文章題目 :《Spermidine Ameliorates Nonalcoholic Steatohepatitis through Thyroid Hormone-Responsive Protein Signaling and the Gut Microbiota-Mediated Metabolism of Bile Acids》
發布期刊 :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*
作者單位 :浙江工業大學生物技術與生物工程學院
DOI https://doi.org/10.1021/acs.jafc.2c02729
引用試劑 :HepG2 cells 、HAKATA胎牛血清
影響因子 :5.279
論文簡述
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.
使用產品
在該研究過程中 ,科研團隊研究人員使用了HAKATA的產品:HepG2 人肝癌細胞(貨號: H019)/HAKATA胎牛血清(貨號: HN-FBS-500) 。
能夠為該研究提供助力 ,尊龍凱時生物/HAKATA深感榮幸 。
產品信息
產品貨號 :HN-FBS-500
產品規格 :500ml
產品介紹 :該款胎牛血清是一款最具有性價比血清產品 ,采用3次0.1μm 的過濾方法及40餘種質量控製檢測 ,通過本公司腫瘤細胞庫中600多種細胞株驗證 ,細胞增殖速度快 ,狀態良好 ,可放心使用 。
質量標準 :
1 、內毒素含量低 ,三次納米級過濾
2 、嚴格控製批次差異
3 、來源可靠 、可溯源
4 、每個批次均提供檢驗檢疫報告
5 、適合各種常規細胞培養
6 、幹冰運輸 ,建議存儲溫度為-10℃至-20℃
文章題目 :《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》
發布期刊 :Neurochemical Research
作者 :Xiaonan Wang1 · Bei Li1 · Xiaohong Yu1 · Ye Zhou1 · Yue Gao1
論文簡述
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.
使用產品
在該研究過程中 ,科研團隊研究人員使用了HAKATA的產品 :PC-12 大鼠腎上腺嗜鉻細胞瘤細胞
能夠為該研究提供助力 ,尊龍凱時生物/HAKATA深感榮幸 。