Immortalized Rat Hepatic Stellate Cells (HSC-T6)
Cat.No.: CSC-I2673Z
Culture Properties: Adherent
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The HSC-T6 cell line is an immortalized rat hepatic stellate cell (HSC) line established by SV40 large T‑antigen transfection of primary stellate cells isolated from an adult male Sprague‑Dawley rat. Hepatic stellate cells are perisinusoidal liver cells specialized in vitamin A (retinoid) storage; upon liver injury they transdifferentiate into activated myofibroblasts, the principal source of extracellular matrix (ECM) in hepatic fibrosis.
The primary advantage of HSC‑T6 is its constitutively activated, myofibroblast‑like phenotype that faithfully recapitulates fibrogenic HSCs without the need for exogenous activation. Unlike quiescent primary HSCs, which spontaneously activate on plastic and exhibit substantial donor‑to‑donor variability, HSC‑T6 provides a homogeneous, reproducible, and unlimited cell supply for mechanistic studies. The cells robustly express fibrotic markers including α‑smooth muscle actin (α‑SMA), glial fibrillary acidic protein (GFAP), and desmin, and secrete TGF‑β, type I collagen, and other ECM components, closely mimicking the activated HSC phenotype in fibrotic liver.
Additional advantages include rapid growth (doubling time ~10 hours), high homogeneity, experimental reproducibility, and the ability to overcome ethical and technical challenges associated with primary HSC isolation-which is time‑consuming, yields low cell numbers, and is subject to significant lot‑to‑lot variation. HSC‑T6 is also amenable to high‑throughput drug screening and has extensive molecular characterization, including a defined short‑tandem‑repeat (STR) profile and transcriptome analysis, ensuring reliable cell authentication. Owing to these features, HSC‑T6 has become a gold‑standard in vitro model for studying hepatic fibrosis, retinoid metabolism, and the pathophysiology of chronic liver diseases such as cirrhosis, as well as for evaluating novel anti‑fibrotic therapies.
Hyaluronic Acid Modified Extracellular Vesicles Targeting Hepatic Stellate Cells to Attenuate Hepatic Fibrosis
Transforming growth factor-beta1 (TGF-β1) plays a pivotal role in promoting hepatic fibrosis, pirfenidone (PFD) could inhibit TGF-β1 signaling pathway to alleviate hepatic stellate cells (HSC) activation mediated hepatic fibrosis. The targeting delivery strategy of PFD to hepatic stellate cells is a challenge. Extracellular vesicles (EVs), cell-derived membranous particles are intraluminal nano-vesicles that play a vital role in intercellular communication, they also be considered as an ideal nano-carrier.
In this study, we developed a target strategy to deliver PFD to HSC with CD44 over-expression by EVs, hyaluronic acid (HA) modified DSPE-PEG2000 endows the active targeting ability of activated HSCs to PFD-loaded EVs.
In both rat hepatic stellate cell line HSC-T6 and rat hepatocyte cell line BRL, HA@EVs-PFD demonstrated the capacity to down-regulate the expression of collagen-synthesis-related proteins and showed superior inhibition efficacy of HSC-T6 activation compared to free PFD. In hepatic fibrosis model, 4 weeks of HA@EVs-PFD treatment resulted in a reduction in liver collagen fibers, significant improvement in hepatic cell morphology, and amelioration of hepatic fibrosis.

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