乳酸菌減弱 tert-butyl hydroperoxide 誘導氧化傷害之護肝作用   全文下載

Hepatoprotective Effect of Lactic Acid Bacteria in the Attenuation of Oxidative Stress from tert-Butyl Hydroperoxide

肝病的發病機制與病程發展是和自由基損傷及氧化壓力有關，而抗氧化劑與自由基清除劑可減弱這種傷害。由於乳酸菌是腸道重要的微生物和天然抗氧化劑，傳統應用在醱酵食品的製造。因此本研究假設乳酸菌可以預防或減少因tert-butyl hydroperoxide（t-BHP）所引起肝細胞的氧化傷害。本研究採用試驗的乳酸菌包括Lactobacillus acidophilus La12, Lactobacillus delbrueckii ssp. bulgaricus Lb23, Bifidobacterium longum Bl36, and Streptococcus salivarius ssp. thermophilus St28的胞內物及其熱致死菌，並分析乳酸脫氫?（Lactate dehydrogenase ; LDH）、丙氨酸轉氨?（alanine aminotransferase ; ALT）、活性氧分子（reactive oxygen species ; ROS）、脂質過氧化物（thiobarbituric acid reactive substances ; TBARS）、榖胱甘?（glutathione ; GSH) 、超氧歧化?（superoxide dismutase ; SOD）、過氧化氫?（catalase ; CAT) 、麩胱甘?還原?（Glutathione reductase ; GR）、穀胱甘?過氧化?（Glutathione peroxidase ; GPx），和穀胱甘?硫基轉移?（Glutathione-S-transferases; GSH-ST）等氧化/抗氧化指標，藉以瞭解乳酸菌對損傷的肝細胞及抗氧化狀態的影響。實驗結果顯示，肝細胞預處理乳酸菌可以減弱t-BHP對肝細胞引起的毒性傷害，乳酸菌是藉由降低活性氧分子的累積與活化抗氧化酵素活性來展現其保護作用，本研究提供一種新的可能機制就是具有抗氧化特性的乳酸菌有助於保護肝臟。"

The pathogenesis and progression of liver disease are associated with free radical injury and oxidative stress, which can be partially attenuated by antioxidants and free radical scavengers. Lactic acid bacteria, which have been traditionally used in the production of various fermented foods, are important intestinal microflora and natural antioxidants. The hypothesis that lactic acid bacteria can prevent or decrease tert-butyl hydroperoxide (t-BHP)-induced oxidative damage in HepG2 cells was investigated. Intracellular extracts and heat-killed cells of Lactobacillus acidophilus La12, Lactobacillus delbrueckii ssp. bulgaricus Lb23, Bifidobacterium longum Bl36 and Streptococcus salivarius ssp. thermophilus St28 were used in this study. Lactate dehydrogenase (LDH), alanine aminotransferase (ALT), reactive oxygen species (ROS), thiobarbituric acid reactive substances (TBARS), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GRd), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) were deter-mined to explore the influence of lactic acid bacteria intervention on cell damage and antioxidative status. Toxic damage to hepatocytes by t-BHP was attenuated by lactic acid bacteria (which exerted protective effects by decreasing the risk of accumulated ROS and by reactivating antioxidant enzymes) in HepG2 cells treated with lactic acid bacteria before t-BHP exposure. The results of this study provide new insights into the mechanisms by which lactic acid bacteria with antioxidative properties can help to protect the liver.