Hepatic stellate cells

High levels of glucose promote the activation of hepatic stellate cells via the p38-mitogen-activated protein kinase signal pathway

L. K. Wu, Liu, Y. C., Ma, G., Shi, L. L., He, X. M., Wu, L. K., Liu, Y. C., Ma, G., Shi, L. L., and He, X. M., High levels of glucose promote the activation of hepatic stellate cells via the p38-mitogen-activated protein kinase signal pathway, vol. 15, p. -, 2016.

The relationship between the p38-mitogen-activated protein kinase (p38-MAPK) signal pathway and high glucose-induced hepatic stellate cell (HSC) activation was investigated in this study. Sixty human HSC samples were randomly selected and used in the control (cultured normally), high-glucose (cultured in the presence of high glucose), and blocking (cultured under high-glucose conditions in the presence of the p38-MAPK inhibitor, SB203580) groups.

Effect of bone marrow mesenchymal stem cells on the TGF-β1/Smad signaling pathway of hepatic stellate

X. E. Sun, Zhang, X. Q., and Liu, M. M., Effect of bone marrow mesenchymal stem cells on the TGF-β1/Smad signaling pathway of hepatic stellate, vol. 14, pp. 8744-8754, 2015.

This study investigated the effect of bone marrow mesenchymal stem cells (BMCs) on the transforming growth factor-β1 (TGF-β1)-induced activation of the Smad signaling pathway in rat hepatic stellate cells (HSCs). There were four experimental groups: 1) a blank control group, 2) a TGF-β1 treatment group, 3) an MSC-combined group, and 4) an induced MSC-combined group. Isolation and culture of rat liver HSCs in vitro and the proliferation of HSCs in each group were detected by MTT method.

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