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    題名: 牛樟芝純化成分抑制幽門螺旋桿菌誘導人類胃上皮細胞的發炎作用;Antrodia camphorata constituents inhibit Helicobacter pylori- induced inflammation in human gastric epithelial cells
    作者: 呂政澤;Chen-Che Lu
    貢獻者: 中國醫藥大學:基礎醫學研究所
    關鍵詞: 幽門螺旋菌;牛樟芝;發炎作用;H. pylori;Antrodia camphorata;inflammation;NF-κB;IL-8
    日期: 2009-07-23
    上傳時間: 2009-08-11 14:35:51 (UTC+8)
    摘要: 幽門螺旋菌 (H. pylori) 是一種微好氧螺旋形狀的革蘭氏陰性菌,會存在於人類的胃以及十二指腸的表皮黏膜上。幽門螺旋菌會引起胃襯的慢性發炎並且與十二指腸、胃潰瘍和以及胃癌的發展有密切關係。幽門螺旋菌對於胃腸道潰瘍的發生有密切相關,一般認為滅除幽門螺旋菌可以使得胃發炎復原,亦可治療潰瘍性疾病。現有多種治療幽門螺旋菌感染的療法,最為普遍使用的是三合一療法,包含了兩種抗生素與一種胃酸分泌抑制劑。然而,在治療幽門螺旋菌感染上,抗生素抗藥性的增加與抗微生物劑的使用有關。因此,根治幽門螺旋菌過程中需要有輔助治療的方法。樟薄孔菌(Antrodia camphorata)是在台灣的一種稀有的藥材,其子果實的名稱是眾所周知的牛樟芝或樟芝。在台灣,牛樟芝對人體的神奇功效,被許多機構廣泛的調查與研究。在本篇論文中,從牛樟芝上分離出13種萃取物。在13種萃取物中,不論是在胃上皮細胞與小鼠巨噬細胞上,AC-3 (15α-Acetyldehydrosulphurenic acid)與AC-10 (Antcin C)對於幽門螺旋菌擁有較高的抑制效果。此外,對於NF-κB以及IL-8的抑制,也顯示出AC萃取物的抗發炎功效。期望此實驗結果可以為治療幽門螺旋菌感染帶來新的方法。

    Helicobacter pylori is a Gram-negative, micro-aerophilic bacterium that inhabits various areas of the stomach and duodenum. It causes a chronic inflammation of the stomach lining and strongly linked to the development of duodenal and gastric ulcers and stomach cancer. It has been well confirmed that infection with H. pylori is an etiological agent of peptic ulcer, and eradication of this organism can not only make the associated gastritis regression but cure these diseases. There are several treatments of H. pylori infection, most common treatment is triple therapy, including two antibiotics and a proton pump inhibitor. However, the increasing of antibiotic resistant rate was associated with the usage of antimicrobial agents in the treatment of H. pylori infection. Thus, the complementary therapeutic methods in eradication of H. pylori were needed. Antrodia camphorata (A. camphorata) is a rare treasure in Taiwan, the fruiting body of A. camphorata is well known by named niu-chang-chih or jang-jy. The miraculous efficacy in human body had been investigated and researched by many organizations in Taiwan. In this study, thirteen compounds were isolated from A. camphorata. Among them, compound 15α-Acetyldehydrosulphurenic acid (number 3) and Antcin C (number 10) had higher inhibition effects on H. pylori-induced inflammatory responses in gastric epithelial cells and mouse macrophage RAW 264.7 cells than other compounds. In addition, these constituents also inhibited the IL-8 protein expression and NF-κB signal activation in H. pylori-infected gastric epithelial cells and it might contribute to the potential role of A. camphorata as an anti-inflammatory action. Results from our study might bring a new method for treating of H. pylori infection.
    顯示於類別:[基礎醫學研究所] 博碩士論文

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