原代肝细胞培养基

肝细胞培养基是为正常人类肝细胞体外培养设计的适于其生长的培养基。是经灭菌的液体培养基，包含必需和非必需氨基酸、维生素、有机和无机化合物、激素、生长因子、微量矿物质和低浓度胎牛血清(5%)。该培养基缓冲体系为重碳酸盐，在含5%CO2的细胞培养箱中平衡后pH值为7.4。该培养基的配方能够选择性的促进正常人类肝细胞体外培养中的增殖和生长，并为其达到理想营养平衡状态提供数量上和质量上的保证。

肝细胞培养基包含500 ml基础培养基，25ml胎牛血清(FBS,目录编号0025)，5ml肝细胞生长添加物(HGS,目录编号5252)和5 ml青霉素/链霉素溶液(P/S,目录编号0503)

1. Widjaja, A.A., Lim, WW., Viswanathan, S. et al. Inhibition of IL-11 signalling extends mammalian healthspan and lifespan. Nature (2024).

For healthspan and lifespan, ERK, AMPK and mTORC1 represent critical pathways and inflammation is a centrally important hallmark1,2,3,4,5,6,7. Here we examined whether IL-11, a pro-inflammatory cytokine of the IL-6 family, has a negative effect on age-associated disease and lifespan. As mice age, IL-11 is upregulated across cell types and tissues to regulate an ERK–AMPK–mTORC1 axis to modulate cellular, tissue- and organismal-level ageing pathologies. Deletion of Il11 or Il11ra1 protects against metabolic decline, multi-morbidity and frailty in old age. Administration of anti-IL-11 to 75-week-old mice for 25 weeks improves metabolism and muscle function, and reduces ageing biomarkers and frailty across sexes. In lifespan studies, genetic deletion of Il11 extended the lives of mice of both sexes, by 24.9% on average. Treatment with anti-IL-11 from 75 weeks of age until death extends the median lifespan of male mice by 22.5% and of female mice by 25%. Together, these results demonstrate a role for the pro-inflammatory factor IL-11 in mammalian healthspan and lifespan. We suggest that anti-IL-11 therapy, which is currently in early-stage clinical trials for fibrotic lung disease, may provide a translational opportunity to determine the effects of IL-11 inhibition on ageing pathologies in older people. Less

2. Harmon, B., Bird, S.W., Schudel, B.R., Hatch, A.V., Rasley, A. & Negrete, O.A.(2016) 'A GenomeWide RNA Interference Screen Identifies a Role for Wnt/?Catenin Signaling during Rift Valley Fever Virus Infection' J Virol. VOL 90

Rift Valley fever virus (RVFV) is an arbovirus within the Bunyaviridae family capable of causing serious morbidity and mortality in humans and livestock. To identify host factors involved in bunyavirus replication, we employed genome-wide RNA interference (RNAi) screening and identified 381 genes whose knockdown reduced infection. The Wnt pathway was the most represented pathway when gene hits were functionally clustered. With further investigation, we found that RVFV infection activated Wnt signaling, was enhanced when Wnt signaling was preactivated, was reduced with knockdown of β-catenin, and was blocked using Wnt signaling inhibitors. Similar results were found using distantly related bunyaviruses La Crosse virus and California encephalitis virus, suggesting a conserved role for Wnt signaling in bunyaviral infection. We propose a model where bunyaviruses activate Wnt-responsive genes to regulate optimal cell cycle conditions needed to promote efficient viral replication. The findings in this study should aid in the design of efficacious host-directed antiviral therapeutics. Less