.D. (1990) Molecular mechanisms of the hepatotoxicity caused by acetaminophen. Semin Liver Dis. 10: 267-278.
30. Jollow, D.J., Mitchell, J.R., Potter, W.Z., Davis, D.C., Gillette, J.R., and Brodie, B.B. (1973) Acetaminophen-induced hepatic necrosis. II. Role of covalent binding in vivo. J Pharmacol Exp Ther. 187: 195-202.
31. Reitman, S., and Frankel, S. (1957) A colorimetric method for the determination of serum glutamic oxalacetic and glutamic pyruvic transaminases. Am J Clin Pathol. 28: 56-63.
32. Sedlak, J., and Lindsay, R.H. (1968) Estimation of total, protein-bound, and nonprotein sulfhydryl groups in tissue with Ellman’s reagent. Anal Biochem. 25: 192-205.
33. Ohkawa, H., Ohishi, N., and Yagi, K. (1979) Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Anal Biochem. 95: 351-358.
34. Aebi, H. (1984) Catalase in vitro. Methods Enzymol. 105: 121-126.
35. Ōyanagui, Y. (1984) Reevaluation of assay methods and establishment of kit for superoxide dismutase activity. Anal. Biochem. 142: 290-296.
36. Günzler, W.A., and Flohé, L. (1984) Assays of glutathione peroxidase. Methods Enzymol. 105: 114-120.
37. Sambrook, J., Fritsch, E.F. and Maniatis, T. (1989) Detection and analysis of proteins expressed from cloned gene. In Molecular Cloning, J. Sambrook, E.F. Fritsch and T. Maniatis, eds. (Cold Spring Harbor, New York: Cold Spring Harbor Laboratory Press): pp. 18.1-18.88.
38. Bradford, M.M. (1976) A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal Biochem. 72: 248-254.
39. Fossati, P., and Prencipe, L. (1982) Serum triglycerides determined colorimetrically with an enzyme that produces hydrogen peroxide. Clin Chem. 28: 2077-2080.
40. Richmond, W. (1973) Preparation and properties of a cholesterol oxidase from Nocardia sp. And its application to the enzymatic assay of total cholesterol in serum. Clin Chem. 19: 1350-1356.
41. Cole, S.P. (1986) Rapid chemosensitivity testing of human lung tumor cells using the MTT assays. Cancer Chemother Pharmacol. 17: 259-263.
42. Lebel, C.P., Ischiropoulos, H., and Bondy, S.C. (1992) Evaluation of the probe 2',7'-dichlorofluorescin as an indicator of reactive oxygen species formation and oxidative stress. Chem Res Toxicol. 5: 227-231.
43. Kobzik, L., Godleski, J.J., and Brain, J.D. (1990) Oxidative metabolism in the alveolar macrophage: analysis by flow cytometry. J Leukoc Biol. 47: 295-303.
44. McManus D.C., Scott B.R., Franklin V., Sparks D.L., and Marcel Y.L. (2001) Proteolytic degradation and impaired secretion of an apolipoprotein A-I mutant associated with dominantly inherited hypoalphalipoproteinemia. J Biol Chem. 276: 21292-21302.
45. Lee, K.J., You, H.J., Park, S.J., Kim, Y.S., Chung, Y.C., Jeong, T.C., and Jeong, H.G. (2001) Hepatoprotective effects of Platycodon grandiflorum on acetaminophen-induced liver damage in mice. Cancer lett. 174: 73-81.
46. Zhang, J., Huang, W., Chua, S.S., Wei, P., and Moore, D.D. (2002) Modulation of acetaminophen-induced hepatotoxicity by the xenobiotic receptor CAR. Science 298: 422-424.
47. Knight, T.R., Ho, Y.S., Farhood, A., and Jaeschke, H. (2002) Peroxynitrite Is a Critical Mediator of Acetaminophen Hepatotoxicity in Murine Livers: Protection by Glutathione. J Pharmacol Exp Ther. 303: 468-475.
48. Shirota, F.N., DeMaster, E.G., Shoeman , D.W., and Nagasawa, H.T. (2002) Acetaminophen-induced suppression of hepatic AdoMet synthetase activity is attenuated by prodrugs of L-cysteine. Toxicol Lett. 132: 1-8.
49. Hattori, A., Yamada, N., Nishikawa, T., Fukuda, H., and Fujino, T. (2001) Protective effect of ajoene on acetaminophen-induced hepatic injury in mice. Biosci Biotechnol Biochem. 65: 2555-2557.
50. Chiu, H., Gardner, C.R., Dambach, D.M., Brittingham, J.A., Durham, S.K., Laskin, J.D., and Laskin, D.L. (2003) Role of p55 tumor necrosis factor receptor 1 in acetaminophen-induced antioxidant defense. Am J Physiol Gastrointest Liver Physiol 285: 959-966.
51. Wu, G., Fang, Y.Z., Yang, S., Lupton, J.R., and Turner, N.D. (2004) Glutathione metabolism and its implications for health. J Nutr. 134: 489-492.
52. Pompella, A., Visvikis, A., Paolicchi, A., Tata, V., and Casini, A.F. (2003) The changing faces of glutathione, a cellular protagonist. Biochem Pharmacol. 66: 1499-1503.
53. Wendel, A., Feuerstein, S., and Konz, K. (1979) Acute paracetamol intoxication of starved mice leads to lipid peroxidation in vivo. Biochem Pharmacol. 28: 2051-2055.
54. Albano, E., Poli, G., Chiarpotto, E., Biasi, F., and Dianzani, M.U. (1983) Paracetamol-stimulated lipid peroxidation in isolated rat and mouse hepatocytes. Chem Biol Interact. 47: 249-263.
55. Toussaint, O., Houbion, A., and Remacle, J. (1993) Relationship between the critical level of oxidative stresses and the glutathione peroxidase activity. Toxicology 81: 89-101.
56. Vermeulen, N.P., Bessems, J.G., and Van de Straat, R. (1992) Molecular aspects of paracetamol-induced hepatotoxicity and its mechanism-based prevention. Drug Metab Rev. 24: 367-407.
57. Lores Arnaiz, S., Llesuy, S., Cutrin, J.C., and Boveris, A. (1995) Oxidative stress by acute acetaminophen administration in. mouse liver. Free Radic Biol Med. 19: 303-310.
58. Rosen, G.M., Singletary, W.V., Rauckman, E.J., and Killenberg, P.G. (1983) Acetaminophen hepatotoxicity. An alternative mechanism. Biochem Pharmacol. 32: 2053-2059.
59. van de Straat, R., de Vries, J., and Vermeulen, N.P. (1987) Role of hepatic microsomal and purified cytochrome P-450 in one-electron reduction of two quinone imines and concomitant reduction of molecular oxygen. Biochem Pharmacol. 36: 613-619.
60. Laskin, D.L., and Pilaro, A.M. (1986) Potential role of activated macrophages in acetaminophen hepatotoxicity. I. Isolation and characterization of activated macrophages from rat liver. Toxicol Appl Pharmacol. 86: 204-215.
61. Laskin, D.L., Gardner, C.R., Price, V.F., and Jollow, D.J. (1995) Modulation of macrophage functioning abrogates the acute hepatotoxicity of acetaminophen. Hepatology. 21: 1045-1050.
62. Michael, S.L., Pumford, N.R., Mayeux, P.R., Niesman, M.R., and Hinson, J.A. (1999) Pretreatment of mice with macrophage inactivatiors decreases acetaminophen hepatotoxicity and formation of reactive oxygen and nitrogen species. Hepatology. 30: 186-195.
63. Kyle, M.E., Miccadei, S., Nakae, D., and Farber, J.L. (1987) Superoxide dismutase and catalase protect cultured hepatocytes from the cytotoxicity of acetaminophen. Biochem Biophys Res Commun. 149: 889-96.
64. Mirochnitchenko, O., Weisbrot-Lefkowitz, M., Reuhl, K., Chen, L., Yang, C., and Inouye, M. (1999) Acetaminophen toxicity. Opposite effects of two forms of glutathione peroxidase. J Biol Chem. 274: 10349-10355.
65. Michiels, C., Raes, M., Toussaint, O., and Remacle, J. (1994) Importance of Se-glutathione peroxidase, catalase, and Cu/Zn-SOD for cell survival against oxidative stress. Free Radic Biol Med. 17: 235-248.
66. Manautou, J.E., Tveit, A., Hoivik, D.J., Khairallah, E.A., and Cohen, S.D. (1996) Protection by clofibrate against acetaminophen hepatotoxicity in male CD-1 mice is associated with an early increase in biliary concentration of acetaminophen–glutathione adducts. Toxicol Appl Pharmacol. 140: 30-38.
67. Lake, B.G., Gray, T.J., Korosi, S.A., and Walters, D.G. (1989). Nafenopin, a peroxisome proliferator, depletes hepatic vitamin E content and elevates plasma oxidise glutathione levels in rats. Toxicol Lett. 45: 221-229.
68. Makowska, J.M., Anders, C., Goldfarb, P.S., Bonner, F., and Gibson, G.G. (1990). Characterization of the hepatic responses to short-term administration of ciprofibrate in several rat strains. Co-induction of microsomal cytochrome P-450 IVA1 and peroxisome proliferation. Biochem Pharmacol. 40, 1083-1093.
69. Chen, C., Hennig, G.E., Whiteley, H.E., and Manautou, J.E. (2002) Protection against acetaminophen hepatotoxicity by clofibrate pretreatment: role of catalase induction. J Biochem Mol Toxicol. 16: 227-234.
70. Nicholls-Grzemski, F.A., Calder, I.C., Priestly, B.G., and Burcham, P.C. (2000) Clofibrate-induced in vitro hepatoprotection against acetaminophen is not due to altered glutathione homeostasis. Toxicol Sci. 56: 220-228.
71. Chen, C., Hennig, G.H., Whiteley, H.E., Corton, J.C., and Manautou, J.E. (2000) Peroxisome-proliferator activated receptor α-null mice lack resistance to acetaminophen hepatotoxicity following clofibrate exposure. Toxicol Sci. 57: 338-344.
72. Reichl, D., and Miller, N.E. (1989) Pathophysiology of reverse cholesterol transport: insights from inherited disorders of lipoprotein metabolism. Arteriosclerosis. 9: 785-797.
73. Barter, P.J., and Rye, K.A. (1996) Molecular mechanisms of reverse cholesterol transport. Curr Opin Lipidol. 7: 82-87.
74. Miyazaki, A., Sakuma, S., Morikawa, W., Takiue, T., Miake, F., Terano, T., Sakai, M., Hakamata, H., Sakamoto, Y., and Natio, M. (1995) Intravenous injection of rabbit apolipoprotein A-I inhibits the progression of atherosclerosis in cholesterol-fed rabbits. Arterioscler Thromb Vasc Biol. 15: 1882-1888.
75. Rubin, E.M., Krauss, R.M., Spangler, E.A., Verstuyft, J.G., and Clift, S.M. (1991) Inhibition of early atherogenesis in transgenic mice by human apolipoprotein A-I. Nature. 353: 265-267.
76. Benoit, P., Emmanuel, F., Caillaud, J.M., Bassinet, L., Castro, G., Gallix, P., Fruchart, J.C., Branellec, D., Denefle, P., and Duverger, N. (1999) Somatic gene transfer of human apoAI inhibits atherosclerosis progression in mouse models. Circulation. 99: 105- 110.
77. Young, C.E., Karas, R.H., and Kuvin, J.T. (2004) High-density lipoprotein cholesterol and coronary heart disease. Cardiol Rev. 12: 107-119.
78. Xydakis, A.M., and Ballantyne, C.M. (2002) Combination therapy for combined dyslipidemia. Am J Cardiol. 90: 21-29.
79. Hu, H., Ahn, N.S., Yang, X., Lee, Y.S., and Kang, K.S. (2002) Ganoderma lucidum extract induces cell cucle arrest and apoptosis in MCF-7 human breast cancer cell. Int J Cancer. 102: 250-253.
80. Minamide, Y., Horie, T., Tomaru, A., and Awazu, S. (1998) Spontaneous chemiluminescence production, lipid peroxidation, and covalent binding in rat hepatocytes exposed to acetaminophen. J Pharm Sci. 87: 640-646.
81. DuBois, R.N., Hill, K.E., and Burk, R.F. (1983) Antioxidant effect of acetaminophen in rat liver. Biochem Pharmacol. 32: 2621-2622.
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