文章题目：《Spermidine Ameliorates Nonalcoholic Steatohepatitis through Thyroid Hormone-Responsive Protein Signaling and the Gut Microbiota-Mediated Metabolism of Bile Acids》

发布期刊：Journal of Agricultural and Food Chemistry

作者：Yinhua Ni, Yating Hu, Xiaoyi Lou, Nianke Rong, Fang Liu, Congrong Yang, Aqian Zheng, Song Yang,Jianfeng Bao,* and Zhengwei Fu*

作者单位：浙江工业大学生物技术与生物工程学院

DOI https://doi.org/10.1021/acs.jafc.2c02729

引用试剂：HepG2 cells 、HAKATA胎牛血清

影响因子：5.279

论文简述

Spermidine, a natural polyamine and physiological autophagy inducer, is involved in various physiological processes.

However, the impact and mechanism of spermidine on nonalcoholic steatohepatitis (NASH) remains unclarifified. We found thatdaily spermidine intake was signifificantly lower in volunteers with liver dysfunction than the healthy controls, and the serum and fecalspermidine levels were negatively correlated with the NASH phenotypes. Spermidine supplementation signifificantly attenuatedhepatic lipid accumulation, insulin resistance, hepatic inflflammation, and fifibrosis in NASH mice induced by a western diet. Theameliorating effffect of spermidine on lipid accumulation might be partly regulated by thyroid hormone-responsive protein (THRSP)signaling and autophagy. Moreover, spermidine altered the profifile of hepatic bile acids (BAs) and microbial composition andfunction. Furthermore, spermidine reversed the progression of hepatic steatosis, inflflammation, and fifibrosis in mice with preexistingNASH. Therefore, spermidine ameliorates NASH partly through the THRSP signaling and the gut microbiota-mediated metabolismof BAs, suggesting that spermidine might be a viable therapy for NASH.

使用产品

在该研究过程中，科研团队研究人员使用了HAKATA的产品：HepG2 人肝癌细胞（货号: H019）/HAKATA胎牛血清（货号: HN-FBS-500）。

能够为该研究提供助力，EBET易博生物/HAKATA深感荣幸。

产品信息

产品货号：HN-FBS-500

产品规格：500ml

产品介绍：该款胎牛血清是一款最具有性价比血清产品，采用3次0.1μm 的过滤方法及40余种质量控制检测，通过本公司肿瘤细胞库中600多种细胞株验证，细胞增殖速度快，状态良好，可放心使用。

质量标准：

1、内毒素含量低，三次纳米级过滤

2、严格控制批次差异

3、来源可靠、可溯源

4、每个批次均提供检验检疫报告

5、适合各种常规细胞培养

6、干冰运输，建议存储温度为-10℃至-20℃

文章题目：《The Neuroprotective Effect of GM-1 Ganglioseside on the Amyloid-Beta-Induced Oxidative Stress in PC-12 Cells Mediated by Nrf-2/ARE Signaling Pathway》

发布期刊：Neurochemical Research

作者：Xiaonan Wang1 · Bei Li1 · Xiaohong Yu1 · Ye Zhou1 · Yue Gao1

论文简述

Alzheimer’s disease (AD) is characterized by the accumulation of amyloid-β (Aβ) plaques, tau tangles, neuroinfammation,oxidative stress, and progressive memory defcits. Aβ deposition could exacerbate oxidative damage and cellular apoptosis.GM-1 ganglioseside (GM-1) has previously been reported to exhibit neuroprotective efects in rodents and patients with AD.However, the substantial impacts and mechanism of GM-1 on Aβ-induced oxidative stress remain elusive. The present studyused PC-12 pheochromocytoma cells treated with Aβ25–35 peptide to construct the AD model in vitro. Aβ25–35 administration alone inhibited cell viability and facilitated cell apoptosis in the range doses of 10 μM to 30 μM. At the same time,GM-1 supplementation promoted cell proliferation and rescued cell apoptosis in a dose-dependent fashion ranging from 5to 30 μM. In parallel, GM-1 treatment alleviated Aβ-induced oxidative stress by increasing the level of antioxidant enzymesand decreasing the content of malondialdehyde (MDA). The nuclear factor-E2-related factor 2 (Nrf2) is a crucial mediatorof antioxidant response. We reported herein that GM-1 could activate Nrf-2 in the PC-12 cells co-treated with Aβ25–35, following with the activated expression of antioxidant response elements (ARE)-mediated antioxidant and detoxifying genes.Consistently, knock-down of Nrf-2 via siRNA abolished the benefcial decrease of Aβ-induced oxidative stress by GM-1treatment, indicating that GM-1-improved oxidative stress was regulated by the Nrf-2 signaling pathway. Collectively, GM-1could alleviate Aβ25–35-induced oxidative damage mediated through the Nrf-2/ARE signaling pathway, which might be apotential agent for AD treatment.

使用产品

在该研究过程中，科研团队研究人员使用了HAKATA的产品：PC-12 大鼠肾上腺嗜铬细胞瘤细胞

能够为该研究提供助力，EBET易博生物/HAKATA深感荣幸。