本文系Food Science and Human Wellness原创编译，欢迎分享，转载请授权。
鼠李糖乳杆菌Fmb14可降低尿酸诱导的HepG2细胞死亡率
图1 鼠李糖乳杆菌Fmb14 CFE对高尿酸条件下HepG2细胞凋亡的影响
鼠李糖乳杆菌Fmb14缓解尿酸诱导的HepG2细胞活性氧（ROS）并恢复线粒体膜电位（MMP）
图2 CFE对尿酸诱导的HepG2细胞ROS和MMP凋亡的影响
鼠李糖乳杆菌Fmb14在尿酸诱导的HepG2细胞中降低NLRP3相关通路的基因表达
图3 鼠李糖乳杆菌Fmb144靶生物标志物对UA诱导的焦亡的改善作用
鼠李糖乳杆菌Fmb14可降低嘌呤饮食诱导的高尿酸血症小鼠肝焦亡
图4 鼠李糖Fmb14对嘌呤诱导的高尿酸血症小鼠肝损伤及相关生物标志物mRNA水平的改善作用
鼠李糖乳杆菌Fmb14处理通过抑制NLRP3缓解高尿酸血症小鼠肝脏焦亡
图5 鼠李糖乳杆菌Fmb14可改善高尿酸血症诱导的焦亡
图6 鼠李糖乳杆菌Fmb14可改善线粒体损伤及相关细胞凋亡
Lacticaseibacillus rhamnosus Fmb14 ameliorates hyperuricemia-induced hepatocyte pyroptosis via NLRP3 inflammasome cascade inhibition
Hongyuan Zhaoa, Xiaoyu Chena, Li Zhangb, Fanqiang Menga, Libang Zhoua, Zhaoxin Lua,*, Yingjian Luc,*
a College of Food Science & Technology, Nanjing Agricultural University, Nanjing 210095, China
b Institute of Vegetable, Gansu Academy of Agricultural Sciences, Lanzhou 730070, China
c College of Food Science & Engineering, Nanjing University of Finance and Economics, Nanjing 210023, China
*Corresponding author.
Abstract
Hyperuricemia is a high-risk factor for the development of gout and renal fibrosis, but the adverse effects of hyperuricemia on the liver have been seriously neglected. This research investigated the ameliorating effect of Lacticaseibacillus rhamnosus Fmb14 on hyperuricemia induced liver dysfunction both in vitro and in vivo. Cell free extracts of high dose L. rhamnosus Fmb14 treatment reduced the death rate of HepG2 cell lines from 24.1% to 14.9% by inhibiting NLRP3 recruitment, which was mainly activated by reactive oxygen species release and mitochondrial membrane potential disorder. In purine dietary induced hyperuricemia (PDIH) mice model, liver oedema and pyroptosis were ameliorated after L. rhamnosus Fmb14 administration through downregulating the expression levels of NLRP3, caspase-1 and gasdermin-D from 1.61 to 0.86, 3.15 to 1.01 and 5.63 to 2.02, respectively. L. rhamnosus Fmb14 administration restored mitochondrial inner membrane protein (MPV17) and connexin 43 from 2.83 and 0.73 to 0.80 and 0.98 respectively in PDIH mice, indicating that dysbiosis of mitochondrial membrane potential was restored in liver. Intriguingly, PDIH pyroptosis stimulates the process of apoptosis, which leads to severe leakage of hepatocytes, and both of pyroptosis and apoptosis were decreased after L. rhamnosus Fmb14 treatment. Therefore, L. rhamnosus Fmb14 is a promising biological resource to maintain homeostasis of the liver in hyperuricemia and the prevention of subsequent complications.
ZHAO H Y, CHEN X Y, ZHANG L, et al. Lacticaseibacillus rhamnosus Fmb14 ameliorates hyperuricemia-induced hepatocyte pyroptosis via NLRP3 inflammasome cascade inhibition[J]. Food Science and Human Wellness, 2024, 13(4): 2174-2186. DOI:10.26599/FSHW.2022.9250181.
或点击下方阅读原文查看文章
长按二维码关注我们！
