Alleviative effect of Lactobacillus fermentum on HepG2 liver cells from lipid accumulation in palmitic acid fatty liver induction model via the attenuation on Nrf2

• Main Authors: Hsu, Meng-Wei, 徐孟微
• Other Authors: Wu, Ming-Chang
• Format: Others
• Language: en_US
• Published: 2018
• Online Access: http://ndltd.ncl.edu.tw/handle/xm7m9k

碩士 === 國立屏東科技大學 === 食品科學國際碩士學位學程 === 106 === Non-alcoholic fatty liver disease (NAFLD) is a common liver disease in Taiwan due to changes in diet and lifestyle. There is an increase in disease prevalence and some patients will progress to end-stage liver disease, liver cancer, diabetes population. Moreover, NAFLD is an important risk factor for the development of diabetes. The incidence may be associated with insulin resistance, lipid peroxidation and abnormal cytokines(such as TNF-α) related. Lactic acid bacteria can enhance intestinal barrier function, immune system, hepatoprotection, but mammals’ intestinal lactic acid bacteria could induce intestinal enzyme to produce ROS, through Nrf2 pathway to produce a protective effect. Nrf2 can act for cellular defense function to resist the pressure caused by oxidation and electron affinity and protect cells from cancerous chemical properties. It is the key transcription factor for regulation of foreign bodies and cells against oxidative damage. However, the mechanism of the lactic acid bacteria to improve Nrf2 is whether through the immune system is not clear. In this study, bacteria’s strain of different vegetables and fruits fermentation broths will be carried out to identify lactic acid bacteria. Then, cell experiment will be conducted to observe the mechanism of selected lactic acid bacteria on the regulation of Nrf2 in NAFLD condition. In my results show that I found the two lactic acid bacterials (NO. 2 and 4) are same species, Lactobacillus fermentum, from Chinese stinky tofu sauce　and compare with BCRC10357. The culture supernatant of MRS from the lactic acid bacterials (NO. 2, 4 and BCRC10357) inhibited the oil accumulation in HepG2 cells by palmitic acid-induced fatty liver model (Negative group). Furthermore, the western blotting show that the protein expression of Nrf2 was increased compared with the negative group after treated with the supernatant from the lactic acid bacterials (NO. 2, 4 and BCRC10357). The metabolites from the lactic acid bacterials may be inhibit the fatty liver formation via enhancing the antioxidant activity in HepG2 cells. It is expected that the consumption of fermented vegetable-fruit extract can reduce the prevalence of NAFLD patients.